Everything You’ve Always Wanted to Know About Fish Allergy

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There are tens of thousands of different types of fish swimming around our seas, of which we eat several hundred. Each of those types of fish contains differing amounts of different allergens in different parts of their bodies. Some of those fish harbour bacteria and parasites that also produce allergy-like symptoms. All of which makes diagnosing fish allergy quite difficult. But getting a proper diagnosis is worth the effort because you can probably eat some species of fish, and you don’t want to miss out on all those healthy vitamins and fatty acids if you don’t have to.

And now for the details, which include:

What is an allergy to fish?

There are more than 32,400 species individual species of finned fish, mainly categorised into two classes; bony fish (Osteichthyes) and cartilaginous fish (rays and sharks—the Chondrichthyes). The most frequently eaten species are bony fish and they belong to a limited number of orders:

• Gadiformes—the cod-like (e.g. cod, hake, pollock)
• Salmoniformes—the salmon-like (e.g. salmon, trout, char)
• Perciformes—the perch-like (e.g. tuna, mackerel, barracuda)
• Clupeiformes—the herring-like (e.g. herring, pilchard)
• Cypriniformes— the carp-like (e.g. carp, anchovy)
• Siluriformes—the catfish-like (e.g. catfish, pangasius)
• Pleuronectiformes—flatfishes (e.g. sole, flounder, whiff)

Although those fish are the most commonly consumed, there are about different 800 types available to eat around the world, and what gets eaten varies according to regional availability and local eating habits.

The most popular fish in Europe are tuna, salmon and cod, followed by Alaska Pollock, hake and herring. In America, pangagius, tilapia and catfish are also commonly consumed. In the southern hemisphere, flathead, Asian carps, barramundi and sharks are often on the menu.

In 2019, the EU was the 5^th largest producer of fish and the US the 6^th largest, coming in behind China, Indonesia, India, and Vietnam. Within the EU, the biggest consumers of fish are the Portuguese (at an average of 58 kg per person) and the smallest are the Czechs (at an average of about 6 kg per person).

Fish is the main or only source of animal protein in many developing countries and, in the last few years, consumption of fish has been on the rise in other countries, due to its reputation for being, among other things, good for your brain, good for your heart and able to reduce the risk of certain types of cancer.

Unfortunately, this increase in consumption has also been associated with an increase in reports of fish allergy in a small percentage people. This happens because their body’s immune system mistakes one or more harmless fish proteins for toxic invaders and creates IgE antibodies against them. The next time they eat fish, 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.

We consume several parts of the fish. Fish muscle is cooked, fried, pickled, or eaten raw, fish eggs (caviar) are often enjoyed as a delicacy, fish collagen (and its hydrolysed form, gelatin) is added to many food products, and fish blood (hemin) is used by the food industry as an additive or processing aid.

Although fish muscle contains the most allergens, all parts of the fish can cause allergic reactions (although the blood only seems to provoke allergic reactions in fish processing workers).

Fish allergy is not a new phenomenon. One of the first documented cases comes from Flemish doctor Jan Baptista van Helmont, who reported several asthmatic attacks following the ingestion of fish in his magum opus, Ortus medicinae (translated into English as Oriatrike or, Physick refined in 1662).

And fish allergy was at the heart of a 1921 study that kick-started the scientific investigation of allergy. A few years after the war, doctor Carl Prausnitz happened to read a report of a patient who had received a blood transfusion from a donor who was allergic to horses and had subsequently become allergic to horse dander.

Curious as to whether the blood of an allergic person might contain a substance that could sensitise someone else, Prausnitz decided to investigate. He took some serum from a colleague—Heinz Küstner—who was allergic to fish, and some serum from a non-allergic colleague, and injected it into his own skin. The next day, he injected fish extract into the same areas and got a positive result—a classic weal and flare reaction—proving that sensitivity could be transferred from an allergic to a non-allergic person by something present in blood serum (which we now know to be IgE antibodies). This experiment later became known as the ‘Prausnitz–Küstner (PK) test’ and it was widely used to investigate sensitisation.

Fish allergens can provoke reactions when we eat fish, when we inhale cooking or processing vapours and when we touch it. How a person is initially exposed to fish allergens seems to determine whether or not they develop a food allergy (generally when exposed to food via the gut or skin) or a respiratory allergy (generally when exposed to aerosolised proteins). Typical allergic reactions can range from mild to life-threatening.

As well as immediate, IgE-mediated reactions, fish also causes non-IgE-mediated, delayed reactions, and mixed reactions (that involve both IgE- and non-IgE-mediated mechanisms). These include atopic dermatitis (AD), aka allergic eczema—which I shall now just call ‘eczema’ (although, strictly-speaking, AD is the most common subtype of eczema)—food protein-induced enterocolitis syndrome, (FPIES) and eosinophilic oesophagitis (EoE).

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, the first letter of the species and a number reflecting the order in which they were identified. For example, one of the most important allergens used for diagnostic purposes is a parvalbumin from the Baltic cod—Gadus callarias—named Gad c 1.

There are thousands of different types of fish, all containing different allergens. To date, 40 allergens from around 17 different species of fish (see Table 36), mainly those commonly consumed in Europe, have been described and are officially recognised by the World Health Organization/International Union of Immunological Societies.

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How common is fish 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

IgE-mediated allergy to fish is relatively common in some parts of the world, but much less so in others. The percentage of people with fish allergy is generally higher in coastal countries, which tend to have a higher fish consumption (and certainly more fish-processing industries) than land-locked countries.

A 2016 review of 61 studies carried out worldwide revealed that the prevalence of fish allergy varies between 0% and 7%, partly due to geography and different study populations, and partly due to the method of diagnosis. When people are sent a questionnaire and asked to self-report any allergies, the percentage rate tends to reach around 7%, but when oral food challenge tests—the gold standard of food allergy diagnosis—are carried out, the prevalence is generally reported to be between 0% and 0.3%.

In 2023, a team of researchers investigating the prevalence of the 8 biggest food allergens in Europe reviewed 60 fish-related studies carried out in the whole region and calculated that around 0.45% of Europeans had been diagnosed with fish allergy during their lifetimes. The percentage of people who had either failed a food challenge or had a convincing history of reacting to fish and therefore had a confirmed allergy was much lower, at 0.05%.

The highest prevalence rates in Europe tend to be reported in populations that traditionally eat a lot of seafood. The European EuroPrevall project has carried out community-based surveys in several European centres and has reported that allergies to fish in both children and adults are more common among Icelanders and people who live in Mediterranean countries, and more often involve white fish rather than oily fish.

In Spain, fish has been reported to be the third most common food allergen, behind egg and milk, in children under 2 years old, demonstrating a clear link between the introduction of the food into a child’s diet and the appearance of reactions. Fish allergy also shows up early in Iceland, where a prevalence of 0.22% has been noted in infants under the age of 1.

Fish is also a popular food in the Scandinavian countries, although the studies from this region of their world are even older, so the current prevalence of fish allergy is uncertain. In 1982, Finnish parents reported it to be one of the most common allergenic foods among children under 6 years old. A 2005 study of two generations of Fins and Russians reported that 0.3% of Finnish children and 2.8% of their mothers and 0.2% of Russian children and 1.9% of their mothers were sensitised to fish.

In Norway, parent reports of food allergy in their toddlers in 1999 produced an estimated fish allergy prevalence of 3% in the under 2-year-olds but, when questioned 6 months later, the numbers of reactions being reported to food were down by two thirds. Six years later in Denmark, 898 children and 936 adults were given oral food challenges with cod to confirm food allergies in their population; none of the children had allergic reactions and 2 (0.2%) of the adults did.

Studies using food challenges always give much lower numbers than studies using questionnaires or skin prick and/or blood tests, but they are not necessarily representative because they include far fewer people, in part because they are expensive and time consuming and consent is often not given for the testing, but also because, according to standard practice, food challenges for IgE-mediated allergies tend to be given to people with an unsure clinical history who are unlikely to react to the food. The real prevalence rate is probably somewhere in between that estimated by challenges and that estimated by lab tests.

Accordingly, the prevalence of fish allergy among children in the UK and Turkey as measured by food challenges has been found to be 0.0006% and 0.0002%, respectively. In comparison, according to parental report, fish is the seventh most common food trigger of reactions among British 11-year-olds living on the Isle of Wight, and the fifth among 15-year-olds, giving a combined prevalence of 0.7%.

Elsewhere in Europe, a 2004 German study reported that, according to skin prick tests, 0.5% of the adult population were sensitised to herring and 0.4% to mackerel (Germany being the only country in the most recent European studies to register a higher rate of allergy to oily fish than to white fish). A year later in France, 6672 schoolchildren aged 9–11 years were given skin prick tests and 0.7% were found to be sensitised to fish.

In the US, a 2019 survey of a nationally representative panel of adults estimated a prevalence of fish allergy of 0.9% (about 2.2 million people), 2 in 5 of whom developed their allergy during adulthood. (Allergies in this case were determined using a set of questions and symptom criteria developed by a panel of experts) A similar survey of (the parents of) children reported a fish allergy prevalence of 0.6% (about 400,000 children), almost half (49%) of whom had a history of severe allergic reactions.

In Canada, a 2010 telephone survey of 9667 random people with questions about their food allergies reported a ‘perceived’ prevalence of fish allergy of 0.51% and a ‘probable’ prevalence (based on clinical history or physician diagnosis) of fish allergy of 0.48% for the whole population; 0.18% for children and 0.56% for adults.

In Australia, where fish is popular than in other English-speaking countries, a study that included 2,999 children with allergies reported that 5.6% of them were allergic to seafood with the most common food triggers in the category being shellfish (prawns), followed by white fish, tuna and salmon.

In the Middle East, where seafood is commonly consumed, a questionnaire-based study in Kuwait found fish to be the second most common allergen among schoolchildren aged between 11 and 14 and put the prevalence of fish allergy (based on a history of convincing reactions) at 1.6%. Another questionnaire-based study in the United Arab Emirates reported that fish was the third most common food allergen among children aged between 6 and 9 and put the prevalence of fish allergy at around 2.6%.

Fish allergy is also common in Asia where fish is a popular food and introduced relatively early into a child’s diet—as early as 6 months old—although fish allergy is not uniformly common in this large region of the world.

In Vietnam, research has revealed that seafood is the most common cause of allergic reactions, with a questionnaire-based study among the parents of 2- to 6-year-old children in two different regions in Vietnam reporting that crustaceans are the most common cause of reactions in young children, followed by fish, and a population-based survey conducted among University students aged 16–50 years reporting that the prevalence of doctor-diagnosed fish allergy of 1.6%, sandwiched in between the numbers of diagnosed allergy to crustaceans and to molluscs.

A parent questionnaire of preschool children in northern Thailand revealed that fish was the third most commonly reported food allergen, after shrimp and milk, and a 2012 survey of 2,034 Thai, 6,498 Singaporean and 11,434 Filipino students found that 0.29%, 0.26% and 2.29% of them reported a convincing fish allergy.

In Korea, a nationwide survey of the parents of Korean schoolchildren reported a prevalence of convincing immediate-type symptoms to fish in 0.32% of the children, with fish being reported as the fourth most likely food group to provoke anaphylaxis, after fruits, crustaceans and nuts.

In China, the prevalence of fish allergy lies between 0.17% – 0.21% according to a study that examined children in 3 Chinese cities in the south west and south east of the country. In one of those cities, 0.21% (1 in 477) infants under the age of 1 tested positive for a sensitisation to fish, and fish was not mentioned at all as a cause of reactions in a survey about Hong Kong Chinese preschoolers.

Non-IgE-mediated and mixed allergies

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

About 2.6% of the global population is estimated to be affected by eczema, or 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.

Adults with eczema tend to be allergic to different foods than young children; namely those which are cross-reactive with airborne allergens—like celery, carrots, hazelnuts and shellfish—and those which people tend to start eating when they’re older (such as fish, in Western countries).

An old review of the records of American children with eczema seen at one medical centre during a 13-year period reported that 6% were allergic to fish (the 6^th most common food trigger), and a more recent review of Thai children with eczema seen at a medical centre during the period of 1 year reported that 13% were sensitised to fish (the 8^th most common allergen). This number is probably greater than the one reported in the American study because a) it refers to sensitisation, and more people are sensitised to foods than are allergic to them, and b) because fish is a more common staple in Asia so more people are likely to be sensitised and allergic to it.

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

Research from the Czech Republic has put the prevalence of fish allergy among adolescents and adults with eczema somewhere between 11% and 13% and has shown that only around 1 in 3 may suffer from a worsening of their skin condition after eating fish, while the rest will experience classic IgE-mediated symptoms.

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.

FPIES to fish is more common in southern European and Mediterranean countries than it is elsewhere. In France, studies involving children with FPIES have reported fish to be the second or third most common trigger, behind cow’s milk and, occasionally, egg. In Spain, it’s the second most common trigger in children, behind milk, and it’s the most common trigger—tied in first place with shellfish—in adults. In Italy, it was the second most common trigger but the most recent study put it at number one. In Greece, it ‘s also the most common trigger and in Turkey, it’s number 2.

This contrasts with countries like the US and Australia, where the most common FPIES triggers are milk, soy and grains. But lest we think that English-speaking people just don’t like to eat fish, a British study of paediatric patients seen at one London clinic during a 3-year period reported fish as the second most common trigger.

FPIES, as allergists are in the process of discovering. is not just a childhood illness, and FPIES to fish in particular is more commonly found in adolescents and adults, (even American adults) second as a trigger only to crustaceans. In fact, fish and shellfish are by far the most common triggers for adult FPIES than any other food, wherever you find yourself in the world (5) and, although the list of trigger foods is getting longer, currently, children show more ‘geographic heterogeneity’—i.e. different foods trigger the condition in different parts of the world, probably because of different cultural eating habits—in their triggers than adults, although whether this is because of a difference in the mechanisms and risk factors of FPIES in adults, or whether this is due to the fact that we still have a lot to learn about adult FPIES, including all the triggers, is currently unknown.

Many cases of FPIES in the Mediterranean are caused by white fish, like hake and sole, as well as by anchovies and sardines, and the great majority of people with FPIES seem to be allergic to a single fish, rather than multiple species.

Cases of eosinophilic oesophagitis (EoE) have 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.

As far as fish is concerned, it is very rarely a reported trigger for EoE. To date, the only cases seem to be reported in Spain, where EoE was found to be triggered by fish in 8 out of 42 adults in one study, and 4 out of 64 patients in another.

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Will it go away?

IgE-mediated allergy

Fish allergy generally develops in childhood, when fish is introduced into the diet (sensitisation may even occur earlier, via breast milk), although suddenly becoming allergic to fish during adulthood is not unusual. And, unlike allergies to milk and egg, fish allergy is often persistent.

A 2004 national phone survey of Americans revealed that only about 3.5% of the fish-allergic reported outgrowing their allergies. A review of children who had been to an allergy clinic in Turkey after suffering an anaphylactic reaction to food between 2010 and 2020 reported that those who had an allergy to seafood were much less likely to outgrow it than those who were allergic to another food; of the 9 children who had had a severe reaction to seafood, only 1 had outgrown their allergy, compared to the 40% (30 of 74) who outgrew their allergy to milk, for example. A Greek study that tested 52 fish allergic children over a period of 9 years reported that 4 of them outgrew their allergy during the study period.

It’s not all bad news. Another Greek study revealed that almost two thirds (19 of 29, 65.5%) children who had been allergic to fish when they were 3 years old had outgrown their food allergy by the time the study had finished (when they were aged between 8 and 14). Those whose allergy did not resolve, however, were at an increase risk of developing hyperactive airways and wheezing when they reached school age.

But tolerance of fish does tend to increase with age and, over time, many people with fish allergy will see their immune system’s reactivity decrease and will discover that they can tolerate less allergenic fish species like tuna and swordfish.

A retrospective analysis of 81 fish-allergic Portuguese patients published in 2020 revealed that 60—almost three quarters—of them achieved tolerance to at least one fish species during the decade they were followed up on, and 5 of them (8%) became tolerant to all fish species. Most achieved some sort of tolerance between the age of 10 and 11, and tuna was generally the first and most widely-tolerated fish, followed by cod, salmon and hake.

There are also documented cases of spontaneous allergy resolution, including the case of a Portuguese boy who experienced his first reactions— difficulty breathing, hives and vomiting—when he was around 10 months old after eating hake and mackerel but was able to eat a variety of fish by the age of 14.

And there’s the case of a 68-year-old man with a history of anaphylaxis triggered by fish who not only started testing negative to several types of fish he had previously tested strongly positive to, but was also able to start eating salmon, cod and halibut again without experiencing any allergic reactions.

Non-IgE-mediated and mixed allergies

The news is less positive when it comes to non-IgE-mediated conditions to fish. A 2013 review of children with eczema reported that those who were allergic to fish were less likely to see their symptoms resolve than children with eczema who were allergic to most other foods.

Similarly, when it comes to FPIES, all of the published research suggests that, compared with FPIES to milk or other solid foods, fish-induced FPIES is more likely to have a later resolution. If indeed, it resolves at all.

Some research has produced a relatively optimistic prognosis for Spanish children with fish-induced FPIES, with one study reporting that FPIES to fish and egg resolves in 3 of 4 children by the age of 5, and another one that followed 135 children with FPIES (56 of whom had fish as a trigger) over a 10-year period stating that tolerance was mostly reached at the age of 2 and a half, and another that followed 70 people diagnosed with FPIES to fish when they were children for 20 years stating that 4 in 5 outgrew their condition during childhood

However, smaller studies following a few children with fish-induced FPIES have also highlighted that FPIES to fish resolves relatively slowly compared to FPIES to other foods, with a study of 16 children reporting that only 3 had achieved tolerance by the age of 4 and a half, and another study reporting that children with FPIES to fish generally outgrew the condition a year later than those with FPIES to other solid foods. And only 5 of their 12 patients had managed to outgrow their condition at all by the end of the study period.

In Italy, research has proposed an even less optimistic outlook for children with FPIES to fish, with one study of 70 children (56 with FPIES to fish) reporting that FPIES to fish took longer to resolve than FPIES to other foods (and noting that only 1 in 3 children in the whole group managed to outgrow their condition by the age of 8 and a half), and another study following 3 children with fish-induced FPIES reporting that none had achieved tolerance by the age of 6.

In Greece, a recent study (1) reported that half of their small group of fish-allergic subjects had not managed to outgrow their condition during the 10 years that they were followed and, in Turkey, fish-induced FPIES has also been found to be persistent.

Likewise, in the US, one study reported that none of their paediatric patients had managed to outgrow FPIES to fish by the age of 5, and another study of older children (aged between 6 and 17) stated that cases of FPIES to fish were the least likely to resolve.

However, some children may eventually be able to tolerate less allergenic types of fish; a small Spanish study that followed 14 infants with FPIES for up to 7 years after diagnosis reported that, while only 4 became tolerant to all fish, 3 were able to tolerate swordfish by the end of the study period.

Cases of FPIES in adults are even less likely to resolve, with one study of seafood-induced FPIES in Spanish adolescents and adults finding that only 4 of 25 people were ultimately able to tolerate their triggers (3 of them had the condition for about 3 years before it resolved, and 1 had it for 21 years) and another study of Spanish adults with FPIES reporting that, the longer an adult had symptoms, the less likely their condition was to resolve. In this study, 18 of 107 adults achieved tolerance and 10 were able to eat small amounts of their trigger foods without showing symptoms by the end of the study period.

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Risk factors for fish allergy

A risk factor for any food allergy is atopy. An atopic person is someone who is prone to developing an allergic reaction in response to a trigger. Studies have shown that the presence of other allergies is a risk factor for allergic reactions to food. This is no different when it comes to fish allergy.

Several studies have found that the majority of people with an allergy to fish are likely to have other allergies, like the 43 seafood-allergic children in this American study, 63% of whom had allergic rhinitis (hay fever), 54% of whom had asthma, 32% of whom had eczema and about half of whom had other food allergies.

Or the 43 fish-allergic adults in this Dutch study, 55% of whom had asthma, allergic rhinitis and eczema, and most of whom had other food allergies (55% to peanut, 47% to hazelnut and 42% to walnut).

Or the 167 seafood-allergic children in this Australian study, 94% of whom had ‘co-existent atopic disease’ (notably, asthma).

Or the 29 fish-allergic children in this Greek study, two thirds of whom were also allergic to egg and most of whom also had asthma.

Working with fish. Although the prevalence of fish allergy in the general population hovers at around 1%, it reaches rates of up to 8 % among fish processing workers.

Workers in the fishing industry are exposed to all sorts of fish proteins in their work environment; the wet ones they breathe in from processing fresh fish, the dry ones they breathe in from processing fish meal, and the ones that get into their bodies through skin breaks and cuts while they are handling fish. Occupational allergy and asthma is acknowledged as a serious health problem affecting seafood-processing workers.

Various studies from the UK and South Africa report a prevalence of occupational asthma between 8% and 36% and a prevalence of contact dermatitis between 3% and 11 %.

Smoking and working with fish. Research also finds that people who work in the fish processing industry and smoke have an even higher risk of becoming sensitised to fish and developing occupational asthma, even when they have no previous history of allergy.

Race has been reported as a risk factor for fish allergy. Several American studies have found that African Americans and Hispanics have a higher risk of getting fish allergy than white Americans.

The first was the 2004 phone survey in which black people reported the highest rates of seafood allergy.

More recently, a 2016 study reported a big difference in the prevalence of fish allergy between different ethnicities, finding that 3.4% of white children were sensitised to fish, compared to 16.16% of Hispanic children and 34.39% of African American children. The latter also had higher rates of eczema and asthma that the other 2 ethnicities, and the Hispanic children had higher rates of eczema than the white children, but similar rates of asthma.

A 2020 study confirmed a higher prevalence of fish allergy (and asthma) amongst African Americans compared to white children and a recent review of intensive care admissions between 2010 and 2015 involving American and Canadian children found that fish was the second most common trigger of anaphylaxis among black and Hispanic children.

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Cross reactions to finned fish

Technically-speaking, a person can be allergic to onetype of fishand 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 in the 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.

Fish is considered one of the food families with the highest rates of cross-reactivity and there are many reports of people being sensitised or allergic to several species of fish.

Test tubes studies have found a high level of potential cross-reactivity between closely related fish such as cod and eelpout (aka burbot) and among fishes that are distantly related—like cod and plaice, mackerel or herring, cod and wolffish, cod and dentex and cod and swordfish, as well as between the roe from different species of fish. This is probably because of the β‐parvalbumin protein they all contain, and its highly conserved structure.

However, just because cross-reactivity is proven in a test tube does not mean that it will be accompanied by actual symptoms of allergy. For example, in an American study of 11 fish-allergic children and young adults, 8 people had positive skin prick tests to 10 species of fish and 3 to at least 2 fish species. When they were given oral challenges, however, 7 of them had allergic reactions to only 1 fish, one to 2 fish species and two to 3 types of fish.

And when researchers went through 13 years’ worth of medical records of adults patients visiting an allergy clinic in Texas, they found that just fewer than a third (29%) had actually reacted to more than one fish.

In fact, the fish-allergic are probably allergic to fewer types of fish than they think. In a Dutch study, researchers gave 43 fish-allergic adults who were sensitised to multiple species of fish a questionnaire to fill in about their eating habits and the reactions that they had had to the various types of fish they had eaten. 59% of the those questioned reported reacting to all of the fish that they had tried. However, after examining the results of their skin and blood tests to different species of fish and comparing these to the questionnaire answers, the researchers concluded that there was not much correlation between the results of the lab tests and the patients’ reports of allergy or tolerance to those species.

In fact, fish allergy sufferers are only thought to have about a 1 in 2 chance of having allergic reactions to other species of fish. This might be because, while the secondary and tertiary structures (the shape) of parvalbumins are very similar, the primary structure (the amino acid sequence) is often quite different.

In an American phone survey of 14,948 random people, of the 58 (0.4 %) people who reported an allergy to fish, 5 (9%) reported reacting to two types of fish and 13 (22%) to over 3 types, and in a study in which 9 American adults with fish allergy were given oral food challenges with several different fish, 4 reacted to more than one fish. Similarly, a study of 95 Australian children reported that 93% were sensitised to several types of fish but that only one third had had allergic reactions to at least two species.

In some countries like Japan, however, people with fish allergy have reported a lot of cross-reactions. A 2016 survey filled out by 95 people with fish allergies (about 1 in 4 of whom had a doctor’s diagnosis of fish allergy) found that 88% of those surveyed reported reactions to at least 3 types of fish. Although most people experienced skin symptoms, around 1 in 3 said that they experienced respiratory symptoms. None of these people actually underwent a formal food challenge, however.

Fish can, on rare occasions, cross-react with shellfish but, because the major allergenic proteins in fish and shellfish are different, people are more likely to be allergic to one group or the other, but not to both. In the American telephone survey mentioned previously, for example, only 0.2% of the people with a seafood allergy reported an allergy to both fish and shellfish.

The main allergen responsible for a cross-reaction between fish and shellfish is tropomyosin. Although examples are rare, there are a smattering of case reports reporting a tropomyosin-induced cross-reaction. One such case is the one that kicked off the entire effort to confirm that vertebrate tropomyosins were allergens in the first place. It involves a 19-year-old man who was 13 when he started having symptoms to several species of fish and molluscs. A thorough work-up confirmed that he was reacting to the tropomyosins in the fish and shellfish. His reactions to fish involved digestive pain and wheezing, but no skin symptoms.

Another case is that of an 11-year-old boy who was admitted to hospital in Spain with breathing problems after eating shrimp for the first time. Although he was known to be allergic to fish—he had experienced mild symptoms confined to the mouth and throat (oral allergy syndrome) after eating hake and cod before—he was not known to be allergic to shellfish; he had also eaten octopus before, without problem. Blood tests revealed that he was sensitised to several types of fish, shrimp and several other arthropods, as well as molluscs including octopus.. Further tests revealed that he was reacting to fish and shellfish tropomyosins.

A third case report mentioning such a cross-reaction involves a 16-year-old girl who had several episodes of anaphylaxis after eating food containing both shellfish and fish. Lab tests revealed that she was allergic to several types of shellfish and anchovies.

Cross reactions, or co-allergies, between fish and shellfish seem to be more frequent in people with the non-IgE-mediated disease food protein–induced enterocolitis syndrome (FPIES). Both Spanish and American studies have noted associations between reactions to fish and reactions to shellfish, with Spanish research in particular finding that about half of adults with fish-induced FPIES react to shellfish, and just over half (55%) of adults with shellfish-induced FPIES react to fish.

Those who are allergic to fish but fancy trying a different type of aquatic creature should be warned that more exotic creatures like frog and crocodile may also be off the menu.

Researchers at a hospital in Luxembourg tested patients allergic to fish and allergic to fish and frog and found that they both shared cross-reactive forms of parvalbumin, and Japanese researchers have advised some fish-allergic patients to avoid the local delicacy, bullfrog.

As for crocodiles, they also contain parvalbumins that fish-allergic people react to, and at least one case of anaphylaxis to crocodile meat has been reported.

Finally, land animals are not necessarily safe for people allergic to fish, either: thanks to those pesky parvalbumins, fish-chicken syndrome is a thing. This term was coined in the lab in 2016, after researchers took some patients who were allergic to both fish and chicken and used blood samples samples to demonstrated that a large majority reacted to several allergens— parvalbumin as well as aldolase and enolase—in both fish meat and chicken meat.

Luckily, these kinds of reactions—like this case of someone who was allergic to fish developing asthma after eating chicken—are pretty rare and there appears to be no cross-reactivity between fish eggs and chicken eggs.

Image by Joshua Chekov on Unsplash

Symptoms of fish allergy

Fish 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 fish

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 fish 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.

There are three main routes to developing an IgE-mediated allergy to fish, and the route taken affects the type of allergy that you get and the principal symptoms that go with it.

1. You can become allergic to fish via gastrointestinal sensitisation—i.e. by eating it. This tends to produce the ‘classic’ signs of allergy.

The classic symptoms of fish allergy include:

• oral allergy syndrome (OAS, commonly manifesting as ‘itchy’ or ‘burning’ symptoms often limited to the mouth, sometimes also swollen lips and cheeks)
• facial swelling
• hives
• sudden-onset vomiting
• stomach pain
• diarrhoea

Oral allergy syndrome is often the first subjective symptom experienced by someone who is having an allergic reaction to fish, and it’s often followed by a feeling of tightness in the chest, an irritated nose and stomach cramps.

Pro tip: If you suddenly start to feel itchiness or swelling in your throat and/or mouth and/or lips while you’re eating something you know contains fish, you should stop eating immediately before the symptoms get worse.

Adults with a classic allergy most commonly report skin symptoms—hives, swelling (angioo-oedema), flushing and itchiness—followed by respiratory symptoms—shortness of breath, chest tightness, wheezing, cough and throat swelling.

That said, fish is one of the foods most likely to provoke anaphylaxis, although this varies significantly between patient populations and countries.

For example, a Portuguese review found that fish accounted for 18.8% of the cases of anaphylaxis in children and 6.7% of the cases in adults in 2016, in Italy, those numbers are around 8–9% for children and 7% for adults whereas, according to one review, fish only caused around 2.1% of the cases of anaphylaxis in children admitted to a Korean hospital between 2009 and 2013.

Fish meat is not the only cause of anaphylaxis. There are also a number of reports of anaphylactic reactions to fish eggs (roe/caviar) from various types of fish, including beluga caviar, salmon, kingfish and whitefish. Although many of the cases have been reported in adults, there have also been reports of reactions in children. It’s not uncommon for a person to have serious reactions to fish roe but not to react to fish meat.

Collagen and gelatin can also provoke serious reactions.

Although the vast majority of these types of reactions are caused by eating fish, some can be caused by indirect contact with fish, for example being kissed by someone who has just eaten fish, or inhaling the vapour of cooking fish, or even eating chicken fed with fish-based fodder.

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.

Fish has also been reported to cause other types of severe symptoms, including acute pancreatitis, a sudden inflammation of the pancreas which generally manifests as stomach pain and can normally be treated with no lasting damage.

2. You can become allergic to fish via inhalation—i.e. by breathing allergens in. This generally results in respiratory symptoms, although it can eventually lead to the ‘classic’ symptoms of food allergy.

The symptoms include:

• blocked or runny nose, itchy nose, sneezing, mucus draining from your nose into your throat (rhinitis)
• red, itchy eyes (conjunctivitis)
• wheezing
• feeling of chest tightness
• shortness of breath
• coughing

Most cases of respiratory allergy to fish can be found among people who work in the seafood industry and are exposed to aerosolised fish proteins as splashback while gutting, de-heading and deboning fish, in steam while cooking fish or in dust while bagging fishmeal, as well as when they clean the processing line and storage tanks with high pressured water.

Occupational asthma is particularly common. Asthmatic symptoms have been reported among fishermen who work on board fishing vessels and people employed in land-based seafood processing factories, such as salmon processors in Sweden, Spain and the UK, trout processors in Denmark, Spain and the UK, and anchovy processors in Spain and South Africa, as well as workers processing a range of other fresh fish, people producing fishmeal and employees on fish farms.

In fact, so many workers suffer from respiratory problems because of occupational exposure to aerosol allergens generated during seafood processing that the International Fishing Industry Safety & Health Conference put out a statement after their 2019 conference recommending that better measures be taken to protect workers from nebulised fish.

The good news for people processing fish is that research shows that occupational asthma is more commonly associated with shellfish (4–36%) than with bony fish (2–8%).

In Greenland, a study of seafood workers has revealed that people who work with fish are less likely to become sensitised to the food they process than people who process shellfish, but they do run a relatively high risk of becoming sensitised to the fish parasite Anisakis simplex (more on that nematode later), and the longer they work as fish processors, the more likely they are to become sensitised to it.

The risk of becoming allergic to Anisakis simplex has also been reported in a South African study that also noticed a sex difference between the symptoms experienced by workers; men were more likely to be sensitised to fish or have an airway obstruction, whereas women were more likely to get asthma-like symptoms. This, the authors suggested, was probably due to gendered work tasks (the men were engaged in more manual and dusty fishmeal production tasks while the women worked in the humid cannery), and the fact that a large proportion of the women were seasonal workers who were unlikely to return to work if their asthma symptoms persisted.

This last factor, incidentally, leads to what is called ‘the healthy worker survivor effect’ which describes the fact that people who remain employed tend to be healthier than those who leave, something that has to be taken into account when studying occupational diseases because it means that the number of people affected by severe symptoms of allergy could be underestimated.

The Greenland study also reported that people who did not directly work with seafood, but worked in administration, packing or landing, for example, also ran a small risk of becoming sensitised to fish.

Typically, workers in the seafood industry seem to get hay fever-type symptoms first before later developing asthma.

Although some seafood workers who develop respiratory symptoms are able to eat seafood without problems, others end up experiencing allergic reactions after eating fish or shellfish, most commonly skin symptoms (hives) and gastrointestinal symptoms.

You don’t have to work with fish to develop a respiratory allergy to them; for example, research has reported cases of children who develop breathing problems when they inhale the vapours of cooking fish.

3. You can become allergic to fish by touching it and developing a contact allergy. This generally results in rashes but can later lead to respiratory and ‘classic’ symptoms of allergy.

There are 2 main forms of contact allergy that you can get from regularly touching fish; contact urticaria (CU) and protein contact dermatitis (PCD).

Allergic contact urticaria basically looks like hives; an itchy, a weal and flare reaction that occurs within 10 to 60 minutes of touching the food and disappears within 24 hours.

Protein contact dermatitis describes allergic (or non-allergic) eczema-like reactions to food proteins. It can be chronic or recurrent and tends to occur on the hands, wrists and arms with periods of intensified reactions when you can feel of itching or tingling a few minutes after contact with the food you’re allergic to.

Sometimes symptoms of both contact urticaria or protein contact dermatitis extend to the face, either because someone touches their face with contaminated hands or because of airborne allergens.

Contact allergies are often experienced by professional food handlers because they are more likely to develop when a person is continuously exposed to allergens and to things that affect the integrity of their skin, such as wet working conditions.

Several cases of contact allergy have been documented in the seafood processing industry in Norway, Denmark, Germany and South Africa.

A study carried out in Greenland noted that women were more likely than men to suffer from skin symptoms because of the different tasks they carried out; men were more likely to carry out service, handling and packing tasks, whereas women were more likely to handle fish and to be engaged in lab work and thus more exposed to wet work and gloves which irritate the skin.

Research has also revealed that:

• it’s the liquid (‘fish juice’) from the fish, which has a high protein content, that is most likely to be causing the sensitisation
• the longer the fish has been dead, the more frequent and worse the reactions are likely to be
• workers are likely to suffer chapping and eczema during work and dry skin after work
• people with mutations in their filaggrin—a structural protein essential for the development and maintenance of the skin barrier—are likely to experience more severe symptoms (these mutations, incidentally, affect about to 1 in 10 Europeans and 1 in 20 Asians)

However, working in a kitchen may be more hazardous than working in a processing plant as far as developing a contact allergy is concerned. A French study of fishermen and chefs determined that chefs were more likely to develop contact allergies to fish, probably because they don’t use gloves.

Many of the chefs involved in the study were atopic, a condition which precludes people from working in the French fishing industry; aspiring fishermen with allergies like eczema and asthma tend to be declared medically unfit to work in the profession. So another reason for the lack of reported cases among fishermen may be the fact that the men do not report any contact allergies.

However, backing up this research is the fact that case reports of cooks and restaurant workers developing contact allergies to fish abound.

In Spain, a couple of cases were reported involving fish-cleaners who developed protein contact dermatitis, not because of the actual (cuttle)fish they were cleaning, but because of the smaller fish in the digestive tract of the shellfish.

Workers generally develop symptoms on their hands anywhere between one month to several years after starting work. These contact allergies can develop into food allergies that can include anaphylactic symptoms.

In such cases, the only thing you can do is quit your job, and many do. Not that this always works out, as in the case of a Japanese sushi chef who, after a year of handling raw fish with his bare hands, first got itchy hands before developing OAS as well as breathing problems, diarrhoea and stomach cramps when he ate fish. He then became a sweet maker but developed an allergy to the white bean paste he used to make Japanese sweets after 6 months in that job. No word on what he did after that, but hopefully he had professional interests that lay outside of the food industry.

Not that you have to work in a kitchen to develop a serious contact allergy to fish, as in the case of the German delivery driver who worked for a decade delivering fish and other seafood stored on crushed ice. Although he initially wore the plastic protecting clothing and long-sleeved gloves that were provided for him, over the years his workload and time pressure increased, so he stopped bothering.

After 8 years on the job, he developed conjunctivitis (pinkeye) then contact urticaria on his hands and forearms, which became generalised hives after carrying a full container of seafood pressed against his stomach. This then turned into a food allergy, and he developed hives, facial swelling (angio-oedema), nausea and vomiting after eating fish. He was transferred to another job cleaning fish transport tanks, but on his first day of cleaning developed respiratory symptoms and had to go to hospital. Presumably he also had to find another job which did not involve seafood.

And you don’t have to process, deliver or cook fish to suffer from an occupational contact allergy to them; a case of contact allergy to herring has also been reported in a dolphinarium worker.

That’s not the only case of contact allergy that’s been caused by feeding sea creatures. One study reported that a woman developed contact allergies at her job which involved feeding fish and crabs and found that it was the high histamine content in the food itself that was causing her symptoms, rather than her contact with the fish and shellfish.

Finally, you don’t have to work at all to suffer from contact allergies—in Italy, cases of children developing contact urticaria to fish have also been recorded—and symptoms may be serious. According to a survey of the general American public carried out in 2004, some of the worst reactions described involved skin contact and/or inhalation, although these people were still able to eat fish.

Still, an American study which followed 197 children diagnosed with fish allergy and put on strict fish avoidance diets reported that 29 had had at least two contact reactions with fish in the years after their diagnosis, and 28 of 29 had only suffered from skin symptoms. One of the children had developed localised hives and wheezing. So people with fish allergies who come into contact with fish are likely to have mild reactions.

Delayed reactions to fish

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 fish are eczema (atopic dermatitis, AD), food protein induced enterocolitis syndrome (FPIES) and eosinophilic oesophagitis (EoE).

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

It can be caused by allergy to fish meat and/or collagen/gelatin. A study of 332 Czech patients over the age of 14 with AD, 35 of whom were allergic to fish, reported that people with fish-induced eczema suffered significantly more from persistent lesions (defined as only experiencing a period of less than a month without eczematous lesions somewhere on the body).

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)

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
• dehydration
• transient weakness and shivering (possibly hypothermia)
• lethargy
• weight loss

In general, the symptoms of adolescents and adults seem to be less dramatic than those of younger children, with fewer requiring emergency care.

People who experience severe symptoms of acute FPIES may have a longer-lasting form of the disease. FPIES to fish may also take longer to outgrow than FPIES to other foods.

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)
• abdominal pain
• 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 suspect that you’re allergic to fish, it’s important that you see your GP/family doctor and get a referral to an allergy clinic for further testing.

Threshold for reactions

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 fish is 2.6 mg. (Note: in this case, the ‘population allergic to fish’ is 82 people who were given a DBPCFC.)

26.7 mg was the dose needed to produce a response in 10% of the test subjects, and 418 mg was the dose needed to provoke a reaction in half of the test subjects.

Some studies have found even lower doses are needed for especially sensitive people to feel subjective (i.e. noticeable only to them, such as an itching mouth) reactions: 2.11 mg for one person during a codfish food challenge in one study and 0.7 mg for 10% of the subjects in another study also testing cod.

Note: we’re talking about milligrams of cod protein. The content of parvalbumin—the fish allergen generally responsible for the worse reactions—varies a lot per fish. A study that calculated the parvalbumin content for several popular fish found that tuna contained <0.05 mg of parvalbumin per gram of raw fish meat, mackerel contained 0.3–0.7 mg per gram of raw meat, salmon, trout and cod 1–2.5 mg per gram of raw meat, and carp, herring and redfish >2.5 mg per gram of raw meat. This amount was 20–60% lower when the fish was cooked.

In other words, a serving size of 200 g of cod fillet could contain about 400 mg of parvalbumin (assuming 2.5 mg per gram of meat and a 20% reduction when cooked). Which is just under the dose needed to provoke a reaction in about half of all people who are allergic to fish. But the same amount of tuna would contain at least 50 times less.

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.

Fish has been specifically implicated in cases of food-dependent exercise-induced anaphylaxis (FDEIA).

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

A 2013 study identified seafood as the third most common cause of food-induced anaphylaxis German adults in situations involving cofactors.

Please note: the amount of fish 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, that does not mean that they will continue to be mild.

Image by Ivan Samkov on Pexels

Diagnosing fish allergy

Diagnosing an allergy to a specific fish is not as easy as it may sound. Globally, we consume hundreds of species from different fish families. Each fish contains different amounts of allergens, and perhaps several versions (isoforms) of those allergens, each of which can vary in their allergenicity and in how they react to different cooking methods. Regional differences in how those fish are prepared and consumed can also alter the pattern of sensitisation and produce different symptoms.

A diagnosis of fish allergy will primarily be based on your clinical history—a record of consistent symptoms following the consumption of fish or fish-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).

In the case of fish, a giving a clinical history can be complicated by the fact that it can be difficult to know which species of fish you ate which triggered your symptoms, for example because of vague or misleading labelling, or because you were eating out on holiday. However, the more precise you can be in identifying the type fish that gave you symptoms, the better your chances of getting an accurate diagnosis.

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 fish

Skin tests

An IgE-mediated sensitisation to fish is typically confirmed by a skin prick test, which involves someone placing a small sample of fish 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, but it is generally used to rule out an allergy rather than to confirm one, because it has excellent negative predictive value—if the skin weal is under a certain size, you are highly unlikely to have an allergy—but poor positive predictive value—the skin weal has to be very large before an allergist can say with any kind of confidence that you probably have an allergy.

However, commercially available fish extracts for skin testing are very limited compared to the wide variety of fish that we eat and can become allergic to. Some people are allergic to a specific fish (family) and that fish may not be represented in the range of extracts available.

Additionally, fish extracts are not standardised. One study carried out on 26 commercial fish extracts from five different companies revealed a greater than 10-fold variation in protein content and allergen concentration between the different manufacturers and fish species. The extracts also contained too little of some of the major allergens, including parvalbumin and collagen.

The preparation of fish allergen extracts is complicated by the fact that parvalbumin is found only in white muscle, and fish like tuna have a lot of red muscle in their torso, which means that any samples taken from this region will be missing a vital diagnostic allergen. Fish like tuna and cod also have an uneven distribution of parvalbumin in their white muscle, meaning that you really have to know the fish that you’re sampling from to be sure that you’re getting the right amount of allergen.

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 (in this case, raw or boiled fish) and then it is used to prick your skin. When the food is in liquid form, the technique is actually the same as the one used for the skin prick test and, when the food is solid, it’s 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, although this will depend on which part(s) of the fish has (have) been sampled. The lab used by the clinic can also prepare the extract in specific ways which may add to its efficacy.

Although skin testing is generally considered a safe procedure, there have been some rare cases of severe reactions reported in children and adults as a result of prick to prick testing, so when this type of test is carried out for fish, it needs to be done by well-trained personnel who are equipped to deal with potentially severe reactions.

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.

For more specific information, a component blood test—aka Component Resolved Diagnosis (CRD)—can be carried out. Instead of using extracts of whole foods containing only (heat-stable, plentiful) allergens, the CRD tests the reaction of IgE antibodies in your blood to isolated, individual proteins. This improves the diagnostic sensitivity of the test as allergens that would otherwise be missing from the whole food extract or exist only in tiny amounts are present in concentrated form in the CRD test.

This type of test enables the doctor to see exactly which allergen(s) you react to, which allows them to determine whether you are sensitised to cross-reactive allergens that are unlikely to produce symptoms, and whether you are sensitised to certain allergens that could affect your management plan.

Component blood tests are also made up of very large panels of allergens which include many other foods and aerollergens that the allergist may want to check your reaction to and can help to determine whether or not a sensitisation to a cross-reactive allergen will be symptomatic or not.

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 fish allergens would require special preparation and is therefore only likely to be done for research purposes.

Additionally, as it is with 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.

Work is being done to produce new and improved blood tests, but component testing is not yet considered a routine diagnostic method.

A positive skin or blood test does not mean that you are allergic to something. While skin prick tests and blood tests 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. And, although your tests may indicate sensitivity to several types of fish, you are actually very unlikely to show symptoms to all of them.

A positive 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.

Neither can the results of your blood or skin test predict how severe your reaction to eating some fish might be; having a large skin weal in response to a prick or a high level of IgE in your blood do not mean that you will have a serious allergic reaction if you accidentally eat a some fish hidden in a pastie.

Food challenge

The only way to get a definitive diagnosis of fish allergy, and to have some idea of how severe your reactions may be and how much fish—and which fish—is needed to provoke them, is to undergo an oral food challenge. This generally involves eating a very small amount of fish, 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.

Oral food challenges are generally undertaken either when someone’s history and their test results disagree (i.e. they have negative tests results but their history strongly suggests an allergy, or vice versa) or to check whether someone has outgrown their allergy to ensure that they don’t unnecessarily restrict their diet or worry about hidden allergens in processed foods.

Practically speaking, most people do not undergo this kind of test since it requires a lot of time and resources. And oral challenges are rarely, if ever, offered to people whose history includes severe reactions to a suspected food. Whenever possible, allergy diagnoses are based on a combination of medical history and lab tests.

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

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 of a certain fish 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 fish
• to allow some fish-allergic patients to include some form of fish in their diets

If you fail your food challenge—an allergy is proven—the doctor can then advise you on the dietary precautions to take to avoid further reactions. The general advice is to avoid all fish. However, it may be that you are only allergic to certain species of fish and that you can eat others without problems. (See the Managing fish allergy section later.) If you want to find out, you will need to do further testing.

Diagnosing non IgE-mediated and mixed reactions to fish

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

Eczema is 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 had mixed results, having been described as reliable and child-friendly and also as not being as good as the APT in diagnosing certain food allergies.

Elimination diets and food challenges

While these 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, the first step towards a diagnosis involves reintroducing the foods one by one into the diet and seeing if the symptoms return. If the symptoms don’t disappear, it could be that the diet has not been restricted enough or that other foods should (also) be considered for 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;

• to identify a culprit food in cases of allergies to multiple foods
• to confirm the development of tolerance to a trigger food, which is often done between 12 to 18 months after the most recent reaction
• to identify alternative fish that can be eaten without symptoms in order to avoid an unnecessarily restrictive diet (in cases of allergy to bony fish, an allergist may try testing tolerance to cartilaginous fish and vice versa)

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

Although oral challenges normally provide a measure of certainty as far as food allergies are concerned, a team of Spanish and Italian doctors have warned that around 1 in 8 of their paediatric patients have passed an oral food challenge to fish only to react to it when exposed to it again at home the following day. They have therefore suggested that anyone with suspected FPIES to fish and a history of severe reactions be given more than one supervised challenge, just to make sure.

In very rare cases, a child may be introduced to a fish that they seem to tolerate a few times before developing FPIES to that fish, too. Sometimes a new allergy develops to another type of fish. Why this happens is unknown, but it may be that the new fish is very similar to, though not quite the same as, the fish that the child is allergic to and, at first, their immune system tolerates it only to subsequently recognise the new fish as something that should be defended against.

The previous research also mentions the case of a child who passed a challenge to cod but then had a reaction to hake a few days later, thus you cannot assume that, if you’ve gained tolerance to one fish, you can now also tolerate other fish, even those which are part of the same order, like cod and hake (Gadiformes).

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 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.

Differential diagnosis

Not all adverse reactions to fish can be blamed on an allergy; some are due to parasites, toxins or histamine hiding in the fish. Some are due to additives added during processing. Here are the most common alternative diagnoses that are considered if eating fish has made you suffer from allergy-like symptoms, but your allergy tests have been negative or inconclusive.

Ciguatera fish poisoning

Ciguatera toxicity is the most commonly reported seafood-toxin illness in the world. Globally, up to 500,000 people are thought to be affected by Ciguatera poisoning every year and that number is thought to represent only 2–10% of the actual cases.

Ciguatoxin is a potent neurotoxin that is created by the biotransformation of toxins produced by microscopic marine algae (Gambierdiscus toxicus) that accumulate in the muscles of fish. The algae stick to coral and seaweed that are eaten by herbivorous fish. Larger carnivorous fish eat those fish and, in turn, are eaten by large fish and gradually there is a toxin build-up.

Ciguatera poisoning is endemic to the tropics, namely the South Pacific and Caribbean, but it can be found anywhere that the contaminated fish—notably reef fish like moray eel, barracuda, grouper, amberjack, parrotfish, red snapper, sea bass, surgeon fish and Spanish mackerel—is consumed. Thanks to international trade and the popularity of the specific species of fish it affects, this can be pretty much anywhere, although tight, process-oriented controls throughout the food chain make that less likely.

Still, ciguatera poisoning affects 3% of tourists in endemic regions, and climate change is likely to make the problem worse. It has also been speculated that ciguatoxin may accumulate in farm-raised fish because of feed composed of wild fish contaminated with the toxin.

Symptoms generally occur within 6 hours of eating contaminated fish, and consist of gastrointestinal, neurological and cardiovascular symptoms.

Gastrointestinal symptoms usually begin within 6 to 12 hours of eating the toxic fish and resolve within 1 to 4 days. They include nausea, vomiting, upset stomach and diarrhoea.

The neurologic symptoms usually appear after the gastrointestinal symptoms, sometime within the first two days of illness. They include headaches, tingling fingers or toes, muscle aches, numbness, vertigo, metallic taste in the mouth, blurred vision, poor muscle control that causes clumsy movement (ataxia), itchy skin and hallucinations. A distinctive neurologic symptom is ‘hot-cold reversal’, when is when cold objects feel like they’re burning when you touch them.

Cardiac symptoms may occur during the early stage of the illness and include low blood pressure and a slow heart rate, which may necessitate emergency medical care. The illness is rarely fatal, but it can be if a person goes into cardiovascular shock or suffers from severe dehydration during the initial period of illness.

Neuropsychological symptoms may appear in the days or weeks after the initial illness and include confusion, reduced memory, difficulty concentrating, depression or irritability, anxiety and fatigue or feeling under the weather (malaise).

Symptoms usually resolve spontaneously within 1 to 4 days, but they—especially the neuropsychological ones—may also persist for months or years, and can even recur periodically.

There is no known antidote for ciguatera poisoning. The toxin is heat-stable, and therefore, cooking or freezing does not eliminate the toxin from the fish tissue. The only kind of prevention that works is avoiding the fish that are most likely to be contaminated, and especially the head, liver, intestines or roe (eggs) of the fish, which are associated with greater symptom severity.

People who have had the illness before can get it again, and certain things that can trigger a recurrence of the symptoms have been identified, including alcohol, caffeine, fish, chicken, pork, nuts, seeds and eggs and doing anything that can bring on dehydration, such as physical over-exertion. These should all be avoided for 3–6 months after intoxication, or until all symptoms have resolved.

Scombroid (histamine) poisoning

Scombroid poisoning—aka histamine toxicity—is caused by eatingcertain types offish that have spoilt because they were stored under suboptimal conditions (i.e. stored in temperatures over 0°C during fishing or processing).

The name ‘scombroid’ is derived from the family name of the fish that were originally implicated in this type of poisoning—tuna and mackerel, the Scombridae family. However, other non-scombroid fish species can also cause scombroid poisoning, including mahi-mahi, herring, amberjack, bluefish, marlin, swordfish, pilchards, sardines and anchovies.

These fish all contain naturally high levels of the amino acid histidine and have bacteria containing the enzyme histidine decarboxylase living on their gills, external surfaces and guts. When a dead fish is exposed to air temperatures above 4°C, the bacteria invade the muscle tissues and start converting the histidine to histamine, which ends up reaching levels that are 200 to 500 times higher than those in properly stored fish.

Affected fish don’t smell or look any different from untainted fish, although the skin may appear honeycombed after cooking. People who have experienced scombroid poisoning often mention that the fish had a ‘peppery’ or metallic taste.

Unfortunately, histamine is resistant to heat; once it is produced, cooking will not diminish its concentration. The only way to make sure that fish is not affected is to keep it properly refrigerated.

Cases of scombroid poisoning were first described in 1799 in Britain, before new medical reports emerged in the 1950s when outbreaks were reported in Japan. They have since been documented worldwide in numerous countries and in numerous different settings including restaurants, schools, army barracks and medical conferences.

Scombroid symptoms typically occur within 2 hours of consuming spoilt fish. The most common are flushed skin, rash, headache and diarrhoea. Less common symptoms include stomach pain, nausea, blurred vision, dizziness and heart palpitations. Severe reactions include swelling of the face and tongue, breathing problems, anaphylactic shock, cardiac arrest and death.

People with medical conditions like asthma and cardiac disease are more likely to experience severe symptoms than people who are otherwise healthy. To date, somewhat reassuringly, only one death has been reported. Because histamine is the main chemical responsible for allergic reactions, scombroid poisoning can easily be confused with fish allergy.

Symptoms normally go away after 6 to 8 hours, but someone who’s experienced scombroid poisoning may feel generally unwell for a couple of days. Most people get better quickly after taking some antihistamines, even those with severe symptoms. Without treatment, symptoms tend to resolve within 12 hours to 2 days.

Histidine is normally found in dark meat fish, like tuna. In 2010, in what is, so far, the largest recorded outbreak, 71 soldiers of the French Armed Forces based in Dakar became ill with scombroid poisoning after eating lunch at the military catering facility. There were 3 fish on the menu that day, tuna, shark and salmon, and the tuna was identified as the culprit. 107 soldiers actually ate the tuna, but it turns out that the amount that you eat matters, too; those who ate more than 1 piece were 3 to 6 times more likely to get ill than those who ate one piece or less.

Their symptoms began during or shortly after lunch and the most common were a sensation of warmth, flushing, headache, weakness, rapid/weak pulse and diarrhoea. Most of the soldiers recovered within a few hours, but 16 had to be taken to hospital where they recovered the following morning.

You’re unlikely to catch scombroid poisoning in developed countries from fish served in a reputable restaurant and caught by commercial companies, due to strict regulations governing fish storage in fishing vessels and general standards of hygiene in most commercial kitchens. Cases of poisoning are generally caused by recreationally caught fish. In developing countries, you might catch a bout from seafood-containing street food.

Symptoms that can distinguish scombroid poisoning from fish allergy include sensations of tingling and burning around the mouth, headache and dizziness (as opposed to feeling faint).

The fish parasite Anisakis simplex

Anisakis simplex is a parasitic nematode (roundworm) that mainly infects fish—including hake, mackerel, herring, salmon, tuna, whiting, anchovies and sardines—and can cause health problems in humans who become accidental hosts by eating eating raw, marinated or undercooked fish that’s infected with live larvae.

There are actually several types of parasitic worm that can be found in seafood and cause reactions in humans—namely Pseudoterranova decipiens, Anisakis physeteris, Nybelinia surmenicola—but A. simplex is the most frequent culprit.

Anisakis simplex can cause problems for people in 2 ways:

1. Tissue damage: the parasitic worm can penetrate into your innards, forming a mass called a granuloma. This infection is called anisakiasis and it normally lasts about 3 weeks before the worm dies and is expelled from the body. If it isn’t naturally expelled, it can be removed through either endoscopy or surgery. Symptoms depend on where the worm ends up:
   • If it burrows into your stomach wall, it causes acute symptoms that occur 2–8 h after eating, often in the form of severe abdominal pain
   • If it burrows into your intestinal wall, it causes chronic symptoms that occur 5-7 days after eating and can manifest as mild stomach pain, nausea, vomiting, diarrhoea, intestinal obstruction and sometimes fever
2. Allergy: the worm itself contains allergens that people can become allergic to. One of the allergens (Ani s 3) is tropomyosin, which could be responsible for cross-reactions among the shellfish-allergic. Some experts believe that a person must first be infected with the worm before becoming sensitised and developing an allergy to it. Symptoms of allergy to A. simplex usually occur between 15 minutes to 6 hours after eating fish and include typical allergic symptoms such as gastrointestinal pain, rashes, facial swelling, asthma and, occasionally, anaphylaxis

Because the symptoms mimic other, more common, illnesses, anisakiasis—the name for the intestinal infection caused by larvae of the genus Anisakis—especially the chronic, intestinal version, is often misdiagnosed as a myriad of conditions including a wide range of cancers, acute appendicitis, intestinal endometriosis, intestinal obstruction, pancreatitis, peritonitis, gastritis, gastric ulcers, ovarian cysts, tumours, hernia, Kounis syndrome or Crohn’s disease.

Scientists from The Netherlands were the first to report on the existence of Anisakis in the 1960s, when epidemics of anisakiasis occurred in the Netherlands due to the consumption of lightly salted herring. Nowadays, the vast majority (over 90%) of reported reactions to Anisakis come from Japan, where raw seafood is an integral part of the diet; over 2,500 cases are estimated to occur annually.

A recent study of anisakiasis cases reported between 2000 and 2017 in the European union found a total of 236 cases (at least 62 of which were caused by eating pickled anchovies), with the highest incidence in Spain, followed by Italy. Just over half of the symptoms involved the skin (with itchiness being the most common symptoms, affecting just over a third of people) following by stomach pain, which affected a third of patients.

Another study of anisakidosis cases—cases due to infection by the larvae of Anisakidae family, which includes Anisakis simplex—admitted to hospital in Spain during a 19-year period noted an increase in numbers that the authors suggested might have several explanations; notably an increasing awareness of the condition and better diagnostic tools, as well as the growing popularity of raw or uncooked seafood and the possibility that the rate of fish and shellfish infestations might be increasing due to current aquaculture and fishing practices.

Fish dishes that are considered high-risk include Japanese sushi and sashimi, Dutch/Belgian pickled, salted or smoked herring, Nordic gravlax, Hawaiian lomi-lomi, South American ceviche/cebiche (a cold dish that includes raw fish or shellfish marinated in citrus and seasoning), Italian salted anchovies and Spanish boquerones en vinagre (pickled anchovies).

Although the Anisakis larva can be killed by cooking, freezing and salting its allergens are resistant to heating or freezing and can still trigger allergies after the larva is killed, so people with Anisakis allergies should avoid seafood altogether.

Anisakis simplex doesn’t just cause problems for people who eat fish, it also causes symptoms including respiratory allergy and contact dermatitis in people who work with fish such as fishermen, fishmongers, workers in fish-processing industries, cooks and restaurant workers, as well as farmers who use fish meal.

Additives

Sometimes ingredients added during processing and canning of fish—like spices or monosodium glutamate—can also trigger symptoms which are similar to allergic reactions, such as rashes, headaches and respiratory symptoms. Canned tuna containing a soy additive has also caused a case of exercise-induced anaphylaxis.

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Image by Jakub Żerdzicki on Unsplash

Good to know

Airborne fish proteins may be more of a problem than you might think.

Fish allergens can lurk in unexpected places. A study carried out in 143 Norwegian homes found fish allergens in the mattresses of 46% of the bedrooms. In smaller homes, or homes with just one floor, the chances of finding fish allergens lurking in bedrooms went up significantly: up to 72% of mattresses contained fish protein.

This could be a problem for children with an impaired skin barrier—with eczema, for example—because evidence increasingly shows that early life exposure to food allergens through the skin, rather than through the gut, can cause allergies

And not eating fish does not guarantee that you will avoid allergic reactions. A Spanish study of 21 children who had been diagnosed as toddlers with fish allergy found that, even on a strict avoidance diet, most (19 of the 21) had experienced several allergic reactions—generally wheezing or hives—after accidentally inhaling fish odours or vapours. In most cases, these episodes occurred at home when fish was being fried, boiled, or simply being served to people sitting next to them.

Just to make things more difficult, some children are actually allergic only to fish vapours—they can actually eat fish with no reaction, but just a whiff of cooking steam and they can experience anything from hay fever symptoms to wheezing and even, in rare cases, to anaphylaxis.

Even buying food in the first place can be hazardous; fish allergens have been detected in the air at fish markets, so if you’re (with) someone who is very sensitive to fish, beware your local fishmonger’s or fishermen’s market.

Doing your best to avoid these nebulous hazards is important because constantly provoking your immune system with floating fish allergens might delay the development of tolerance.

Not digesting your fish properly increases your risk of an allergic reaction.

Fish allergens are much less able to trigger an allergic reaction when they have undergone proper gastric digestion. Research has shown that cod that has been properly digested in the stomach is 10 000 less allergenic than badly digested cod, and an increase of the pH in the stomach from 2.5 to 2.75 is all that it takes to stop the fish proteins from being broken down. When people who are allergic to cod undergo a food challenge with badly digested cod-proteins, their thresholds for allergic reactions are much lower than they otherwise would be.

There are all sorts of reasons that a person might have a stomach pH that’s lower than it should be, including stomach surgery, age (both newborns and older people tend to produce too little acid), bacterial infection, chronic stress and the long- term use of antacid medication. All of these factors can increase stomach pH which results in the incomplete digestion of food, leaving allergens intact and putting someone at higher risk of being sensitised to food or having an allergic reaction to it.

It’s possible to become allergic to fish again after outgrowing your allergy.

This is what happened to 2 children, a 2-year-old and a 5-year-old, who reacted to sole and cod. They had positive skin prick and blood tests to cod, sole and hake but, after a fish-free diet of 3 and 4 years respectively, their tests became negative and they both passed oral food challenges, so fish was reintroduced in their diet and they ate it regularly. However, after 8 months, the first child developed oral allergy syndrome to cod, sole, tuna and salmon and, after 2 months, the second child got an itchy mouth, swollen lips and shortness of breath after eating sole. Their skin and blood tests to cod and sole were positive again and they had to eliminate fish from their diets once more.

You can develop an allergy to fish after an organ transplant or a blood transfusion.

Although food allergies can develop after different types of transplant, a liver transplant is by far the type of operation that’s most likely to result in a new food allergy, often to multiple foods. Fish is around the 7^th most common allergy in these cases, although in countries where it’s more commonly eaten, like Japan, it will be more frequent.

Children are much more likely to develop an allergy after a liver transplant than adults (especially to fish); 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. We don’t yet know why this is so, 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.

There are a few risk factors associated with a liver transplantation-associated food allergy (LTFA), although the only one which is universally reported is being younger than 2 years old. Other risk factors include having an Epstein-Barr Virus infection and having a personal or familial history of allergy, including eczema, asthma or hay fever. One study reported having eczema at the time of the transplantation as being a big risk factor.

Symptoms generally manifest within two years of the liver transplantation, and normally involve the skin; facial swelling (angio-oedema) and hives (urticaria) 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.

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. A review of the transplant cases seen over a 14 year period at a hospital in Thailand reported that, of the 8 children who developed an allergy to fish after their transplant, just one outgrew it.

Although less common, there are also reports of people developing new allergies to fish after bone marrow transplants, both in children and in adults.

You can also develop a food allergy after a blood transfusion. This happened to an 8-year-old boy who was being treated for his cancer with chemotherapy and blood platelet transfusion. After his third round of treatment, he suffered an anaphylactic attack after after eating some salmon (which he had done many times before without problem). The good news is, this kind of allergy by ‘passive transfer’ tends to resolve; after pinpointing the problem, the blood from the donor was taken out of circulation and the boy was able to continue his treatment with other blood. His allergy disappeared after a few months and he was able to eat fish again.

Similarly, you can also get a food allergy after a cord blood transplantation (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 type of allergy also tends to go away.

There is some evidence to suggest that early consumption of fish may prevent the development of allergy.

Studies that have analysed the diet of a few thousand infants for the first few years of their lives have found that regular fish consumption during the first year of life is associated with a reduced risk of food and general allergies at 4 years old and 5 years old.

Specifically, studies of large numbers of infants have found that children who are introduced to fish before the age of 9 months are less likely to suffer from hay fever.

The protective effect of introducing fish into a child’s diet between 6 and 9 months also extends to the prevention of eczema, asthma and wheezing.

Conversely, research has found that the late introduction of fish into the diet (after 8 months of age) is correlated with a child’s sensitisation to food and (especially, and strangely) inhalant allergens.

However, the evidence from this strand of research is somewhat mixed. For example, a 2016 study found that fish intake in infancy might reduce the risk of eczema and hay fever, and also concluded that a mother’s fish intake during pregnancy had no effect on their child’s of getting an allergy. However, another study found that if a mother ate fish during her pregnancy, her child was 43% less likely to get eczema.

And another study found that the early introduction of fish into a child’s diet was associated with less eczema and less of a likelihood to suffer from asthma, but did not confer any benefits as far as food allergy was concerned.

Finally, a 2016 meta-analysis which examined the data provided by the previous studies concluded that the evidence that early introduction to fish was associated with reduced allergic sensitisation was not that strong, because of things like study bias and the researcher’s inability to properly compare the studies because they were too different.

As often is the case, when it comes to studies involving food and allergies, nothing is straightforward. Still, the idea of introducing a variety of solid foods to infants during the first year of their life is catching on among allergists, and the potential advantages generally seem to outweigh the disadvantages. If you are considering introducing your child to solid foods early in life, especially if anyone in your close family has allergies or related health problems, ask your doctor for advice.

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