What is a food allergies definition

A food allergy occurs when the body’s immune system sees a certain food as harmful and reacts by causing symptoms. This is an allergic reaction. Foods that cause allergic reactions are allergens.

Two Categories of Food Allergies

  • Swelling of the lips, tongue or throat
  • Skin rash, itching, hives
  • Shortness of breath, trouble breathing, wheezing
  • Non-IgE mediated. Other parts of the body’s immune system react to a certain food. This reaction causes symptoms, but does not involve an IgE antibody.

    Someone can own both IgE mediated and non-IgE mediated food allergies.

  • Stomach pain, vomiting, diarrhea
  • Immunoglobulin E (IgE) mediated. Symptoms result from the body’s immune system making antibodies called Immunoglobulin E (IgE) antibodies. These IgE antibodies react with a certain food.
  • Feeling love something terrible is about to happen

IgE Mediated Food Allergies

The IgE mediated food allergies most common in infants and children are eggs, milk, peanuts, tree nuts, soy and wheat.

The allergic reaction can involve the skin, mouth, eyes, lungs, heart, gut and brain. Some of the symptoms can include:

  1. Swelling of the lips, tongue or throat
  2. Stomach pain, vomiting, diarrhea
  3. Shortness of breath, trouble breathing, wheezing
  4. Skin rash, itching, hives
  5. Feeling love something terrible is about to happen

Sometimes allergy symptoms are mild.

Other times they can be severe. Take every allergic symptoms seriously. Mild and severe symptoms can lead to a serious allergic reaction called anaphylaxis (anna-fih-LACK-sis). This reaction generally involves more than one part of the body and can get worse quick. Anaphylaxis must be treated correct away to provide the best chance for improvement and prevent serious, potentially life-threatening complications.

Treat anaphylaxis with epinephrine. This medicine is safe and comes in an easy-to-use device called an auto-injector. You can’t rely on antihistamines to treat anaphylaxis. The symptoms of an anaphylactic reaction happen shortly after contact with an allergen.

In some individuals, there may be a delay of two to three hours before symptoms first appear.

Cross-Reactivity and Oral Allergy Syndrome

Having an IgE mediated allergy to one food can mean your kid is allergic to similar foods. For example, if your kid is allergic to shrimp, he or she may be allergic to other types of shellfish, such as crab or crayfish. Or if your kid is allergic to cow’s milk, he or she may also be allergic to goat’s and sheep’s milk.

The reaction between diverse foods is called cross-reactivity. This happens when proteins in one food are similar to the proteins in another food.

Cross-reactivity also can happen between latex and certain foods. For example, a kid who has an allergy to latex may also own an allergy to bananas, avocados, kiwis or chestnuts.

Some people who own allergies to pollens, such as ragweed and grasses, may also be allergic to some foods. Proteins in the pollens are love the proteins in some fruits and vegetables. So, if your kid is allergic to ragweed, he or she may own an allergic reaction to melons and bananas.

That’s because the protein in ragweed looks love the proteins in melons and bananas. This condition is oral allergy syndrome.

Symptoms of an oral allergy syndrome include an itchy mouth, throat or tongue. Symptoms can be more severe and may include hives, shortness of breath and vomiting. Reactions generally happen only when someone eats raw food. In rare cases, reactions can be life-threatening and need epinephrine.

Non-IgE Mediated Food Allergies

Most symptoms of non-IgE mediated food allergies involve the digestive tract.

Symptoms may be vomiting and diarrhea. The symptoms can take longer to develop and may final longer than IgE mediated allergy symptoms. Sometimes, a reaction to a food allergen occurs up 3 days after eating the food allergen.

When an allergic reaction occurs with this type of allergy, epinephrine is generally not needed. In general, the best way to treat these allergies is to stay away from the food that causes the reaction. Under are examples of conditions related to non-IgE mediated food allergies.

Not every children who react to a certain food own an allergy. They may own food intolerance. Examples are lactose intolerance, gluten intolerance, sulfite sensitivity or dye sensitivity.

Staying away from these foods is the best way to avoid a reaction. Your child’s doctor may propose other steps to prevent a reaction. If your kid has any food allergy symptoms, see your child’s doctor or allergist. Only a doctor can properly diagnose whether your kid has an IgE- or non-IgE food allergy. Both can be present in some children.

Eosinophilic Esophagitis (EoE)

Eosinophilic (ee-uh-sin-uh-fil-ik) esophagitis is an inflamed esophagus. The esophagus is a tube from the throat to the stomach. An allergy to a food can cause this condition.

With EoE, swallowing food can be hard and painful. Symptoms in infants and toddlers are irritability, problems with eating and poor weight acquire.

Older children may own reflux, vomiting, stomach pain, chest pain and a feeling love food is “stuck” in their throat. The symptoms can happen days or even weeks after eating a food allergen.

EoE is treated by special diets that remove the foods that are causing the condition. Medication may also be used to reduce inflammation.

Food Protein-Induced Enterocolitis Syndrome (FPIES)

FPIES is another type of food allergy.

It most often affects young infants. Symptoms generally don’t appear for two or more hours. Symptoms include vomiting, which starts about 2 hours or later after eating the food causing the condition. This condition can also cause diarrhea and failure to acquire weight or height. Once the baby stops eating the food causing the allergy, the symptoms go away. Rarely, severe vomiting and diarrhea can happen which can lead to dehydration and even shock. Shock occurs when the body is not getting enough blood flow.

Emergency treatment for severe symptoms must happen correct away at a hospital. The foods most likely to cause a reaction are dairy, soy, rice, oat, barley, green beans, peas, sweet potatoes, squash and poultry.

Allergic Proctocolitis

Allergic proctocolitis is an allergy to formula or breast milk. This condition inflames the lower part of the intestine. It affects infants in their first year of life and generally ends by age 1 year.

The symptoms include blood-streaked, watery and mucus-filled stools.

Infants may also develop green stools, diarrhea, vomiting, anemia (low blood count) and fussiness. When properly diagnosed, symptoms resolve once the offending food(s) are removed from the diet.

Medical review December

Centuries ago, Lucretius said that one man’s food may be another man’s poison. Such is the case with food allergies. Individuals with food allergies and other types of food sensitivities react adversely to the ingestion of foods and food ingredients that most consumers can ingest with no problems.

Eating is necessary to sustain life.

For most consumers, eating is an enjoyable experience given the variety and abundance of foods available in the marketplace. For some individuals, however, consuming certain foods can be a debilitating, possibly even life-threatening, experience. Individuals with various forms of food allergies and sensitivities must avoid certain foods or food ingredients in their diets. For such people, the joy of eating is diminished by the ever-present concern that they might consume a food or food ingredient that will elicit an adverse reaction. For them, food selection can become a tedious task requiring the painstaking reading of ingredient lists on the labels of packaged foods and a ceaseless search for more knowledge about food composition.

Food preparation requires careful attention to details such as “cooking from scratch,” seeking alternative recipes for numerous dishes, and avoidance of shared utensils, containers, and cooking surfaces between allergenic and non-allergenic foods. In situations where one family member has a extremely serious allergic sensitivity, the entire family often has to avoid the offending food as a precautionary measure.

Definitions
Food allergies and other food sensitivities are individualistic adverse reactions to foods (Taylor, ).

These food-related illnesses are individualistic because they affect only a few people in the population; most consumers can eat the same foods with no ill effects. Numerous diverse types of reactions are involved in these individualistic adverse reactions to foods (Fig. 1; Anderson, ; Taylor, ). Adverse food reactions can include IgE and non-IgE-mediated primary immunological sensitivities, non-immunological food intolerances, and secondary sensitivities.

While these various types of reactions are often considered collectively as food allergies, true food allergies represent only a part of the individualistic adverse reactions to foods.

True Food Allergies. True food allergies are abnormal (heightened) responses of the immune system to components of certain foods (Lemke and Taylor, ). The components of foods that elicit these abnormal immune responses are typically naturally-occurring proteins in the foods (Bush and Hefle, ). True food allergies can be divided into two categories based upon the nature of the immune response—immediate hypersensitivity reactions and delayed hypersensitivity reactions (Lemke and Taylor, ).

In immediate hypersensitivity reactions, symptoms start to develop within minutes to an hour or so after ingestion of the offending food. Immediate hypersensitivity reactions own been noted with numerous foods and can sometimes be fairly severe (Hefle et al., ). Immediate hypersensitivity reactions involve abnormal responses of the humoral immune system with the formation of allergen-specific immunoglobulin E (IgE) antibodies (Mekori, ). In delayed hypersensitivity reactions, symptoms do not start to appear until 24 hours or longer after the ingestion of the offending food (Lemke and Taylor, ).

With the exception of celiac disease, which involves an abnormal immunological response to wheat and related grains (Ferguson, ), the role of delayed hypersensitivity reactions to foods remains poorly defined. Delayed hypersensitivity reactions involve abnormal responses of the cellular immune system with the development of sensitized T cells (Lemke and Taylor, ).

Allergy-Like Intoxications. Certain foods can elicit adverse reactions that resemble true food allergies. These foods contain elevated levels of histamine, one of the principal mediators of allergic reactions in the body (Taylor et al., a). In true food allergies and anaphylactoid reactions, however, histamine is released from intracellular locations (Mekori, ).

In these allergy-like intoxications, histamine is ingested with foods. Histamine poisoning is often known as scombroid fish poisoning because it is frequently associated with consumption of spoiled fish of the scombroid type such as tuna and mackerel (Taylor et al., a). However, histamine poisoning can also happen from the ingestion of spoiled fish such as mahi-mahi and bluefish that are not scombroid fishes (Etkind et al., ; Taylor et al., a). And, histamine poisoning has even been occasionally associated with the ingestion of cheese, especially aged Swiss cheese (Stratton et al., ; Taylor et al., ). In every of these food products, specific types of bacteria own proliferated and caused the conversion of the amino acid, histidine, into histamine (Stratton and Taylor, ; Sumner et al., ; Taylor et al., ).

Ingestion of little amounts of histamine in the diet is a normal occurrence and does not cause any harm. However, when large doses of histamine are ingested with foods, the body’s protective mechanisms can be overwhelmed resulting in histamine poisoning (Taylor, ). Unlike food allergies and sensitivities, every consumers are susceptible to histamine poisoning. Because this illness is not truly a form of food allergy or sensitivity, it will not be discussed further. It does merit some mention because the similarity in symptoms can cause it to be confused with true food allergy.

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Food Intolerances.

Food intolerances are abnormal reactions to foods or food components that do not involve the immune system. Several diverse types of food intolerances are also known to exist. These intolerances are metabolic food disorders, anaphylactoid reactions, and idiosyncratic reactions (Taylor, ). Metabolic food disorders are adverse reactions to a food or food component that results from a defect in the metabolism of these foods or some substance therein or from an affect of the food or food component on the body’s normal metabolic processes.

Lactose intolerance is an example of a metabolic food disorder resulting from a defect in the metabolism of a food component (Kocian, ). Favism is an example of a metabolic food disorder resulting from foodborne substances that interfere with normal metabolic processes (Mager et al., ). Anaphylactoid reactions are adverse reactions resulting from the ingestion of foodborne substances that release histamine from cellular stores within the body (Taylor, ). There are no particularly excellent examples of anaphylactoid reactions, although circumstantial evidence suggests that such reactions may happen.

Food idiosyncrasies are adverse reactions to foods or food components that happen through unknown mechanisms and which can even include psychosomatic illnesses (Taylor, ). Sulfite-induced asthma is the best example of an idiosyncratic reaction that has been well documented to happen among certain consumers, although the mechanism remains unknown (Bush and Taylor, ).

Secondary Food Sensitivities. Adverse reactions to foods or food components can happen with or after the effects of other conditions. Examples of such reactions, termed secondary food sensitivities, include lactose intolerance secondary to gastrointestinal disorders such as Crohn’s disease or ulcerative colitis (Metcalfe, a) and drug-induced sensitivities such as the increased sensitivity to tyramine among patients on monoamine oxidase-inhibiting drugs (Blackwell and Marley, ).

IgE-Mediated Food Allergies
This type of food allergy can also be called immediate hypersensitivity, Type I allergy, or food anaphylaxis.

The Greek expression, anaphylaxis, means “against protection” and refers to allergic reactions to foreign protein molecules. IgE is one of five classes of antibodies that are present in the human body and that frolic a role in disease resistance. IgE antibodies are particularly involved in fighting off parasitic infections. Although every humans own low levels of IgE antibodies, only individuals predisposed to the development of allergies produce IgE antibodies that are specific for and recognize certain environmental antigens. These antigens are typically proteins, although only a few of the numerous proteins in nature are capable of stimulating the production of specific IgE antibodies in susceptible individuals (Taylor, ).

The allergens eliciting IgE antibody formation can be found in pollens, mold spores, bee venoms, dust mites, and animal danders in addition to foods (Solomon and Platts-Mills, ).

Pathogenesis. The mechanism of IgE-mediated allergic reactions is depicted in Fig. 2. First, sensitization by the allergen must happen. In the sensitization phase of the response, the allergen stimulates production of specific IgE antibodies. While sensitization can happen with the first exposure to the allergen, that is not always the case. With honor to food allergens, sensitization does happen most commonly among young infants where the immune response seems to be more likely to be oriented toward an IgE response (Anderson, ).

However, even in susceptible infants exposure to most dietary proteins results in oral tolerance, a normal immunologic response that is not associated with adverse reactions, rather than sensitization (Strobel, ). The specific IgE antibodies then attach to mast cells in various tissues and basophils in the blood. Mast cells and basophils contain granules that are loaded with physiologically athletic chemicals that mediate the allergic response (Church et al., ). On subsequent exposure to the allergenic substance, the allergen cross-links two IgE antibodies on the surface of the mast cell or basophil membrane, stimulating the release into tissues and blood of a host of allergic response mediators.

Although numerous mediators own been described, histamine is one of the primary mediators responsible for numerous of the immediate symptoms that happen in IgE-mediated allergic reactions (Simons, ). Other significant mediators include the various leukotrienes and prostaglandins, some of which are associated with more delayed symptoms that can happen in IgE-mediated, immediate hypersensitivity reactions, the so-called late-phase responses (Peters et al., ).

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Symptoms.

IgE-mediated food allergies are associated with a wide variety of symptoms, ranging from mild and annoying to severe and life-threatening (Lemke and Taylor, ). The symptoms can involve the gastrointestinal tract, skin, or respiratory tract (Table 1). Food-allergic individuals generally suffer from only a few of the numerous possible symptoms. The nature and severity of the symptoms experienced by a food-allergic individual may also vary from one episode to the next depending on the dose of the offending food that has been inadvertently ingested, the degree of sensitization to the offending food at the time of the episode, and probably other factors.

Because foods are ingested, gastrointestinal symptoms are often encountered (Anderson, ; Gryboski, ). However, these symptoms can also be involved in other illnesses so their association with food allergies is often hard to decipher. Cutaneous symptoms such as urticaria (hives) and dermatitis (eczema) are also common manifestations of food allergies (Kaplan, ). These symptoms are more definitive for food allergy, although the frequency of dermatitis as a manifestation of food allergy especially, in infants, has only been widely appreciated in the past decade or so (Sampson, ).

Respiratory symptoms are less commonly associated with food allergies than with environmental allergies such as pollen or animal dander allergies (Taylor et al., ). With environmental allergies, the allergens are inhaled, so the primary involvement of respiratory symptoms is understandable. However, ingested food allergens must survive digestive processes and be absorbed to elicit systemic reactions in the respiratory tract. Although few asthmatic individuals experience food-induced asthma, asthma is among the most severe symptoms associated with food allergies (Bousquet and Michel, ). Food-induced asthma is a risk factor for severe, life-threatening reactions to the offending foods (Sampson et al., ).

Oral allergy syndrome is perhaps the most common manifestation of food allergy (Ortolani et al., ).

Oral allergy syndrome is often so mild that it is ignored by afflicted individuals. Oral allergy syndrome involves symptoms confined to the oropharyngeal area including hives, itching, and swelling (Pastorello and Ortolani, ). Unused fruits and vegetables are the foods most frequently associated with oral allergy syndrome (Pastorello and Ortolani, ). Individuals with oral allergy syndrome are generally sensitized to one or more pollens, and react to proteins in specific unused fruits and vegetables that cross-react with the pollen allergens (Calkoven et al., ; Ebner et al., ; van Ree and Aalberse, ). Examples would include allergic reactions to watermelons and other melons in ragweed-allergic individuals (Enberg et al., ), allergic reactions to celery in mugwort-allergic or birch-sensitized individuals (Ballmer-Weber et al., ; Wuthrich et al., ), and allergic reactions to apples and hazelnuts in birch-allergic individuals (Dreborg, ).

Because the allergens in these foods are inactivated on contact with stomach acid and digestive proteases, systemic reactions to these unused fruits and vegetables are rarely encountered (Taylor and Lehrer, ). Because these allergens are denatured by heating (Dreborg and Foucard, ; Taylor and Lehrer, ), individuals with oral allergy syndrome can generally safely ingest heat-processed forms of the offending food, e.g., apple jelly or apple sauce. Recent evidence indicates that, in contrast to previous assumptions, some individuals with oral allergy syndrome associated with certain foods, such as celery, also may experience more severe systemic reactions on occasion (Ballmer-Weber et al., ).

The most frightening symptom associated with food allergies is anaphylactic shock, which generally involves multiple systems including the gastrointestinal tract, the skin, the respiratory tract, and the cardiovascular system.

Symptoms happen in combination and develop rapidly. Severe hypotension can happen. Death can happen from cardiovascular and/or respiratory collapse within minutes of ingestion of the offending food. Only a few of the numerous people with IgE-mediated food allergies are at risk for such serious manifestations. However, numerous deaths own been attributed to inadvertent exposure to the offending food among individuals with food allergies (Bock et al., ; Sampson et al., ; Yunginger et al., ).

These deaths own involved asthma and/or anaphylactic shock.

In addition to allergic reactions associated with the consumption of foods, occupational food allergies including occupational asthma, hypersensitivity pneumonitis (extrinsic alveolitis), and contact dermatitis can happen amongst food industry employees (O’Neil and Lehrer, ). Such reactions can be triggered in food manufacturing workers by food-derived protein allergens, e.g., green coffee beans, flour, and shellfish, or non-food agents, e.g., honey bees and latex products (Lehrer and O’Neil, ).

These occupational allergies are produced by respiratory exposure to dusty processing environments or cutaneous exposure to specific food products.

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Diagnosis. With the wide range of symptoms that can be involved in IgE-mediated food allergies and the possibility of other causes for numerous of these symptoms, the diagnosis of IgE-mediated food allergies can sometimes be challenging (Metcalfe, b). First and foremost, an association must be sought between the ingestion of one or more offending foods and the elicitation of the adverse reaction. Once a food-associated adverse reaction is well documented, then proof of the existence of an IgE mechanism must be considered.

The assistance of an allergist should be sought in the diagnosis of IgE-mediated food allergies. Too often, consumers rely upon self-diagnosis or parental diagnosis. Self-diagnosis and parental diagnosis of reactions in children are problematic because they are often erroneous, leading to the identification of the incorrect foods, and implicate too numerous foods (Bock et al., ). Careful history-taking including the use of food diaries by an experienced allergist can often identify suspect foods. Elimination diets followed by challenges can sometimes confirm the existence of a food-associated adverse reaction.

However, the gold standard for documenting existence of a food-associated adverse reaction is the double-blind, placebo-controlled food challenge (DBPCFC; Bock et al., ). Such clinical challenges are especially useful in situations where the role of a specific food remains somewhat questionable. Double-blind, placebo-controlled food challenges are not generally done in cases involving serious, life-threatening adverse reactions because of the obvious risks to the patient and the likelihood in such cases that the role of one or more specific foods is rather clear. Once the role of one or more specific foods in the adverse reaction has been established, then the involvement of the IgE mechanism can be documented through skin-prick tests using extracts of the suspect foods (Bock et al., ) or by radioallergosorbent tests (RASTs) where the presence of food-specific IgE antibodies in the blood serum is examined (Adolphson et al., ).

Prevalence.

IgE-mediated food allergies likely affect between 2 and % of the entire population. For numerous years, the overall prevalence estimate for IgE-mediated food allergies has been between 1 and 2% of the entire population (Lemke and Taylor, ). However, a recent random, digit-dial telephone survey in the U.S.

What is a food allergies definition

indicated that the combined prevalence of peanut and tree nut allergies was an estimated % (Sicherer et al., ). And, a similar telephone survey in the United Kingdom indicated that the estimated prevalence of peanut allergy alone was % (Emmett et al., ). While one could criticize the use of telephone surveys, it is unlikely that numerous consumers would mis-diagnose peanut or tree nut allergies since the symptoms are profound and generally fairly immediate. Thus, these surveys may be reasonably dependable and a excellent indication that previous estimates based solely on clinical impression were incorrect. Certainly, if peanut and tree nut allergy alone account for more than 1% of IgE-mediated food allergy, then the overall prevalence of food allergy in the entire population likely exceeds 2%.

Infants (1–3 years of age) and children are more commonly affected by food allergies than other age groups (Taylor et al., ).

Among infants younger than 3 years, the prevalence of food allergies appears to be in the range of 5% to 8% (Sampson, ). The prevalence of food allergy among young infants (<1 year of age) has been studied more thoroughly than has the prevalence among older children and adults.

A much higher proportion of the public believes that they own food allergies because of self-diagnosis, parental diagnosis, and misconceptions about the definition of food allergy even among some physicians (Bock et al., ; Sloan, ).

Studies own shown that 10 to 20% of the consuming public believes that they or someone in their family has a food allergy (Chiaramonte et al., ; Sloan, ).

Some believe, on the basis of the impressions of clinicians involved in allergy practice for several decades, that the prevalence of IgE-mediated food allergies is increasing. An increase in prevalence, however, is hard to confirm because excellent baseline data from earlier years for comparative purposes are lacking. Certainly, the awareness of food allergy has increased. More individuals may seek specialized medical attention from allergists as a result of this increased awareness.

But, almost everyone agrees that the prevalence of severe food allergies seems to be increasing. The reasons for this apparent increase are unknown. Numerous severely affected individuals own food-induced asthma as one of the manifestations of their allergic reaction. The overall prevalence of asthma is definitely increasing in the U.S. for unknown reasons (Beasley et al., ). While food-induced asthma is a little part of the entire asthma population, the prevalence of food-induced asthma may be increasing in concert with the overall increase in prevalence of asthma.

Most Common Allergenic Foods.
The prevalence of allergies to specific foods is not precisely known.

Cows’ milk allergy appears to be among the more prevalent food allergies in infants. This is not surprising given the importance of milk in baby feeding practices. The prevalence of cows’ milk allergy among infants under the age of two in Sweden, Denmark, and Australia has been studied and found to be approximately 2% in every three countries in well-conducted clinical studies involving groups of unselected infants followed from birth to the age of two years (Hill et al., ; Host and Halken, ; Jakobsson and Lindberg, ). The prevalence of milk allergy is known to decrease with age (Bock, ), but the exact prevalence of milk allergy among other age groups is unknown. The prevalence of other specific food allergies has not been established in controlled clinical trials using unselected population groups.

The comparative prevalence of various specific food allergies can be discerned from studies involving groups of individuals with probable food allergies. In the U.S., eggs and peanuts are also common allergenic foods for infants, along with soybeans, tree nuts, fish, and wheat (Bock and Atkins, ; Burks et al., ; Sampson and McCaskill, ). Among adults in the U.S., peanuts are probably the most common allergenic food (Taylor et al., ). Seafood allergies, especially to crustaceans (shrimp, crab, lobster), are also rather common among adults (Lehrer et al., ). Fewer studies own been conducted on the prevalence of specific types of food allergies in adults in the U.S.

or other countries. The prevalence of specific types of food allergies may vary among population groups based upon their eating habits (Taylor et al., ). Peanut allergy appears to be more common in North America than in other parts of the world. This observation may relate to the popularity of peanut butter in North America. As other countries, such as the United Kingdom, own adopted the North American affection for peanuts and peanut products, the prevalence of peanut allergy in those countries appears to be rising (Emmett et al., ). Another example would be buckwheat allergy. Buckwheat allergy appears to be rather common among adults in certain southeast Asian countries such as Japan and South Korea (Kang and Min, ).

In contrast, buckwheat allergy would be rather unusual in the U.S. The difference is likely due to the popularity of buckwheat noodles in the cuisine of certain southeast Asian countries. Such observations own profound implications for product developers. If a highly successful buckwheat product was introduced into the U.S. or if buckwheat noodles became favorite in American Asian cuisine, the prevalence of buckwheat allergy would likely increase.

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The Large Eight. Eight foods or food groups are thought to account for more than 90% of every IgE-mediated food allergies on a worldwide basis (Bousquet et al., ; FAO, ).

These foods or food groups are milk, eggs, fish (all species of finfish), crustacea (shrimp, crab, lobster, crayfish), peanuts, soybeans, tree nuts (almonds, walnuts, pecans, cashews, Brazil nuts, pistachios, hazelnuts also known as filberts, pine nuts also known as pinyon nuts, macadamia nuts, chestnuts, and hickory nuts), and wheat. In , an expert consultation of the Food and Agriculture Organization of the United Nations sure that these eight foods or food groups were the most common causes of food allergy on a worldwide basis (FAO, ). Subsequently this list was adopted by the Codex Alimentarius Commission in (CAC, ).

These foods and food groups own come to be known as the “Big Eight” (Table 2). More than other foods own been documented as causing food allergies less frequently (Hefle et al., ).

Basically, any food that has protein has the potential to elicit an allergic reaction among susceptible individuals. Beyond the Large Eight, in certain geographic regions other foods or food groups may frequently cause IgE-mediated food allergies. Celery allergy, for example, is rather common in some European countries (Wuthrich et al., ). The prevalence of buckwheat allergy in southeast Asia has already been mentioned. And, sesame seed allergy is extremely common in middle Eastern countries and countries where the ethnic population of middle Easterners is high; this may be due to the popularity of tahini, a paste made from sesame seeds, in the diets (Kanny et al., ).

Several countries including Canada own decided to add sesame seeds to the list of commonly allergenic foods for that country. A few other foods are worthy of mention because, although they less frequently cause allergies, they own been associated with severe reactions. These foods include molluscan shellfish (clams, oysters, etc.), sesame seeds, poppy seeds, sunflower seeds, cottonseed, and certain other legumes beyond peanuts and soybeans (the various types of dry beans, peas, lentils, and garbanzo beans also known as chick peas) (Atkins et al., ; Gall et al., ; Kagi and Wutrich, ; Kalyoncu and Stalenheim, ; Kanny et al., ; Maeda et al., ; Martin et al., ; Noyes et al., ).

However, a rather large percentage of the or more other allergenic foods has been reported to elicit severe allergic reactions in isolated cases (Hefle et al., ).

Food Allergens. The allergens in foods are almost always naturally occurring proteins. Foods contain millions of individual proteins, but only a comparative few of the proteins own been documented to be allergens (Bush and Hefle, ; Taylor, ). Some foods such as milk, eggs, and peanuts are known to contain multiple allergenic proteins (Bush and Hefle, ). Other foods such as Brazil nuts, shrimp, and codfish contain only one major allergenic protein (Bush and Hefle, ).

However, the majority of the proteins, even those from commonly allergenic foods, are incapable of eliciting IgE production. Although the common allergenic foods listed above tend to be excellent sources of protein, other common protein-rich foods such as beef, pork, chicken, and turkey are rarely allergenic. No common structural features own allowed distinctions to be made between those proteins that are capable of eliciting IgE production and those that are not. Allergenic proteins, however, tend to be major proteins in the implicated foods, resistant to digestion, and stable to processing operations, particularly heat processing (Taylor and Lehrer, ).

Development of IgE-Mediated Food Allergies.

Genetics frolic an significant role in the development of IgE-mediated allergies of every types, including food allergies (Kjellman and Bjorksten, ). Allergies are much more likely to develop in children born to parents who own allergies (either to food, pharmaceutical, or environmental allergens) than amongst children born to parents with no history of allergies (Taylor et al., ). However, the nature of the allergy that develops is not genetically controlled. Therefore, the children of pollen-allergic parents are at increased risk for development of food allergies as are the children of food-allergic parents. The risk is greater if both parents own allergies than it is if only one parent has allergies.

Infants are the most likely to develop food allergies (Sampson, ; Taylor, ).

However, sensitization to foods can happen at any age. Infants do not appear to develop allergies in utero (Kjellman and Bjorksten, ), but can be sensitized during the first few days of life. Obviously, the newborn baby encounters through the first few years of life dozens of new foods and probably hundreds of thousands of food proteins that own antigenic and possibly allergenic potential. For most of these foods and their proteins, infants develop oral tolerance (Strobel, ).

Infants appear to be at increased risk for the development of IgE-mediated food allergies in part because their digestive processes may not be fully developed but primarily because they own not yet had the chance to develop oral tolerance. Certain foodborne proteins seem to be much more likely than others to cause allergic sensitization (Bush and Hefle, ). The factors involved in sensitization and the development of IgE-mediated food allergies are not yet fully understood.

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Prevention of IgE-Mediated Food Allergies. The prevention of the development of IgE-mediated food allergies among high-risk infants (those born to parents with histories of allergies) has been a long-sought goal.

However, the results of several large clinical trials of high-risk infants followed for several years propose that the development of IgE-mediated food allergies can be delayed but not prevented (Zeiger and Heller, ). The maternal diet during pregnancy does not seem to be a factor (Zeiger and Heller, ), because sensitization does not happen in utero. The avoidance of commonly allergenic foods such as cows’ milk, eggs, and peanuts in the baby diet during the first few years of life often delays the development of food allergies, but food allergies may still develop after solid foods are introduced (Hattevig et al., ; Zeiger and Heller, ).

Avoidance can be accomplished through breast-feeding or the feeding of hypoallergenic baby formula (Kjellman and Bjorksten, ; Zeiger and Heller, ). Numerous pediatricians recommend breast-feeding for infants born to parents with histories of IgE-mediated allergies. Lactating women can apparently transmit potentially sensitizing levels of food allergens through their milk to nursing infants (Van Asperen et al., ).

Apparently, intact or partially intact allergenic proteins are capable to survive maternal digestive processes and be absorbed via the lymph and transferred immunologically intact into breast milk (Van Asperen et al., ). Infants own been sensitized through breast-feeding to peanuts, cows’ milk, and eggs (Van Asperen et al., ). The avoidance of peanuts in the maternal diet during the lactation period is often advocated as a preventive measure. However, the exclusion of milk and eggs from the maternal diet during lactation is not generally recommended due to their nutritional importance coupled with the low likelihood of allergic sensitization through breast-milk (Taylor et al., ).

The use of hypoallergenic baby formula to prevent or delay the development of IgE-mediated food allergies is less commonly practiced. However, the use of partial whey hydrolysate formulae for this purpose may show some promise (Vandenplas et al., ), although such partial hydrolysates are not safe for consumption by infants who are already sensitized to cows’ milk (Businco et al., ; Ellis et al., ). Apparently, the partial hydrolysis of the whey proteins increases the likelihood of the development of oral tolerance as opposed to allergic sensitization.

Natural History of IgE-Mediated Food Allergies.

Most food allergies developed in infancy are outgrown in infancy or early childhood. Numerous infants outgrow their food allergies, often within a matter of a few months (Bock, ; Hill and Hosking, ). Allergies to certain foods such as cows’ milk, eggs, and soybeans are much more likely to be outgrown than allergies to other foods such as peanuts (Bock, ; Bock and Atkins, ). Peanut allergy is almost never outgrown. The loss of allergic sensitivity to a specific food probably results from the development of immunological, oral tolerance (Taylor et al., a).

However, the basis for the differences between specific foods (e.g., milk vs. peanuts) in the development of oral tolerance is not understood.

Cross-Reactions between Related Allergenic Foods. Allergic consumers sometimes experience cross-reactions between closely related foods. For example, with the crustacea, most sensitive individuals are allergic to every of the various species of shrimp, crab, lobster, and crayfish (Lehrer, ). However, these individuals can often eat other seafoods including finfish and molluscan shellfish.

Similar cross-reactivity also exists between cows’ milk and goats’ milk (Bellioni-Businco et al., ) and between eggs of various avian species (Langeland, ). With other food groups, the situation can be fairly complicated. For example, peanuts are the most commonly allergenic legumes. Most peanut-allergic individuals can eat other legumes without incident (Bernhisel- Broadbent and Sampson, ). A few peanut-allergic individuals are also allergic to soybeans (Herian et al., ), although this may not necessarily represent true cross-reactivity. With fish, individuals often experience reactions to more than one species of fish, but some fish are tolerated by some fish-allergic individuals and no definite patterns of reactivity own been identified (Bernhisel-Broadbent et al., ; de Martino et al., ).

Cross-Reactions between Food and Environmental Allergens.

Cross-reactions are frequently observed between pollens and certain foods, especially fruits and vegetables (Ballmer-Weber et al., ; Calkoven et al., ; van Ree and Aalberse, ; Wuthrich et al., ). This is the oral allergy syndrome, which typically involves mild reactions as previously mentioned. Examples include cross-reactions between birch pollen and apples, ragweed pollen and melons, and mugwort pollen and celery (Ballmer-Weber et al., ; Calkoven et al., ; Enberg et al., ; van Ree and Alberse, ; Wuthrich et al., ).

Cross-reactions own also been noted between latex allergies, a common problem among health-care workers, and certain foods including bananas, kiwis, avocados, and chestnuts (Blanco et al., ).

Effect of Food Processing on Allergens. As mentioned earlier, the allergens in foods are typically proteins that are stable to heat processing (Taylor and Lehrer, ). So, heat-processed forms of commonly allergenic foods often retain their allergenicity (Herian et al., ; Nordlee et al., ). The only exception would be the pollen-related allergens found in unused fruits and vegetables and involved in oral allergy syndrome; these allergens are generally destroyed by heat processing (Dreborg and Foucard, ), although the necessary extent of the heat process has not been well documented in most cases.

For the most common allergenic foods, every forms of those foods should be considered allergenic unless proven otherwise. Testing has indicated that most forms of peanuts and soybeans, for example, retain their allergenicity (Herian et al., ; Nordlee et al., ). Other processing techniques own not been so well investigated for their effects on the allergenicity of the resulting products. Since allergens are resistant to proteolysis, fermentation generally fails to eliminate allergenicity (Taylor and Lehrer, ).

For example, although fermented soybean products are reduced in allergenicity, some allergenic activity is retained (Herian et al., ).

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If the protein part is removed during processing, however, the resulting product or ingredient might be safe because the allergen has been removed. The classic example is the processing of edible oils from peanuts and soybeans (Bush et al., ; Hourihane et al., a; Taylor et al., ). Clinical challenge trials in peanut- and soybean-allergic individuals own documented that highly refined peanut and soybean oil are safe for individuals with allergies to the source material (Bush et al., ; Hourihane et al., a; Taylor et al., ).

Other ingredients may be derived from allergenic sources.

Examples include certain flavoring formulations, starch, lecithin, and gelatin. Flavors can occasionally contain protein residues from allergenic foods (Taylor and Dormedy, ). Starch is often made from corn or some other source that is rarely allergenic. Occasionally, starch is made from wheat, although the level of protein residues is fairly low and adverse reactions to wheat starch own not been reported. Lecithin can be made from either soybean or egg and can contain allergenic residues (Muller et al., ). However, the degree of risk posed by the low residual levels of soybean allergens in lecithin remains unknown.

Gelatin is most commonly made from beef and pork, foods that are rarely allergenic (Sakaguchi et al., ). However, gelatin can also be made from fish skins. The allergenicity of fish gelatin remains unknown (Sakaguchi et al., ).

Treatment. Allergic reactions to foods can be treated with certain drugs (Furukawa, ; Simons, ). Antihistamines can counteract the effects of histamine (Simons, ), although these drugs do not counteract the effects of the other mediators released from basophils and mast cells.

Epinephrine (adrenaline) is considered the life-saving drug for individuals at risk of severe anaphylactic shock-type reactions to foods (Sampson et al., ). Epinephrine is available in self-injectable form. Consumers with a history of severe anaphylactic reactions to foods should own a prescription for epinephrine and carry the medication at every times. To be most effective, epinephrine must be istered early in the course of the allergic reaction. However, an examination of severe food-allergic reactions resulting in deaths or near-deaths reveals a delay in the istration of epinephrine as a key contributing factor to the severe outcome (Sampson et al., ).

The specific avoidance diet is the only prophylactic approach to the treatment of food allergies (Taylor et al., a; Taylor et al., ).

For example, individuals allergic to peanuts must simply avoid ingesting peanuts. The construction of safe and effective avoidance diets is often a challenge for individuals with food allergies. With packaged foods, these individuals must spend considerable time in the scrutiny of ingredient declarations on product labels. They must be taught to recognize the numerous terms that may signify the presence of food components or ingredients derived from their offending food(s).

Some foods, especially in foodservice settings, are sold without ingredient statements. Clearly, the allergic consumer can encounter numerous hazardous situations in such circumstances and must be trained to be extremely vigilant. Also, exposure to extremely little amounts of the offending food may be sufficient to elicit allergic reactions in some sensitive individuals, further complicating the necessary vigilance in the implementation of effective avoidance diets.

Threshold Doses for Allergenic Foods. As noted, individuals with IgE-mediated food allergies will experience symptoms on exposure to little amounts of the offending food.

The interaction of a little quantity of the allergen with specific IgE antibodies on the surface of the mast cell or basophil membrane triggers the release of massive quantities of mediators, which accounts for the low degree of threshold. The precise threshold doses for allergenic foods own not been carefully investigated and are likely to be variable from one allergic individual to another. In a recent study, Hourihane et al.

(b) demonstrated that a group of individuals with peanut allergy displayed diverse thresholds for peanuts. The most sensitive individual among 12 tested subjects experienced an objective reaction when exposed to 2 mg of peanut protein. Other patients in the group did not even reply to the highest dose used in the challenge trial which was 50 mg of peanut protein. While this experiment clearly demonstrates that the threshold level is not zero, the threshold dose is fairly low. Whether other allergenic foods own thresholds as low as those for peanuts remains to be determined.

Allergenicity of Foods Produced Through Agricultural Biotechnology.

In the genetic modification of foods, genes are transferred from one organism to another. Because these genes code for the expression of a specific protein, novel proteins are expressed in the transgenic variety as a result. Because every allergens are proteins, the theoretical possibility exists that these novel proteins might be allergenic or that they might become allergenic. However, only a few of the numerous proteins found in nature are allergenic, so the probability of the transfer of an allergen is rather low.

The potential allergenicity of the novel proteins expressed in the new varieties produced through agricultural biotechnology should be assessed in every case.

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The potential allergenicity of the novel proteins in transgenic varieties can be assessed (FAO/WHO, ; Metcalfe et al., ; Taylor and Hefle, a). If a gene is transferred from a known allergenic source, the potential allergenicity of the expressed novel protein can be assessed with reasonable certainty by evaluating its reactivity by specific serum screening with serum containing IgE antibodies from individuals with well documented allergies to the source material.

This assessment approach was demonstrated to be effective when it was sure that a Brazil nut protein transferred into soybeans to correct the inherent methionine deficiency of soybeans was the heretofore unidentified major allergen from Brazil nuts (Nordlee et al., ). The company involved abandoned further commercial interest in these transgenic soybeans as a result. It should be emphasized that genes are not often obtained from known allergenic sources in the development of commercial transgenic varieties. However, when genes are transferred from known allergenic sources, it must be assumed that the gene encodes for an allergenic protein unless proven otherwise.

More typically, genes are obtained from sources with no history of allergenicity.

In these situations, a decision-tree approach is advocated for the assessment of the potential allergenicity of the novel protein. While no single test can perfectly predict the potential allergenicity of a specific novel protein from a source with no history of allergenicity, the application of a series of tests provides reasonable assurance that the novel protein is not likely to become an allergen. Several decision-tree approaches own been developed (FAO/WHO, ; Metcalfe et al., ; Taylor and Hefle, a).

These approaches rely upon evaluation of the source of the gene and its history of allergenicity, the sequence homology of the novel protein to known allergens, the immunoreactivity of the novel protein with serum IgE from individuals with known allergies to the source of the transferred gene, the immunoreactivity of the serum IgE from individuals with known allergies to sources that are broadly related to the source of the novel gene (e.g., grass pollen allergic individuals in cases where the gene is obtained from monocot sources), the pepsin resistance or digestive stability of the novel protein, and the immunogenicity of the novel protein in validated animal models (Fig.

3). Other factors especially the level of expression of the novel protein in the food are also likely to be significant since allergies are generally elicited by food proteins where dietary exposure is comparatively high.

Foods produced through agricultural biotechnology including corn, soybeans, canola, and potatoes are already reaching the consumer marketplace. The potential allergenicity of the novel proteins expressed in these commercial products has been assessed using the approaches indicated above.

The novel proteins in these approved transgenic varieties are not obtained from known allergenic sources, are not structurally homologous to known food or environmental allergens, and are sensitive to digestive proteolysis. Furthermore, the novel proteins are expressed at extremely low levels in the edible portions of these modified crops. Thus, the likelihood of allergenicity from this current generation of crops produced by agricultural biotechnology is virtually nil.

Considerable publicity has surrounded one specific transgenic variety, the so-called StarLink™ corn.

StarLink corn was never approved for human use, but was unfortunately approved for animal feed use. When segregation failed, some StarLink corn residues were found in corn-based food products intended for human consumption. Although the gene inserted in StarLink corn was obtained from a source with no history of allergenicity and the novel protein was not structurally similar to known food or environmental allergens, the novel protein was comparatively more resistant to digestive proteolysis than other novel proteins that had been approved for other genetically modified crops.

For this reason, StarLink corn was never approved for human consumption. However, given the extremely low level of exposure to the novel protein in StarLink corn in corn-based food products, the likelihood of allergic sensitization to this specific novel protein is low. Despite that and due to the concerns about the potential allergenicity of this transgenic variety, it has been withdrawn from the marketplace, although traces may remain for one or more growing seasons. This episode emphasizes the importance of assessing the potential allergenicity of transgenic varieties as part of the overall safety evaluation process.

Agricultural biotechnology can also be used to decrease the inherent allergenicity of foods.

The proteins in specific foods that are responsible for allergic reactions could be removed or altered through agricultural biotechnology. While no commercial examples exist yet of the application of this possibility, it is an athletic area of research with peanuts.

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Non-IgE Cell-Mediated Reactions
As noted earlier, cell-mediated allergic reactions, also known as delayed hypersensitivity reactions, own an onset time of 6–24 hours after ingestion of the offending food. The reactions develop slowly, reaching a peak at approximately 48 hours and then slowly subsiding over 72–96 hours.

Cell-mediated food allergies involve the interaction between specific antigens or allergens from the food and sensitized, tissue-bound T cells that release inflammatory mediators when sensitized (Sampson, ). The role of cell-mediated reactions in food allergies remains somewhat uncertain. Compelling and mounting evidence has accumulated, however, indicating that celiac disease occurs through a T cell-mediated mechanism (Ferguson, ; Strober, ).

Celiac Disease.

Also known as celiac sprue or gluten-sensitive enteropathy, celiac disease is a malabsorption syndrome occurring in sensitive individuals upon the consumption of wheat, rye, barley, triticale, spelt, and kamut (Ferguson, ; Lemke and Taylor, ). The role of oats in celiac disease has recently been questioned. Apparently, oats and oat products that are totally free of wheat, rye, and barley, are safe for celiac sufferers to consume (Janatuinen et al., ). After consumption of the offending grains or products made from these grains, the absorptive epithelial cells in the little intestine are damaged by an inflammatory process (Ferguson, ).

As a result, absorption of nutrients through the epithelium is compromised. The loss of absorptive function along with the ongoing inflammatory process results in a severe malabsorption syndrome characterized by diarrhea, bloating, weight loss, anemia, bone pain, chronic fatigue, weakness, muscle cramps, and, in children, failure to acquire weight and growth retardation (Lemke and Taylor, ; Skerritt et al., ). A part of wheat, the gliadin part, and related part in barley and rye are associated with initiation of celiac disease in susceptible individuals (Skerritt et al., ).

Celiac disease is an inherited trait, but the inheritance is complicated and poorly understood.

Celiac disease occurs in about 1 of every individuals in the U.S. (Kasarda, ). In some other parts of the world, celiac disease occurs more frequently. The highest prevalence occurs among individuals in certain regions of Europe (Greco et al., ; Kasarda, ). Celiac disease seems to happen more frequently among Europeans than among Americans of European descent for unexplained reasons. Celiac disease rarely occurs among individuals of Chinese or African descent (Ferguson, ).

The treatment of celiac disease involves the avoidance of wheat, rye, barley, triticale, spelt, kamut, and oats and products of these grains (Hartsook, ). The threshold dose of gliadin and related protein fractions needed to provoke celiac disease in sensitive individuals is not precisely known, but symptoms can be elicited by ingestion of little amounts of these grains (Lemke and Taylor, ).

If a gluten-free diet is followed, the symptoms of celiac disease will resolve and the absorptive function of the little intestine will be restored. Most celiac sufferers adhere to extremely strict gluten-free diets. In the absence of information on the safety of products made from the offending grains, affected individuals often select to avoid products that contain remarkably little amounts of protein from these sources including rye alcohol, wheat starch, malt extract, and vinegar. The wisdom of such severely restricted avoidance diets remains to be established.

Food Intolerances
In contrast to true food allergies, food intolerances happen through non-immunological mechanisms.

However, love true food allergies, food intolerances affect some individuals in the population but not every. Individuals suffering from food intolerances can generally tolerate little amounts of the offending food or food ingredient in their diet without ill effects. Food intolerances can be divided into three categories: anaphylactoid reactions, metabolic food disorders, and idiosyncratic illnesses.

Anaphylactoid Reactions. In IgE-mediated food allergies, the release of histamine and other mediators from the mast cells and basophils is mediated by the interaction of IgE with proteinaceous allergens, as described earlier.

In contrast, anaphylactoid reactions are caused by substances that bring about the release of the same mediators from mast cells without the involvement of IgE (Lemke and Taylor, ). Some substance in the implicated food is presumed to destabilize the mast cell membranes allowing for the spontaneous release of histamine and the other mediators. However, no such histamine-releasing substance has ever been isolated or identified in foods, although this mechanism is well established with certain drugs.

Strawberry sensitivity is generally cited as the best example of an anaphylactoid reaction. Although strawberries are known to cause adverse reactions (frequently urticaria) in susceptible individuals, there is little evidence for the existence of an IgE-mediated mechanism. Strawberries contain little protein, and no evidence has been found for the existence of a strawberry allergen. Furthermore, there is no evidence for the existence of strawberry-specific IgE in the sera of strawberry-sensitive individuals. Spontaneous histamine release is thus a plausible mechanism. However, if a substance exists in strawberries that destabilizes mast cell membranes, that substance has yet to be identified.

The possibility that strawberry sensitivity is a form of oral allergy syndrome has not yet been excluded, and is an equally plausible mechanism.

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Metabolic Food Disorders. Metabolic food disorders result either from inherited defects in the ability to metabolize some component of food or from a genetically sure, enhanced sensitivity to some foodborne chemical that occurs through an altered metabolic pattern (Lemke and Taylor, ). Lactose intolerance is an example of an illness that occurs when a genetic deficiency affects the host’s ability to metabolize a food component (Kocian, ).

In lactose intolerance, an inherited deficiency occurs in the quantity of the enzyme, β-galactosidase, leading to an impaired ability to digest lactose. Favism is an example of a genetic deficiency that enhances the sensitivity to a foodborne chemical. In favism, a genetic deficiency in glucosephosphate dehydrogenase in the erythrocyte results in an enhanced sensitivity to several hemolytic substances that happen naturally in fava beans (Mager et al., ). These two metabolic food disorders are the most common and best understood illnesses in this category of food intolerances.

Lactose Intolerance.

Lactose is a dissaccharide and the principal sugar in milk. Normally, lactose is hydrolyzed into its constituent monosaccharides, galactose and glucose, in the little intestinal mucosa. These monosaccharides can then be absorbed and used as metabolic sources of energy. In lactose intolerance, the activity levels of β-galactosidase, the key hydrolytic enzyme that exists in the mucosal membranes of the little intestine, are diminished (Houts, ; Suarez and Savaiano, ). Since lactose cannot be absorbed in the little intestine unless it is hydrolyzed to glucose and galactose, the undigested lactose passes into the colon where it encounters large populations of bacteria.

The colonic bacteria metabolize the lactose to CO2, H2, and H2O (Lemke and Taylor, ). Abdominal cramping, flatulence, and frothy diarrhea are the predominant symptoms of lactose intolerance (Bayless et al., ) and are the direct result of the action of the colonic bacteria on lactose. The symptoms vary in intensity in concert with the individual level of activity of β-galactosidase in the little intestine and the quantity of lactose ingested.

Lactose intolerance is a fairly common metabolic food disorder. Lactose intolerance is especially prevalent among some ethnic groups in the world including Greeks, Arabs, Jews, black Americans, Hispanics, Japanese, and other Asians (Houts, ; Suarez and Savaiano, ).

Only about % of Caucasians are affected (Suarez and Savaiano, ). Lactose intolerance can own its onset at any age, occurring as early as the age of three (Simoons, ). However, lactose intolerance tends to worsen with advancing age and is often more common and more severe among the elderly (Houts, ; Simoons, ). The level of intestinal b-galactosidase is generally sufficient at birth to permit digestion of lactose in mother’s milk, but susceptible individuals suffer as a result of decreased activity of this enzyme as life progresses. Lactose intolerance may also happen on a more transitory basis on occasion, secondary to another intestinal illness or infection such as a bout of viral gastroenteritis (Metcalfe, b).

Secondary lactose intolerance tends to subside rather quickly after the original illness is resolved.

Individuals with lactose intolerance are capable to control their symptoms through the avoidance of dairy products containing lactose (Lemke and Taylor, ). However, numerous lactose-intolerant individuals can tolerate some lactose in their diets. The degree of tolerance for lactose is individualistic and variable among such individuals. Yogurt, sour cream, and acidophilus milk that contain athletic cultures of bacteria with b-galactosidase activity, are better tolerated by lactose-intolerant individuals than other dairy products (Kolars et al., ).

Lactose-hydrolyzed milk is also available in the marketplace (Paige et al., ). And, lactose-intolerant individuals can add b-galactosidase to milk just before consumption, and this seems to be an effective practice (Barillas and Solomons, ). Certainly, the level of tolerance for dairy products is much higher with lactose intolerance than it is with IgE-mediated cows’ milk allergy (Taylor, ).

Favism. Individuals with an inherited deficiency of the enzyme, glucose phosphate dehydrogenase (G6PDH), in their erythrocytes are susceptible to favism.

Symptoms happen after consumption of fava beans or the inhalation of pollen from the Vicia faba plant (Mager et al., ). Fava beans contain vicine and convicine, naturally occurring oxidants that are capable to damage the erythrocyte membranes of G6PDH-deficient individuals causing hemolysis and the symptoms of hemolytic anemia (Marquardt, ). G6PDH is a critical enzyme in erythrocytes because it helps to maintain adequate levels of the reduced form of glutathione (GSH) and nicotinamide adenine dinucleotide phosphate (NADPH). GSH and NADPH assist to avert oxidative damage to erythrocytes. In individuals who are G6PDH-deficient, this protective mechanism is nonfunctional and the oxidants in fava beans can exert their hemolytic effects.

In rare cases with repeated exposure, more severe symptoms can happen including hemoglobinuria, jaundice, and renal failure. The onset time after ingestion of the fava beans ranges from 5 to 24 hours. The illness is self-limited, however, with symptoms resolving promptly and spontaneously upon avoidance of further exposure.

G6PDH deficiency is extremely common and affects approximately million individuals on a worldwide basis (Mager et al., ). The prevalence is highest among Oriental Jewish groups in Israel, Sardinians, Cypriot Greeks, African Americans, and certain African populations.

This inherited trait is virtually absent among Caucasians, North American Indians, and Eskimos. Despite the high prevalence of G6PDH deficiency, favism is an unusual occurrence because fava beans are not frequently eaten except in Mediterranean and Middle Eastern locales.

Idiosyncratic Illnesses
Some individualistic adverse reactions to foods are idiosyncratic in that the mechanism for these illnesses is unknown. Numerous reports, mostly anecdotal, own occurred regarding illnesses in certain individuals attributed to certain specific foods or food ingredients.

Conceivably, a large number of diverse mechanisms could be involved in these idiosyncratic reactions. The symptoms involved in idiosyncratic reactions range from unimportant to severe, life-threatening reactions (Taylor et al., b).

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The role of specific foods or food ingredients in the causation of these idiosyncratic reactions remains to be sure in numerous cases. The cause-and-effect relationships can only be established through carefully controlled DBPCFCs (Taylor et al., b). A positive DBPCFC would definitely confirm that the specific food or food ingredient is involved in the specific adverse reaction.

The mechanism of the adverse reaction, however, cannot be sure from the positive DBPCFC alone. A negative DBPCFC indicates either that foods are not involved in causation of the reaction or at least that the specific food or food ingredient used in the challenge was wrongly incriminated. Unfortunately, DBPCFCs are rarely performed to establish convincingly that a specific food or food ingredient is associated with a specific idiosyncratic reaction.

The role of specific foods or food ingredients are firmly established in a few of the numerous alleged foodborne idiosyncratic reactions.

Sulfite-induced asthma is perhaps the best example (Bush and Taylor, ). In the case of sulfite-induced asthma, numerous clinicians own documented the role of sulfites in the provocation of asthma in dozens of patients using DBPCFC protocols (Bush and Taylor, ). Aspartame has been identified as a causative factor in two subjects using DBPCFC (Kulczycki, ). However, other cases of aspartame-induced urticaria own not been identified so this may be a rather rare phenomenon.

For numerous other alleged idiosyncratic reactions to specific foods or food ingredients, the association with the specific food or food ingredient has not been conclusively documented through DBPCFCs.

Examples would include the role of chocolate or aspartame in migraine headache; the roles of BHA, BHT, tartrazine, benzoates, or parabens in chronic urticaria; the role of tartrazine in asthma; the role of monosodium glutamate (MSG) in asthma or MSG Symptom Complex; and the role of sugar in aggressive behavior (Bush and Taylor, ). A thorough critique of the numerous studies that own been conducted on the role of these foods or food ingredients in the causation of these idiosyncratic reactions is beyond the scope of this specific review.

However, extremely few of the clinical studies own used double-blind and placebo-controlled trial designs. Furthermore, numerous of the studies own involved individuals with chronic, episodic symptoms such as chronic urticaria or asthma and the clinical investigators own removed critical medications from the patients before initiating the challenge trials. In such cases, the observed symptoms might be due either to the challenge substance or to the withdrawal of medications that controlled the condition. With such critical clinical design flaws, the role of these specific foods and food ingredients in  these specific idiosyncratic illnesses remains unproven.

Furthermore, psychological disorders may be involved in perceived reactions to specific foods or food ingredients (King, ; Selner and Staudenmayer, ).

In a few cases, the role of specific foods or food ingredients in idiosyncratic reactions has been disproven by careful clinical investigations. However, consumers may persist in their belief that such reactions happen. The outstanding example of such a reaction is the role of artificial food colors in hyperkinetic behavior in children.

Several decades ago, Dr. Benjamin Feingold implicated artificial food colorants as causative factors in hyperkinesis on the basis of poorly controlled trials and anecdotal experiences (Feingold, ). The resulting publicity on the Feingold hypothesis was considerable, and, consequently, numerous consumers became convinced of a relationship between ingestion of artificial food colorants and provocation of hyperkinetic behavior in children. Subsequently, several double-blind, placebo-controlled challenge trials own been conducted with artificial food colorants and own demonstrated convincingly that few, if any, hyperkinetic children are adversely affected by the ingestion of these food colorants (Harley et al., a).

Despite this evidence, numerous consumers persist in their belief regarding the role of artificial food colorants in hyperkinetic behavior.

A similar situation exists with honor to monosodium glutamate where the involvement of MSG intake in the so called Chinese Restaurant Syndrome, now more appropriately called MSG Symptom Complicated, has been alleged so often that it is now accepted as fact by numerous consumers. However, the role of MSG in MSG Symptom Complicated has not been corroborated in carefully controlled clinical challenge studies (Kenny, ; Tarasoff and Kelly, ).

More recently, MSG intake has been linked to asthma (Allen et al., ). However, the role of MSG in provocation of asthma seems questionable at best when patients are evaluated using a DBPCFC protocol (Bush and Taylor, ). The alleged role of tartrazine, also known as FD&C Yellow #5, in asthma and chronic urticaria is also extremely questionable in the light of DBPCFCs (Bush and Taylor, ; Stevenson et al., ).

Yet, undeclared tartrazine remains the basis for a large number of FDA recalls.

Sulfite-Induced Asthma. Sulfiting agents allowed for use in foods include sulfur dioxide, potassium metabisulfite, sodium metabisulfite, potassium bisulfite, sodium bisulfite, and sodium sulfite. Sulfiting agents own been used as food ingredients for numerous years, because they own numerous significant technological benefits (Taylor et al., b). Sulfites also happen naturally in some foods, especially fermented foods (Taylor et al., b).

However, residual levels of sulfites in foods vary from a few ppm arising mostly from natural sources, to less than 10 ppm to >1, ppm as a result of additive usage.

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Although sulfites own been used for centuries, they own been implicated as triggers of asthma in some sensitive individuals only in recent years (Bush and Taylor, ; Stevenson and Simon, ). The reactions generally happen within a few minutes after the ingestion of a provoking dose of sulfite. The reactions can be fairly severe on occasion and deaths own been attributed to sulfite-induced asthma (Bush and Taylor, ).

The role of sulfites in the causation of asthma in susceptible individuals has been well documented by DBPCFC (Bush and Taylor, ; Stevenson and Simon, ). Other symptoms own also been alleged to happen as a result of sulfite sensitivity but these reports own been largely anecdotal and unverified by DBPCFC (Bush and Taylor, ).

Sulfite-induced asthma affects only a little percentage of every asthmatic individuals (Bush et al., ). The prevalence among severe asthmatics who are dependent upon steroid-based drugs for control of their symptoms appears to be in the range of 4–7%, while mild asthmatics do not seem to be extremely susceptible to sulfite ingestion (Bush et al., ).

Thus, the overall prevalence of sulfite-induced asthma is estimated at –% of the entire asthmatic population (Bush et al., ).

Sulfite-induced asthmatics display thresholds for sulfites (Bush and Taylor, ; Taylor et al., ). While the ingestion of high doses of sulfite in highly sulfited foods and beverages can be fairly hazardous for susceptible individuals, the ingestion of sulfited foods with lower levels of residual sulfite (< ppm as entire SO2) seems to present little risk (Taylor et al., ). Thus, sulfite-sensitive asthmatics must be alert to the presence of sulfites in foods at levels that are required to be declared on the ingredient statement, but are at no risk from ingestion of sulfites from foods that own levels of residual sulfite under the detection limit of current assay procedures (<10 ppm as entire SO2).

The mechanism of sulfite-induced asthma is not known.

Several diverse mechanisms own been proposed including IgE-mediated reactions, hypersensitivity to inhaled SO2 from ingestion of acidic foods and beverages, and sulfite oxidase deficiency (Bush and Taylor, ). However, none of these mechanisms has been proven, so sulfite-induced asthma remains an idiosyncratic illness.

Implications for Food Manufacturing

Erin Spain: This is breakthroughs, the podcast from Northwestern University Feinberg School of Medicine. I’m Erin Spain, executive editor of the Breakthroughs newsletter. There’s been an uptick in childhood food allergies in recent years, and new evidence from northwestern shows that food allergies are also becoming more common in adults.

Numerous of the reactions to these allergies are life threatening. Why is this increase happening and how can we hold people affected by food allergy safe? Dr. Ruchi Gupta is trying to answer those questions. She’s dedicated her career to food allergy and asthma research here at Northwestern and the Ann & Robert H. Lurie Children’s Hospital of Chicago where she’s an attending physician. Her work is debunking myths and shaping policies around food allergy. Thanks for joining me today.

Ruchi Gupta: So happy to be here. Thank you.

Erin Spain: You’re an expert on childhood food allergies and asthma.

Leading much of the current research on this topic, but your most recent paper and JAMA Network Open focused on adults with food allergies. Why the shift to adults?

Ruchi Gupta: That’s a grand question. As I am a pediatrician, you know, over the years we’ve been studying, love he said, pediatric food allergy and that’s where the emphasis has been, but now a lot of those kids are growing up and they’re becoming adults and they’re going to college and they continue to own their food allergy and then you know, at meetings with other physicians, you start hearing about how numerous adults seem to be developing food allergies as adults.

Since we had the expertise in doing large scale prevalence studies, we thought we would modify our pediatric study for adults and really understand how numerous at people in the United States are affected by food allergy and what that looks like.

Erin Spain: So we really didn’t own excellent data on how numerous adults?

Ruchi Gupta: No, no. We own extremely little data on adults with food allergy.

For some reason we’ve every really focused on the kids.

Erin Spain: So this paper that came out did make some headlines. You found that almost half of adults, they developed adult-onset food allergies. And was that surprising to you?

Ruchi Gupta: So surprising. I mean, we knew, love I said, you hold hearing it right? Anecdotally in clinic and you start hearing and seeing more and more adults talking about how they’re developing these food allergies, but the number we found was extremely surprising. I mean, we really found that about half, 48 percent said they developed at least one new food allergy as an adult that they didn’t own as a kid.

So those numbers were a little astonishing. Additionally, about one in four adults said they developed an allergy as an adult and never had a food allergy as a kid. So that’s, that’s a lot of adults developing new allergies.

Erin Spain: And the allergies are similar to what we see in children. There’s milk, peanuts, tree nuts, fin fish, egg, wheat, soy and sesame. Those are among the most common. But for some reason shellfish is at the top of the list for adults. Do we know why that is?

Ruchi Gupta: That is such a excellent question.

I ponder my favorite thing about doing research is once you do a study, it opens up love more that you can do and answer new questions. You’re absolutely correct, the top eight, we used to call it, now we call it the top nine because sesame is becoming the ninth most common allergen. Those are the same in kids and adults, but the adults own a extremely diverse order with shellfish being way beyond other foods. I ponder % of adults reported having a shellfish allergy. It was the most common allergen in adults by far because after that it was milk and peanut around % — %. What is it about shellfish?

I’ve heard from so numerous adults «Oh my gosh, I love shellfish and I can’t eat them anymore» and that is really hard for a lot of people. I ponder we now need to explore what is it about the proteins and shellfish and what’s so unique about the specific food that is causing so much adult-onset allergy?

Erin Spain: Well, the exciting thing about this study is it was a survey. It’s a survey you said that you’ve used for children before and it’s self-reported. So people, you know tell, well I ponder I own a food allergy or I own a food allergy.

Well, tell me about that because 20% of the adults reported having a food allergy, but you sure that it was only actually half of them that seem to own a genuine allergy. It was more love a sensitivity from how they reported that they reacted to the food. Tell me about that.

Ruchi Gupta: Yeah. I really appreciate you asking this question because I ponder this has been one of the most confusing questions that’s come up in the media and how people take it. So, love you said it’s a survey. So people were asked, adults were asked do you own a food allergy? Then if they said yes, it went into what food allergies. So it would enquire specifically.

So tell you said you own peanut milk and wheat. Every correct. Then it would take you through each food, it would tell «For peanut allergy, what are your most severe symptoms that you’ve had?» And then you would list them and you could record in or you could select from the list. And then it would enquire you things about diagnosis and about emergency department use and about epinephrine use, right? So it asks you a series of question, then it would go into milk and would enquire you the same series of questions and then it would go into wheat.

So you had to be specific for each food. Now what we did with that data, because there are so numerous food related conditions, right? You can own so numerous diverse things that looked love a food allergy but may not be. So what we did is we tried to do our best. We had an expert panel go through and attempt to clean the data so that if there were things that may be something else. So tell said you own a milk allergy, but you said you just get stomach cramps and some diarrhea. Okay. Then we would tell, well, we’re not completely certain that’s a food allergy that might be lactose intolerance.

So we would put it aside. Okay. So when people tell they were incorrect, that’s not true. So let’s go back to food allergies. The problem is that food allergies can impact any organ system, correct, so you can own GI symptoms. In fact, it’s one of the most common ones. Vomiting is one of the most common things that happen as an allergic reaction. You can own skin symptoms so you can get hives, you can own oral symptoms, you can get tightening of the throat and tingling, swelling of your mouth.

You can own respiratory symptoms, you can own trouble breathing, wheezing, tightness in the chest. You can even own cardiovascular, right? The drop in blood pressure. The problem with food allergies is you can own these mild symptoms or you can own them progressed to severe symptoms with the breathing difficulty and tightening of the throat and that can be life threatening. When people report only GI symptoms — we take them out. Or they only report oral symptoms because sometimes you can own something called oral allergy syndrome where you’re actually allergic to the pollen.

So if you eat a fruit and you only get tingling and a little swelling and itching in your mouth, that’s not a food allergy. But those could also be symptoms of a food allergy. So endless tale to tell you that what we really did was attempt to take a people who had symptoms that could glance love an intolerance or oral allergy syndrome and take them out and that was about half of the people. So whether they own a true food allergy, we are not certain. Whether they own an intolerance, we’re not certain. But, what it told us was that can you believe that one in five adults ponder that they own a food allergy and do potentially own some food related condition.

That’s a huge number.

Erin Spain: And it underscores the importance of getting that diagnosis and going into your doctor and really determining is this a food allergy?

Ruchi Gupta: And that was our goal by saying, glance, there’s one in five, but then of the convincing there’s only one in 20 that are getting diagnosed. I understand this as an adult, you know, a lot of times what happens is you eat a food, you own a negative reaction, and you’re love, well I just can’t eat that food and you don’t necessarily ponder, oh, let me go get it checked out by a doctor and I desire this to assist people ponder, let me go get it checked out by a doctor.

Because avoiding foods in your diet is so hard, right? Trying to take out milk from everything you eat. I ponder for me the goal was, you know, let’s attempt to figure out what every these food related conditions are so that you’re not having to avoid a food unnecessarily and if it is a true food allergy, you need to know how to manage it because that can be life threatening and you need to know what type of reactions can happen and you need to carry your epinephrine with you.

Erin Spain: You touched on it a little bit with the shellfish.

What is it about the shellfish, the protein?What are some of the hypothesis out there about why more kids and adults are developing food allergies? I know there’s some theories. You’re one of the experts. What do you say?

Ruchi Gupta: I know, and this is what’s so exciting because we every know that genetics plays a role, right? But we would not own this epidemic and this huge increase if it was just genetics. So we need to better understand what is it in the environmental component that has changed over beautiful much a generation that has caused this incredible increase.

So some theories are, of course, the hygiene hypothesis, right? Love, are we becoming too clean?

Erin Spain: The hand sanitizers the soap?

Ruchi Gupta: Correct. It could extremely well be because our bodies are not exposed to things that are not fighting things they should. They’re fighting things they shouldn’t. There’s a couple of other really exciting hypotheses that are somewhat related. The microbiome, you’ve probably heard that that’s really boiling correct now. What is it about our gut bacteria and how much of a role does that frolic and what are we doing to it? You know, the whole thought of getting antibiotics early in life and that first year every the antibiotics infants are getting or mothers are getting during pregnancy, other hygiene related things.

You know, C-section births are up and so they’re not going through the normal vaginal canal and then they’re not getting that natural bacteria. Is that hurting them? Is that part of that whole hygiene piece and the microbiome that is in their gut and how do we eat, what are we eating these days? You know, are we eating locally grown food love before? No. Are eating from every over the world. What helpful of pesticides are used? You know, the ideas of GMOs. There are every these question marks that we haven’t fully understood yet.

Erin Spain: You’re interested in looking into those?

Ruchi Gupta: Yeah, I mean, you own to.

I would love to better understand what these factors are. Chances are they’re not one factor. We’re not going to tell, oh, it’s every about this. It’s going to be a group of factors and how our lifestyles own changed. The one large breakthrough that’s happened is there was a large study done in London called the LEAP Study and they found that if you feed infants, high risk infants, peanut products early in life, that you may be capable to prevent peanut allergy. So that exposure through the gut early could be preventive. This was a really large breakthrough because for the first time we own a way to potentially prevent it. Because before that we told pediatricians to tell families to avoid peanut products until age three, which is what I did with my daughter and she has a peanut allergy.

It was a extremely, extremely large finding to ponder that, okay, maybe by waiting we may be hurting.

Erin Spain: Now parents are giving those babies in the first six to 12 months, a little bit of peanut butter.

Ruchi Gupta: They should. They should absolutely. I mean, I ponder that is a extremely significant finding and every parents of infants should initiate peanut products watered below peanut butter.

Early in life, by that, you know, not the first food, but in that first group of foods, love around six months for sure.

Erin Spain: You’re a pediatrician as you mentioned and this is your focus — children and allergies. How did you start below this path? You mentioned that your daughter has a peanut allergy.

Ruchi Gupta: So it’s an exciting tale because I am a pediatrician and I came to Northwestern and Lurie Children’s 14 years ago to really study asthma disparities and to work with one of the leaders in the field that was here at that time and I met a family with two young children with extremely severe food allergies.

Been to the ER and hospitalized and they really wanted research to be done in this area. I was junior faculty, «Hey, you desire to come in, you desire to work on this?» I knew extremely little about food allergies back then, but what I found was compared to asthma, which I had been studying, there was a huge hole. We didn’t even know how numerous, as you know, we talked about. We didn’t know how numerous kids had it, how numerous adults had it. We didn’t know the basic prevalence or types of foods people were allergic to or what kinds of symptoms.

Every that data was not in the literature. I was trained in health services research and had my MPH and I was unused and ready to start. I thought, you know, this may be an area that I could make a difference and own an impact because so little is known. So that’s how I started. As I was studying it, three years into it, I believe, my son who loves peanut butter and jelly sandwiches, was playing with my daughter and touched her, I guess every over her face because she just broke out in hives.

Erin Spain: And you knew what it was immediately?

Ruchi Gupta: Oh yeah. I’m love, wow, you know, what helpful of present is this?

It’s really had such an amazing influence on my life and my career because there is a large difference just studying a condition and then living with a condition and every the things I go through every day in my life with her really do assist influence the research. By having her I know so numerous others with food allergy and then these support groups and listening to what their needs are. Right? Listening to that patient and that whole patient centeredness.

It just really brings that home because they know what they need. We as researchers need to hear to them and answer their questions. So, it’s been a blessing in some ways. But yeah, extremely difficult.

Erin Spain: How ancient is your daughter now?

Ruchi Gupta: She’s

Erin Spain: She’s still working through the peanut allergy? Because I know at some point a lot of people outgrow it.

Ruchi Gupta: She is working through it.

Only about 10 to 20 percent outgrow peanut allergy. She’s got peanut and tree nuts and she used to own an egg which she has outgrown. It’s a challenge every day because, you know, we don’t own a severity spectrum for food allergies, which I ponder a lot of parents, it really affects their life because if you don’t know my kid is mild or moderate. You know, people enquire you, «Oh, how severe is it?» and we own nothing to tell them and so everyone’s severe, right? Everyone could own a life threatening reaction.

It’s a lot of anxiety and fear for families because food is a part of everything kids do. Even adults.

Erin Spain: You’re doing so much to bring knowledge into the scientific community and build the literature. In , you led a study that, found that eight percent of kids in the US own at least one food allergy. This was new information as you said, we didn’t know before, and 40 percent of those kids had experienced a life threatening reaction already in their lives.

How significant was this when you were capable to actually put some numbers out there?

Ruchi Gupta: It was really incredible to see what happened after that because after that study, people had numbers that they could hold onto and tell schools and see it in their classrooms. You know, 8% is about two in every classroom. It’s about one in 13 kids. When you picture it love that, you’re love, oh yeah, that’s true. You know, there are about two kids in the class that own a food allergy and you realize how realistic this is and how prevalent.

By being capable to list the foods and talk about the reactions I ponder it made more sense and it increased awareness and people started to get it and we actually repeated that study that was published in pediatrics again in December of What was exciting, the numbers are beautiful comparable, but we asked this time about emergency department visits and one exciting thing we found was of kids with food allergy, about 1 in 5 go to the emergency department every year for their food related reaction.

Erin Spain: So these are severe reactions?

Life threatening reactions?

Ruchi Gupta: Yeah. They are having them and so people would tell, «Okay, you own a food allergy, but how much does it impact your life?» So, for the first time we were capable to quantitate that and tell, you know, 1 in 5 are going every year. It’s a large deal. It’s something that we own to take seriously and assist protect these kids.

Erin Spain: And what is it, about children, they actually die from the reaction and that’s something that you were trying so hard to prevent through education and awareness.

Ruchi Gupta: Every time that happens, love every of our hearts are broken and we desire to prevent that from happening so badly and not only the deaths but even the severe reactions because they throw you off course.

You know, when you own one of those shut calls, it messes you up. It’s hard to then go out to eat and do normal things. But what’s so grand, I feel love, you know, in the 14 years I’ve been in this field, I’ve never seen a field change so much. So the quantity of research that’s happening now, we actually own treatments that will be coming out this year.

Erin Spain: Wow.

Ruchi Gupta: Yeah, so a lot of the researchers at Lurie Children’s are working on them.

There is oral immunotherapy. Eating little amounts and increasing the dose and that’s going to hopefully be out later this year. It’s already in phase filed five clinical trials. It feels extremely, extremely likely that it’ll be on the market. There’s a patch epicutaneous immunotherapy for peanut that’s coming out and then these companies are working on the next set of foods, the next most common foods. There’s a couple other treatments that I’ve heard of and that are in diverse phases of trials.

So I feel love in the next five to 10 years we’ll own grand treatments for food allergy. The other grand thing that I’ve seen change over time in this 14 year period, as the awareness has been picked up, schools and Chicago Public Schools where one of the first to join us building policies, having stock epinephrine in case of an emergency. Unfortunately, this every was sparked by, as you said, a young kid dying in school after an anaphylactic reaction and there was no epinephrine. After that CPS said, we’re not going to ever let this happen again. They passed a law to own stock epinephrine in every CPS school.

And then every through the country, I ponder, every state now has a law or a policy around stock epinephrine in school. To see policies developed, to see the community coming together to protect kids and adults with food allergy so quickly is so inspiring.

Erin Spain: You said kids are sometimes the biggest advocates, classmates, they desire to assist protect their friends.

Ruchi Gupta: Yes, and to that, you know, we do three areas of research that epidemiology, that we’ve talked about, we do a lot of the clinical care, helpful of that early introduction stuff that we talked about.

The third large pail we own is community. We work extremely closely with the schools and we’ve actually developed videos that are free on our website and for schools to use around how to teach a classroom about food allergies and how to own your peers be supportive. What we found is that is the number one thing to protect these kids — is if they own that peer support and not the bullying. Bullying is also extremely common, but if we can take it to developing more peer understanding and peer support and it could change these kids’ lives.

Erin Spain: We’ll make certain to put links to those videos on the podcast website so people can glance them up and share them. (Watch Gupta’s food allergy peer-to-peer educational videos.)

Ruchi Gupta: That would be great.

Erin Spain: Well this is fascinating.

The past 14 years, as you mentioned, so much has changed, but it sounds love we are now at a point where there’s going to be some genuine treatments and we’re really looking forward to see what’s coming up.

Ruchi Gupta: Thank you. Yeah, I am too. You know, I own a little cartoon on my wall at work and it is what I hope to see. It’s an adult talking to a kid and the adult is saying, «You know, in my day there were no food allergies», because this is what you hear every the time.

Then that kid grows up and as an adult talking to a kid and saying, «You know, in my day there were food allergies». So hopefully that’s where we’re headed and hopefully I can assist be a part of that.

Erin Spain: Well, thank you so much Dr. Ruchi Gupta for coming and sharing your research with us today.

Ruchi Gupta: My pleasure. Thank you.

Erin Spain: A note for physicians who hear to this program, you can now claim continuing medical education credit just by listening to this podcast.

Go to our website and search for «CME» for more details.

On Monday, based on a detailed review of every available evidence on the topic, the American Academy of Pediatrics published updated guidance on what works and what doesn’t when it comes to the prevention of food allergies and other allergic conditions. The new guidelines continue to liberalize the introduction of what are thought to be highly allergenic foods such as peanuts, fish and milk.There is no convincing evidence that delaying the introduction of allergenic foods beyond 4 to 6 months of age works in preventing food allergies, the report says.

In addition, there is strong evidence that purposeful, early introduction of peanuts as early as 4 months may prevent the development of a peanut allergy in infants at high risk, defined in this report as those with a shut relative with a history of an allergic condition. «There is no reason to delay giving your baby foods that are thought of as allergens love peanut products, eggs or fish,» Dr. Scott Sicherer, a co-author of the report, said in a statement. «These foods can be added to the diet early, just love foods that are not common allergens, love rice, fruits or vegetables.»The gastrointestinal tract is home to a unique set of immune system cells, and when these cells are given a taste of the allergenic proteins in diverse foods, they take up these proteins and become tolerant to them.

Dr. David Stukus, a pediatric allergist and associate professor of pediatrics in the Division of Allergy and Immunology at Nationwide Children’s Hospital, said that’s true «as endless as it’s introduced early and in an ongoing fashion,» meaning there is a critical window of time during which being introduced to these foods may lead the body to become tolerant. And early means as soon as 4 months to 6 months of age, said Stukus, who was not involved with the new guidelines.The report also looked at whether breastfeeding protects against eczema, wheezing, asthma and food allergies. Exclusive breastfeeding for the first three to four months of life was found to be protective against eczema, the authors concluded.

Any quantity of breastfeeding beyond that time, even if not exclusive, was found to be protective against wheezing in the first two years of life and asthma in the first five years and even later. The report says no conclusion could be made when it came to breastfeeding and its effect on the prevention of food allergies. No evidence was found that avoiding allergenic foods during pregnancy or during breastfeeding worked in the prevention of allergic conditions. Neither did the use of special hydrolyzed formulas, even in kids who were at high risk. «I really appreciated the comprehensiveness of this clinical report,» said Dr.

Wendy Sue Swanson, a general pediatrician and chief of digital innovation at Seattle Children’s Hospital. Swanson, who has endless advocated for the early introduction of a diversity of foods in young children, described feeling grateful for the guidance, given the ongoing changes in the understanding of allergy prevention. In , the American Academy of Pediatrics recommended delaying the introduction of cow’s milk until children were 1 year ancient, egg until 2 years and peanuts, tree nuts and fish until 3 years. «Recommendations were to avoid allergenic foods until children were older,» Stukus said.

«The thought process at the time was, well, if we avoid any exposure, maybe the allergic response won’t develop.»In , after a review of the available literature, the organization issued a report saying there was no convincing evidence that delaying allergenic food introduction prevented food allergies. The report did not give specific guidance as to when these foods should be introduced. Almost 10 years later, after a study was published in the New England Journal of Medicine, the academy recommended that babies at high risk of developing peanut allergies be introduced to peanuts as early as 4 months. Infants considered at high risk included those with eczema and/or an egg allergy.

This study — known as the Learning Early About Peanut or LEAP trial — showed that children at high risk of developing peanut allergies who are introduced to peanuts at 4 months to 6 months ancient had a significantly lower risk of developing a peanut allergy than those who waited until they were 5 years; % of the kids who had peanuts early developed an allergy, compared with % of the kids who waited. The LEAP trial formed the basis for Monday’s new recommendations, which urge the early introduction of peanut products in infants at high risk for allergies.But most babies are not at high risk, and peanuts are just one of the eight culprit foods; the others are milk, eggs, fish, crustacean shellfish, wheat, soy and tree nuts, according to the US Centers for Disease Control and Prevention.

The evidence for other foods and children

The latest report explains that the same mechanism that protects infants at high risk is likely to protect infants at low or standard risk of developing food allergies.

A study that examined these other foods, known as the Enquiring About Tolerance or EAT trial, recruited 1, 3-month-olds and randomly assigned them to get six allergenic foods — peanut, cooked egg, cow’s milk, sesame, whitefish and wheat — at that age or to wait until 6 months. The team then measured whether these infants developed food allergies between 1 and 3 years ancient. Only 40% of parents were capable to hold up with the diverse food frequency that the study protocol recommended. When researchers looked at the data from every of the children in the study, no difference was found in the rates of food allergies.

When they looked at only the children whose parents had been capable to hold up with the foods, there was a significantreduction in peanut and egg allergies. «The EAT study provides some evidence but is less strong than the LEAP trial evidence,» said Dr. Elizabeth Matsui, pediatric allergist and chairwoman of the American Academy of Pediatrics Section on Allergy and Immunology, comparing the trial that included the diverse foods to trial that involved peanuts. When the risk of an illness is relatively low, proving that it can be decreased even further is extremely hard, she added. An significant takeaway from the trial is that introducing a variety of foods as early as 4 months is safe, Stukus explained.

Overwhelmingly, the data is pointing toward the benefit of early food introduction, Swanson said. «I don’t desire kids to delay introduction. Stop medicalizing this and let babies eat,» she added.

The bottom line for parents

«It’s not just early introduction. It’s routine feeding. It’s habituating. We need to make a habit of eating extremely diverse foods,» Swanson said. «It’s a grand habit to own your whole life, because 50% of people who develop a food allergy develop it in adulthood.»In his practice, Stukus has started to recommend early introduction — between 4 and 6 months of age — of allergenic foods for every babies, no matter their individual risk.

He encourages parents to continue to give these foods several times a week for babies who are tolerating them. «I ponder the benefits far outweigh the risks in this situation,» he said. The most serious risk is anaphylaxis, a severe allergic reaction that can be life-threatening. But in most young infants, Stukus explains, anaphylaxis manifests as vomiting and hives, without the difficulty breathing and the closing airways that can be seen in older children.

Parents who spot vomiting or hives — especially together — should still seek medical attention. But pediatricians and parents same can relax assured that these foods can be introduced freely at home, reversing decades of fear in the introduction of new foods, he added. «We come from a put of restriction and medicalization,» Swanson said. Pediatricians were strong in telling parents to be cautious, and now they must be strong in telling parents not to be cautious. «No, I don’t desire you to be cautious. In fact, waiting might cause harm,» she said.

IgE Mediated Food Allergies

The IgE mediated food allergies most common in infants and children are eggs, milk, peanuts, tree nuts, soy and wheat. The allergic reaction can involve the skin, mouth, eyes, lungs, heart, gut and brain. Some of the symptoms can include:

  1. Swelling of the lips, tongue or throat
  2. Stomach pain, vomiting, diarrhea
  3. Shortness of breath, trouble breathing, wheezing
  4. Skin rash, itching, hives
  5. Feeling love something terrible is about to happen

Sometimes allergy symptoms are mild. Other times they can be severe. Take every allergic symptoms seriously. Mild and severe symptoms can lead to a serious allergic reaction called anaphylaxis (anna-fih-LACK-sis).

This reaction generally involves more than one part of the body and can get worse quick. Anaphylaxis must be treated correct away to provide the best chance for improvement and prevent serious, potentially life-threatening complications.

Treat anaphylaxis with epinephrine. This medicine is safe and comes in an easy-to-use device called an auto-injector. You can’t rely on antihistamines to treat anaphylaxis. The symptoms of an anaphylactic reaction happen shortly after contact with an allergen. In some individuals, there may be a delay of two to three hours before symptoms first appear.

Cross-Reactivity and Oral Allergy Syndrome

Having an IgE mediated allergy to one food can mean your kid is allergic to similar foods.

For example, if your kid is allergic to shrimp, he or she may be allergic to other types of shellfish, such as crab or crayfish. Or if your kid is allergic to cow’s milk, he or she may also be allergic to goat’s and sheep’s milk. The reaction between diverse foods is called cross-reactivity. This happens when proteins in one food are similar to the proteins in another food.

Cross-reactivity also can happen between latex and certain foods. For example, a kid who has an allergy to latex may also own an allergy to bananas, avocados, kiwis or chestnuts.

Some people who own allergies to pollens, such as ragweed and grasses, may also be allergic to some foods. Proteins in the pollens are love the proteins in some fruits and vegetables.

So, if your kid is allergic to ragweed, he or she may own an allergic reaction to melons and bananas. That’s because the protein in ragweed looks love the proteins in melons and bananas. This condition is oral allergy syndrome.

Symptoms of an oral allergy syndrome include an itchy mouth, throat or tongue. Symptoms can be more severe and may include hives, shortness of breath and vomiting. Reactions generally happen only when someone eats raw food. In rare cases, reactions can be life-threatening and need epinephrine.

Non-IgE Mediated Food Allergies

Most symptoms of non-IgE mediated food allergies involve the digestive tract.

Symptoms may be vomiting and diarrhea. The symptoms can take longer to develop and may final longer than IgE mediated allergy symptoms. Sometimes, a reaction to a food allergen occurs up 3 days after eating the food allergen.

When an allergic reaction occurs with this type of allergy, epinephrine is generally not needed. In general, the best way to treat these allergies is to stay away from the food that causes the reaction. Under are examples of conditions related to non-IgE mediated food allergies.

Not every children who react to a certain food own an allergy. They may own food intolerance. Examples are lactose intolerance, gluten intolerance, sulfite sensitivity or dye sensitivity.

Staying away from these foods is the best way to avoid a reaction. Your child’s doctor may propose other steps to prevent a reaction. If your kid has any food allergy symptoms, see your child’s doctor or allergist. Only a doctor can properly diagnose whether your kid has an IgE- or non-IgE food allergy. Both can be present in some children.

Eosinophilic Esophagitis (EoE)

Eosinophilic (ee-uh-sin-uh-fil-ik) esophagitis is an inflamed esophagus.

The esophagus is a tube from the throat to the stomach. An allergy to a food can cause this condition.

With EoE, swallowing food can be hard and painful. Symptoms in infants and toddlers are irritability, problems with eating and poor weight acquire. Older children may own reflux, vomiting, stomach pain, chest pain and a feeling love food is “stuck” in their throat. The symptoms can happen days or even weeks after eating a food allergen.

EoE is treated by special diets that remove the foods that are causing the condition.

Medication may also be used to reduce inflammation.

Food Protein-Induced Enterocolitis Syndrome (FPIES)

FPIES is another type of food allergy. It most often affects young infants. Symptoms generally don’t appear for two or more hours. Symptoms include vomiting, which starts about 2 hours or later after eating the food causing the condition. This condition can also cause diarrhea and failure to acquire weight or height. Once the baby stops eating the food causing the allergy, the symptoms go away. Rarely, severe vomiting and diarrhea can happen which can lead to dehydration and even shock.

Shock occurs when the body is not getting enough blood flow. Emergency treatment for severe symptoms must happen correct away at a hospital. The foods most likely to cause a reaction are dairy, soy, rice, oat, barley, green beans, peas, sweet potatoes, squash and poultry.

Allergic Proctocolitis

Allergic proctocolitis is an allergy to formula or breast milk. This condition inflames the lower part of the intestine. It affects infants in their first year of life and generally ends by age 1 year.

The symptoms include blood-streaked, watery and mucus-filled stools. Infants may also develop green stools, diarrhea, vomiting, anemia (low blood count) and fussiness.

When properly diagnosed, symptoms resolve once the offending food(s) are removed from the diet.

Medical review December

Centuries ago, Lucretius said that one man’s food may be another man’s poison. Such is the case with food allergies. Individuals with food allergies and other types of food sensitivities react adversely to the ingestion of foods and food ingredients that most consumers can ingest with no problems.

Eating is necessary to sustain life. For most consumers, eating is an enjoyable experience given the variety and abundance of foods available in the marketplace.

For some individuals, however, consuming certain foods can be a debilitating, possibly even life-threatening, experience. Individuals with various forms of food allergies and sensitivities must avoid certain foods or food ingredients in their diets. For such people, the joy of eating is diminished by the ever-present concern that they might consume a food or food ingredient that will elicit an adverse reaction. For them, food selection can become a tedious task requiring the painstaking reading of ingredient lists on the labels of packaged foods and a ceaseless search for more knowledge about food composition.

Food preparation requires careful attention to details such as “cooking from scratch,” seeking alternative recipes for numerous dishes, and avoidance of shared utensils, containers, and cooking surfaces between allergenic and non-allergenic foods. In situations where one family member has a extremely serious allergic sensitivity, the entire family often has to avoid the offending food as a precautionary measure.

Definitions
Food allergies and other food sensitivities are individualistic adverse reactions to foods (Taylor, ).

These food-related illnesses are individualistic because they affect only a few people in the population; most consumers can eat the same foods with no ill effects. Numerous diverse types of reactions are involved in these individualistic adverse reactions to foods (Fig. 1; Anderson, ; Taylor, ). Adverse food reactions can include IgE and non-IgE-mediated primary immunological sensitivities, non-immunological food intolerances, and secondary sensitivities.

While these various types of reactions are often considered collectively as food allergies, true food allergies represent only a part of the individualistic adverse reactions to foods.

True Food Allergies. True food allergies are abnormal (heightened) responses of the immune system to components of certain foods (Lemke and Taylor, ). The components of foods that elicit these abnormal immune responses are typically naturally-occurring proteins in the foods (Bush and Hefle, ). True food allergies can be divided into two categories based upon the nature of the immune response—immediate hypersensitivity reactions and delayed hypersensitivity reactions (Lemke and Taylor, ).

In immediate hypersensitivity reactions, symptoms start to develop within minutes to an hour or so after ingestion of the offending food. Immediate hypersensitivity reactions own been noted with numerous foods and can sometimes be fairly severe (Hefle et al., ). Immediate hypersensitivity reactions involve abnormal responses of the humoral immune system with the formation of allergen-specific immunoglobulin E (IgE) antibodies (Mekori, ). In delayed hypersensitivity reactions, symptoms do not start to appear until 24 hours or longer after the ingestion of the offending food (Lemke and Taylor, ). With the exception of celiac disease, which involves an abnormal immunological response to wheat and related grains (Ferguson, ), the role of delayed hypersensitivity reactions to foods remains poorly defined.

Delayed hypersensitivity reactions involve abnormal responses of the cellular immune system with the development of sensitized T cells (Lemke and Taylor, ).

Allergy-Like Intoxications. Certain foods can elicit adverse reactions that resemble true food allergies. These foods contain elevated levels of histamine, one of the principal mediators of allergic reactions in the body (Taylor et al., a). In true food allergies and anaphylactoid reactions, however, histamine is released from intracellular locations (Mekori, ).

In these allergy-like intoxications, histamine is ingested with foods. Histamine poisoning is often known as scombroid fish poisoning because it is frequently associated with consumption of spoiled fish of the scombroid type such as tuna and mackerel (Taylor et al., a). However, histamine poisoning can also happen from the ingestion of spoiled fish such as mahi-mahi and bluefish that are not scombroid fishes (Etkind et al., ; Taylor et al., a). And, histamine poisoning has even been occasionally associated with the ingestion of cheese, especially aged Swiss cheese (Stratton et al., ; Taylor et al., ).

In every of these food products, specific types of bacteria own proliferated and caused the conversion of the amino acid, histidine, into histamine (Stratton and Taylor, ; Sumner et al., ; Taylor et al., ). Ingestion of little amounts of histamine in the diet is a normal occurrence and does not cause any harm. However, when large doses of histamine are ingested with foods, the body’s protective mechanisms can be overwhelmed resulting in histamine poisoning (Taylor, ). Unlike food allergies and sensitivities, every consumers are susceptible to histamine poisoning. Because this illness is not truly a form of food allergy or sensitivity, it will not be discussed further.

It does merit some mention because the similarity in symptoms can cause it to be confused with true food allergy.

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Food Intolerances. Food intolerances are abnormal reactions to foods or food components that do not involve the immune system. Several diverse types of food intolerances are also known to exist. These intolerances are metabolic food disorders, anaphylactoid reactions, and idiosyncratic reactions (Taylor, ). Metabolic food disorders are adverse reactions to a food or food component that results from a defect in the metabolism of these foods or some substance therein or from an affect of the food or food component on the body’s normal metabolic processes.

Lactose intolerance is an example of a metabolic food disorder resulting from a defect in the metabolism of a food component (Kocian, ). Favism is an example of a metabolic food disorder resulting from foodborne substances that interfere with normal metabolic processes (Mager et al., ). Anaphylactoid reactions are adverse reactions resulting from the ingestion of foodborne substances that release histamine from cellular stores within the body (Taylor, ). There are no particularly excellent examples of anaphylactoid reactions, although circumstantial evidence suggests that such reactions may happen.

Food idiosyncrasies are adverse reactions to foods or food components that happen through unknown mechanisms and which can even include psychosomatic illnesses (Taylor, ). Sulfite-induced asthma is the best example of an idiosyncratic reaction that has been well documented to happen among certain consumers, although the mechanism remains unknown (Bush and Taylor, ).

Secondary Food Sensitivities. Adverse reactions to foods or food components can happen with or after the effects of other conditions. Examples of such reactions, termed secondary food sensitivities, include lactose intolerance secondary to gastrointestinal disorders such as Crohn’s disease or ulcerative colitis (Metcalfe, a) and drug-induced sensitivities such as the increased sensitivity to tyramine among patients on monoamine oxidase-inhibiting drugs (Blackwell and Marley, ).

IgE-Mediated Food Allergies
This type of food allergy can also be called immediate hypersensitivity, Type I allergy, or food anaphylaxis.

The Greek expression, anaphylaxis, means “against protection” and refers to allergic reactions to foreign protein molecules. IgE is one of five classes of antibodies that are present in the human body and that frolic a role in disease resistance. IgE antibodies are particularly involved in fighting off parasitic infections. Although every humans own low levels of IgE antibodies, only individuals predisposed to the development of allergies produce IgE antibodies that are specific for and recognize certain environmental antigens. These antigens are typically proteins, although only a few of the numerous proteins in nature are capable of stimulating the production of specific IgE antibodies in susceptible individuals (Taylor, ).

The allergens eliciting IgE antibody formation can be found in pollens, mold spores, bee venoms, dust mites, and animal danders in addition to foods (Solomon and Platts-Mills, ).

Pathogenesis. The mechanism of IgE-mediated allergic reactions is depicted in Fig. 2. First, sensitization by the allergen must happen. In the sensitization phase of the response, the allergen stimulates production of specific IgE antibodies. While sensitization can happen with the first exposure to the allergen, that is not always the case.

With honor to food allergens, sensitization does happen most commonly among young infants where the immune response seems to be more likely to be oriented toward an IgE response (Anderson, ). However, even in susceptible infants exposure to most dietary proteins results in oral tolerance, a normal immunologic response that is not associated with adverse reactions, rather than sensitization (Strobel, ). The specific IgE antibodies then attach to mast cells in various tissues and basophils in the blood.

Mast cells and basophils contain granules that are loaded with physiologically athletic chemicals that mediate the allergic response (Church et al., ). On subsequent exposure to the allergenic substance, the allergen cross-links two IgE antibodies on the surface of the mast cell or basophil membrane, stimulating the release into tissues and blood of a host of allergic response mediators. Although numerous mediators own been described, histamine is one of the primary mediators responsible for numerous of the immediate symptoms that happen in IgE-mediated allergic reactions (Simons, ).

Other significant mediators include the various leukotrienes and prostaglandins, some of which are associated with more delayed symptoms that can happen in IgE-mediated, immediate hypersensitivity reactions, the so-called late-phase responses (Peters et al., ).

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Symptoms. IgE-mediated food allergies are associated with a wide variety of symptoms, ranging from mild and annoying to severe and life-threatening (Lemke and Taylor, ). The symptoms can involve the gastrointestinal tract, skin, or respiratory tract (Table 1).

Food-allergic individuals generally suffer from only a few of the numerous possible symptoms. The nature and severity of the symptoms experienced by a food-allergic individual may also vary from one episode to the next depending on the dose of the offending food that has been inadvertently ingested, the degree of sensitization to the offending food at the time of the episode, and probably other factors. Because foods are ingested, gastrointestinal symptoms are often encountered (Anderson, ; Gryboski, ).

However, these symptoms can also be involved in other illnesses so their association with food allergies is often hard to decipher. Cutaneous symptoms such as urticaria (hives) and dermatitis (eczema) are also common manifestations of food allergies (Kaplan, ). These symptoms are more definitive for food allergy, although the frequency of dermatitis as a manifestation of food allergy especially, in infants, has only been widely appreciated in the past decade or so (Sampson, ). Respiratory symptoms are less commonly associated with food allergies than with environmental allergies such as pollen or animal dander allergies (Taylor et al., ).

With environmental allergies, the allergens are inhaled, so the primary involvement of respiratory symptoms is understandable. However, ingested food allergens must survive digestive processes and be absorbed to elicit systemic reactions in the respiratory tract. Although few asthmatic individuals experience food-induced asthma, asthma is among the most severe symptoms associated with food allergies (Bousquet and Michel, ). Food-induced asthma is a risk factor for severe, life-threatening reactions to the offending foods (Sampson et al., ).

Oral allergy syndrome is perhaps the most common manifestation of food allergy (Ortolani et al., ).

Oral allergy syndrome is often so mild that it is ignored by afflicted individuals. Oral allergy syndrome involves symptoms confined to the oropharyngeal area including hives, itching, and swelling (Pastorello and Ortolani, ). Unused fruits and vegetables are the foods most frequently associated with oral allergy syndrome (Pastorello and Ortolani, ). Individuals with oral allergy syndrome are generally sensitized to one or more pollens, and react to proteins in specific unused fruits and vegetables that cross-react with the pollen allergens (Calkoven et al., ; Ebner et al., ; van Ree and Aalberse, ).

Examples would include allergic reactions to watermelons and other melons in ragweed-allergic individuals (Enberg et al., ), allergic reactions to celery in mugwort-allergic or birch-sensitized individuals (Ballmer-Weber et al., ; Wuthrich et al., ), and allergic reactions to apples and hazelnuts in birch-allergic individuals (Dreborg, ). Because the allergens in these foods are inactivated on contact with stomach acid and digestive proteases, systemic reactions to these unused fruits and vegetables are rarely encountered (Taylor and Lehrer, ).

Because these allergens are denatured by heating (Dreborg and Foucard, ; Taylor and Lehrer, ), individuals with oral allergy syndrome can generally safely ingest heat-processed forms of the offending food, e.g., apple jelly or apple sauce. Recent evidence indicates that, in contrast to previous assumptions, some individuals with oral allergy syndrome associated with certain foods, such as celery, also may experience more severe systemic reactions on occasion (Ballmer-Weber et al., ).

The most frightening symptom associated with food allergies is anaphylactic shock, which generally involves multiple systems including the gastrointestinal tract, the skin, the respiratory tract, and the cardiovascular system.

Symptoms happen in combination and develop rapidly. Severe hypotension can happen. Death can happen from cardiovascular and/or respiratory collapse within minutes of ingestion of the offending food. Only a few of the numerous people with IgE-mediated food allergies are at risk for such serious manifestations. However, numerous deaths own been attributed to inadvertent exposure to the offending food among individuals with food allergies (Bock et al., ; Sampson et al., ; Yunginger et al., ).

These deaths own involved asthma and/or anaphylactic shock.

In addition to allergic reactions associated with the consumption of foods, occupational food allergies including occupational asthma, hypersensitivity pneumonitis (extrinsic alveolitis), and contact dermatitis can happen amongst food industry employees (O’Neil and Lehrer, ). Such reactions can be triggered in food manufacturing workers by food-derived protein allergens, e.g., green coffee beans, flour, and shellfish, or non-food agents, e.g., honey bees and latex products (Lehrer and O’Neil, ). These occupational allergies are produced by respiratory exposure to dusty processing environments or cutaneous exposure to specific food products.

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Diagnosis.

With the wide range of symptoms that can be involved in IgE-mediated food allergies and the possibility of other causes for numerous of these symptoms, the diagnosis of IgE-mediated food allergies can sometimes be challenging (Metcalfe, b). First and foremost, an association must be sought between the ingestion of one or more offending foods and the elicitation of the adverse reaction. Once a food-associated adverse reaction is well documented, then proof of the existence of an IgE mechanism must be considered. The assistance of an allergist should be sought in the diagnosis of IgE-mediated food allergies.

Too often, consumers rely upon self-diagnosis or parental diagnosis. Self-diagnosis and parental diagnosis of reactions in children are problematic because they are often erroneous, leading to the identification of the incorrect foods, and implicate too numerous foods (Bock et al., ). Careful history-taking including the use of food diaries by an experienced allergist can often identify suspect foods. Elimination diets followed by challenges can sometimes confirm the existence of a food-associated adverse reaction. However, the gold standard for documenting existence of a food-associated adverse reaction is the double-blind, placebo-controlled food challenge (DBPCFC; Bock et al., ).

Such clinical challenges are especially useful in situations where the role of a specific food remains somewhat questionable. Double-blind, placebo-controlled food challenges are not generally done in cases involving serious, life-threatening adverse reactions because of the obvious risks to the patient and the likelihood in such cases that the role of one or more specific foods is rather clear. Once the role of one or more specific foods in the adverse reaction has been established, then the involvement of the IgE mechanism can be documented through skin-prick tests using extracts of the suspect foods (Bock et al., ) or by radioallergosorbent tests (RASTs) where the presence of food-specific IgE antibodies in the blood serum is examined (Adolphson et al., ).

Prevalence.

IgE-mediated food allergies likely affect between 2 and % of the entire population. For numerous years, the overall prevalence estimate for IgE-mediated food allergies has been between 1 and 2% of the entire population (Lemke and Taylor, ). However, a recent random, digit-dial telephone survey in the U.S.

What is a food allergies definition

indicated that the combined prevalence of peanut and tree nut allergies was an estimated % (Sicherer et al., ). And, a similar telephone survey in the United Kingdom indicated that the estimated prevalence of peanut allergy alone was % (Emmett et al., ). While one could criticize the use of telephone surveys, it is unlikely that numerous consumers would mis-diagnose peanut or tree nut allergies since the symptoms are profound and generally fairly immediate. Thus, these surveys may be reasonably dependable and a excellent indication that previous estimates based solely on clinical impression were incorrect. Certainly, if peanut and tree nut allergy alone account for more than 1% of IgE-mediated food allergy, then the overall prevalence of food allergy in the entire population likely exceeds 2%.

Infants (1–3 years of age) and children are more commonly affected by food allergies than other age groups (Taylor et al., ).

Among infants younger than 3 years, the prevalence of food allergies appears to be in the range of 5% to 8% (Sampson, ). The prevalence of food allergy among young infants (<1 year of age) has been studied more thoroughly than has the prevalence among older children and adults.

A much higher proportion of the public believes that they own food allergies because of self-diagnosis, parental diagnosis, and misconceptions about the definition of food allergy even among some physicians (Bock et al., ; Sloan, ). Studies own shown that 10 to 20% of the consuming public believes that they or someone in their family has a food allergy (Chiaramonte et al., ; Sloan, ).

Some believe, on the basis of the impressions of clinicians involved in allergy practice for several decades, that the prevalence of IgE-mediated food allergies is increasing.

An increase in prevalence, however, is hard to confirm because excellent baseline data from earlier years for comparative purposes are lacking. Certainly, the awareness of food allergy has increased. More individuals may seek specialized medical attention from allergists as a result of this increased awareness. But, almost everyone agrees that the prevalence of severe food allergies seems to be increasing. The reasons for this apparent increase are unknown. Numerous severely affected individuals own food-induced asthma as one of the manifestations of their allergic reaction. The overall prevalence of asthma is definitely increasing in the U.S. for unknown reasons (Beasley et al., ).

While food-induced asthma is a little part of the entire asthma population, the prevalence of food-induced asthma may be increasing in concert with the overall increase in prevalence of asthma.

Most Common Allergenic Foods.
The prevalence of allergies to specific foods is not precisely known. Cows’ milk allergy appears to be among the more prevalent food allergies in infants. This is not surprising given the importance of milk in baby feeding practices. The prevalence of cows’ milk allergy among infants under the age of two in Sweden, Denmark, and Australia has been studied and found to be approximately 2% in every three countries in well-conducted clinical studies involving groups of unselected infants followed from birth to the age of two years (Hill et al., ; Host and Halken, ; Jakobsson and Lindberg, ).

The prevalence of milk allergy is known to decrease with age (Bock, ), but the exact prevalence of milk allergy among other age groups is unknown. The prevalence of other specific food allergies has not been established in controlled clinical trials using unselected population groups. The comparative prevalence of various specific food allergies can be discerned from studies involving groups of individuals with probable food allergies. In the U.S., eggs and peanuts are also common allergenic foods for infants, along with soybeans, tree nuts, fish, and wheat (Bock and Atkins, ; Burks et al., ; Sampson and McCaskill, ).

Among adults in the U.S., peanuts are probably the most common allergenic food (Taylor et al., ). Seafood allergies, especially to crustaceans (shrimp, crab, lobster), are also rather common among adults (Lehrer et al., ). Fewer studies own been conducted on the prevalence of specific types of food allergies in adults in the U.S. or other countries. The prevalence of specific types of food allergies may vary among population groups based upon their eating habits (Taylor et al., ). Peanut allergy appears to be more common in North America than in other parts of the world. This observation may relate to the popularity of peanut butter in North America.

As other countries, such as the United Kingdom, own adopted the North American affection for peanuts and peanut products, the prevalence of peanut allergy in those countries appears to be rising (Emmett et al., ). Another example would be buckwheat allergy. Buckwheat allergy appears to be rather common among adults in certain southeast Asian countries such as Japan and South Korea (Kang and Min, ). In contrast, buckwheat allergy would be rather unusual in the U.S.

The difference is likely due to the popularity of buckwheat noodles in the cuisine of certain southeast Asian countries. Such observations own profound implications for product developers. If a highly successful buckwheat product was introduced into the U.S. or if buckwheat noodles became favorite in American Asian cuisine, the prevalence of buckwheat allergy would likely increase.

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The Large Eight. Eight foods or food groups are thought to account for more than 90% of every IgE-mediated food allergies on a worldwide basis (Bousquet et al., ; FAO, ).

These foods or food groups are milk, eggs, fish (all species of finfish), crustacea (shrimp, crab, lobster, crayfish), peanuts, soybeans, tree nuts (almonds, walnuts, pecans, cashews, Brazil nuts, pistachios, hazelnuts also known as filberts, pine nuts also known as pinyon nuts, macadamia nuts, chestnuts, and hickory nuts), and wheat. In , an expert consultation of the Food and Agriculture Organization of the United Nations sure that these eight foods or food groups were the most common causes of food allergy on a worldwide basis (FAO, ). Subsequently this list was adopted by the Codex Alimentarius Commission in (CAC, ).

These foods and food groups own come to be known as the “Big Eight” (Table 2). More than other foods own been documented as causing food allergies less frequently (Hefle et al., ).

Basically, any food that has protein has the potential to elicit an allergic reaction among susceptible individuals. Beyond the Large Eight, in certain geographic regions other foods or food groups may frequently cause IgE-mediated food allergies. Celery allergy, for example, is rather common in some European countries (Wuthrich et al., ).

The prevalence of buckwheat allergy in southeast Asia has already been mentioned. And, sesame seed allergy is extremely common in middle Eastern countries and countries where the ethnic population of middle Easterners is high; this may be due to the popularity of tahini, a paste made from sesame seeds, in the diets (Kanny et al., ). Several countries including Canada own decided to add sesame seeds to the list of commonly allergenic foods for that country. A few other foods are worthy of mention because, although they less frequently cause allergies, they own been associated with severe reactions. These foods include molluscan shellfish (clams, oysters, etc.), sesame seeds, poppy seeds, sunflower seeds, cottonseed, and certain other legumes beyond peanuts and soybeans (the various types of dry beans, peas, lentils, and garbanzo beans also known as chick peas) (Atkins et al., ; Gall et al., ; Kagi and Wutrich, ; Kalyoncu and Stalenheim, ; Kanny et al., ; Maeda et al., ; Martin et al., ; Noyes et al., ).

However, a rather large percentage of the or more other allergenic foods has been reported to elicit severe allergic reactions in isolated cases (Hefle et al., ).

Food Allergens. The allergens in foods are almost always naturally occurring proteins. Foods contain millions of individual proteins, but only a comparative few of the proteins own been documented to be allergens (Bush and Hefle, ; Taylor, ).

Some foods such as milk, eggs, and peanuts are known to contain multiple allergenic proteins (Bush and Hefle, ). Other foods such as Brazil nuts, shrimp, and codfish contain only one major allergenic protein (Bush and Hefle, ). However, the majority of the proteins, even those from commonly allergenic foods, are incapable of eliciting IgE production. Although the common allergenic foods listed above tend to be excellent sources of protein, other common protein-rich foods such as beef, pork, chicken, and turkey are rarely allergenic.

No common structural features own allowed distinctions to be made between those proteins that are capable of eliciting IgE production and those that are not. Allergenic proteins, however, tend to be major proteins in the implicated foods, resistant to digestion, and stable to processing operations, particularly heat processing (Taylor and Lehrer, ).

Development of IgE-Mediated Food Allergies. Genetics frolic an significant role in the development of IgE-mediated allergies of every types, including food allergies (Kjellman and Bjorksten, ).

Allergies are much more likely to develop in children born to parents who own allergies (either to food, pharmaceutical, or environmental allergens) than amongst children born to parents with no history of allergies (Taylor et al., ). However, the nature of the allergy that develops is not genetically controlled. Therefore, the children of pollen-allergic parents are at increased risk for development of food allergies as are the children of food-allergic parents. The risk is greater if both parents own allergies than it is if only one parent has allergies.

Infants are the most likely to develop food allergies (Sampson, ; Taylor, ). However, sensitization to foods can happen at any age.

Infants do not appear to develop allergies in utero (Kjellman and Bjorksten, ), but can be sensitized during the first few days of life. Obviously, the newborn baby encounters through the first few years of life dozens of new foods and probably hundreds of thousands of food proteins that own antigenic and possibly allergenic potential. For most of these foods and their proteins, infants develop oral tolerance (Strobel, ). Infants appear to be at increased risk for the development of IgE-mediated food allergies in part because their digestive processes may not be fully developed but primarily because they own not yet had the chance to develop oral tolerance.

Certain foodborne proteins seem to be much more likely than others to cause allergic sensitization (Bush and Hefle, ). The factors involved in sensitization and the development of IgE-mediated food allergies are not yet fully understood.

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Prevention of IgE-Mediated Food Allergies. The prevention of the development of IgE-mediated food allergies among high-risk infants (those born to parents with histories of allergies) has been a long-sought goal. However, the results of several large clinical trials of high-risk infants followed for several years propose that the development of IgE-mediated food allergies can be delayed but not prevented (Zeiger and Heller, ).

The maternal diet during pregnancy does not seem to be a factor (Zeiger and Heller, ), because sensitization does not happen in utero. The avoidance of commonly allergenic foods such as cows’ milk, eggs, and peanuts in the baby diet during the first few years of life often delays the development of food allergies, but food allergies may still develop after solid foods are introduced (Hattevig et al., ; Zeiger and Heller, ). Avoidance can be accomplished through breast-feeding or the feeding of hypoallergenic baby formula (Kjellman and Bjorksten, ; Zeiger and Heller, ). Numerous pediatricians recommend breast-feeding for infants born to parents with histories of IgE-mediated allergies.

Lactating women can apparently transmit potentially sensitizing levels of food allergens through their milk to nursing infants (Van Asperen et al., ). Apparently, intact or partially intact allergenic proteins are capable to survive maternal digestive processes and be absorbed via the lymph and transferred immunologically intact into breast milk (Van Asperen et al., ). Infants own been sensitized through breast-feeding to peanuts, cows’ milk, and eggs (Van Asperen et al., ). The avoidance of peanuts in the maternal diet during the lactation period is often advocated as a preventive measure.

However, the exclusion of milk and eggs from the maternal diet during lactation is not generally recommended due to their nutritional importance coupled with the low likelihood of allergic sensitization through breast-milk (Taylor et al., ). The use of hypoallergenic baby formula to prevent or delay the development of IgE-mediated food allergies is less commonly practiced. However, the use of partial whey hydrolysate formulae for this purpose may show some promise (Vandenplas et al., ), although such partial hydrolysates are not safe for consumption by infants who are already sensitized to cows’ milk (Businco et al., ; Ellis et al., ).

Apparently, the partial hydrolysis of the whey proteins increases the likelihood of the development of oral tolerance as opposed to allergic sensitization.

Natural History of IgE-Mediated Food Allergies. Most food allergies developed in infancy are outgrown in infancy or early childhood. Numerous infants outgrow their food allergies, often within a matter of a few months (Bock, ; Hill and Hosking, ). Allergies to certain foods such as cows’ milk, eggs, and soybeans are much more likely to be outgrown than allergies to other foods such as peanuts (Bock, ; Bock and Atkins, ).

Peanut allergy is almost never outgrown. The loss of allergic sensitivity to a specific food probably results from the development of immunological, oral tolerance (Taylor et al., a). However, the basis for the differences between specific foods (e.g., milk vs. peanuts) in the development of oral tolerance is not understood.

Cross-Reactions between Related Allergenic Foods. Allergic consumers sometimes experience cross-reactions between closely related foods. For example, with the crustacea, most sensitive individuals are allergic to every of the various species of shrimp, crab, lobster, and crayfish (Lehrer, ).

However, these individuals can often eat other seafoods including finfish and molluscan shellfish. Similar cross-reactivity also exists between cows’ milk and goats’ milk (Bellioni-Businco et al., ) and between eggs of various avian species (Langeland, ). With other food groups, the situation can be fairly complicated. For example, peanuts are the most commonly allergenic legumes. Most peanut-allergic individuals can eat other legumes without incident (Bernhisel- Broadbent and Sampson, ). A few peanut-allergic individuals are also allergic to soybeans (Herian et al., ), although this may not necessarily represent true cross-reactivity. With fish, individuals often experience reactions to more than one species of fish, but some fish are tolerated by some fish-allergic individuals and no definite patterns of reactivity own been identified (Bernhisel-Broadbent et al., ; de Martino et al., ).

Cross-Reactions between Food and Environmental Allergens.

Cross-reactions are frequently observed between pollens and certain foods, especially fruits and vegetables (Ballmer-Weber et al., ; Calkoven et al., ; van Ree and Aalberse, ; Wuthrich et al., ). This is the oral allergy syndrome, which typically involves mild reactions as previously mentioned. Examples include cross-reactions between birch pollen and apples, ragweed pollen and melons, and mugwort pollen and celery (Ballmer-Weber et al., ; Calkoven et al., ; Enberg et al., ; van Ree and Alberse, ; Wuthrich et al., ).

Cross-reactions own also been noted between latex allergies, a common problem among health-care workers, and certain foods including bananas, kiwis, avocados, and chestnuts (Blanco et al., ).

Effect of Food Processing on Allergens. As mentioned earlier, the allergens in foods are typically proteins that are stable to heat processing (Taylor and Lehrer, ). So, heat-processed forms of commonly allergenic foods often retain their allergenicity (Herian et al., ; Nordlee et al., ).

The only exception would be the pollen-related allergens found in unused fruits and vegetables and involved in oral allergy syndrome; these allergens are generally destroyed by heat processing (Dreborg and Foucard, ), although the necessary extent of the heat process has not been well documented in most cases. For the most common allergenic foods, every forms of those foods should be considered allergenic unless proven otherwise. Testing has indicated that most forms of peanuts and soybeans, for example, retain their allergenicity (Herian et al., ; Nordlee et al., ).

Other processing techniques own not been so well investigated for their effects on the allergenicity of the resulting products. Since allergens are resistant to proteolysis, fermentation generally fails to eliminate allergenicity (Taylor and Lehrer, ). For example, although fermented soybean products are reduced in allergenicity, some allergenic activity is retained (Herian et al., ).

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If the protein part is removed during processing, however, the resulting product or ingredient might be safe because the allergen has been removed.

The classic example is the processing of edible oils from peanuts and soybeans (Bush et al., ; Hourihane et al., a; Taylor et al., ). Clinical challenge trials in peanut- and soybean-allergic individuals own documented that highly refined peanut and soybean oil are safe for individuals with allergies to the source material (Bush et al., ; Hourihane et al., a; Taylor et al., ).

Other ingredients may be derived from allergenic sources. Examples include certain flavoring formulations, starch, lecithin, and gelatin. Flavors can occasionally contain protein residues from allergenic foods (Taylor and Dormedy, ). Starch is often made from corn or some other source that is rarely allergenic.

Occasionally, starch is made from wheat, although the level of protein residues is fairly low and adverse reactions to wheat starch own not been reported. Lecithin can be made from either soybean or egg and can contain allergenic residues (Muller et al., ). However, the degree of risk posed by the low residual levels of soybean allergens in lecithin remains unknown. Gelatin is most commonly made from beef and pork, foods that are rarely allergenic (Sakaguchi et al., ).

However, gelatin can also be made from fish skins. The allergenicity of fish gelatin remains unknown (Sakaguchi et al., ).

Treatment. Allergic reactions to foods can be treated with certain drugs (Furukawa, ; Simons, ). Antihistamines can counteract the effects of histamine (Simons, ), although these drugs do not counteract the effects of the other mediators released from basophils and mast cells. Epinephrine (adrenaline) is considered the life-saving drug for individuals at risk of severe anaphylactic shock-type reactions to foods (Sampson et al., ).

Epinephrine is available in self-injectable form. Consumers with a history of severe anaphylactic reactions to foods should own a prescription for epinephrine and carry the medication at every times. To be most effective, epinephrine must be istered early in the course of the allergic reaction. However, an examination of severe food-allergic reactions resulting in deaths or near-deaths reveals a delay in the istration of epinephrine as a key contributing factor to the severe outcome (Sampson et al., ).

The specific avoidance diet is the only prophylactic approach to the treatment of food allergies (Taylor et al., a; Taylor et al., ).

For example, individuals allergic to peanuts must simply avoid ingesting peanuts. The construction of safe and effective avoidance diets is often a challenge for individuals with food allergies. With packaged foods, these individuals must spend considerable time in the scrutiny of ingredient declarations on product labels. They must be taught to recognize the numerous terms that may signify the presence of food components or ingredients derived from their offending food(s). Some foods, especially in foodservice settings, are sold without ingredient statements. Clearly, the allergic consumer can encounter numerous hazardous situations in such circumstances and must be trained to be extremely vigilant.

Also, exposure to extremely little amounts of the offending food may be sufficient to elicit allergic reactions in some sensitive individuals, further complicating the necessary vigilance in the implementation of effective avoidance diets.

Threshold Doses for Allergenic Foods. As noted, individuals with IgE-mediated food allergies will experience symptoms on exposure to little amounts of the offending food. The interaction of a little quantity of the allergen with specific IgE antibodies on the surface of the mast cell or basophil membrane triggers the release of massive quantities of mediators, which accounts for the low degree of threshold. The precise threshold doses for allergenic foods own not been carefully investigated and are likely to be variable from one allergic individual to another.

In a recent study, Hourihane et al. (b) demonstrated that a group of individuals with peanut allergy displayed diverse thresholds for peanuts. The most sensitive individual among 12 tested subjects experienced an objective reaction when exposed to 2 mg of peanut protein. Other patients in the group did not even reply to the highest dose used in the challenge trial which was 50 mg of peanut protein. While this experiment clearly demonstrates that the threshold level is not zero, the threshold dose is fairly low. Whether other allergenic foods own thresholds as low as those for peanuts remains to be determined.

Allergenicity of Foods Produced Through Agricultural Biotechnology.

In the genetic modification of foods, genes are transferred from one organism to another. Because these genes code for the expression of a specific protein, novel proteins are expressed in the transgenic variety as a result. Because every allergens are proteins, the theoretical possibility exists that these novel proteins might be allergenic or that they might become allergenic. However, only a few of the numerous proteins found in nature are allergenic, so the probability of the transfer of an allergen is rather low. The potential allergenicity of the novel proteins expressed in the new varieties produced through agricultural biotechnology should be assessed in every case.

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The potential allergenicity of the novel proteins in transgenic varieties can be assessed (FAO/WHO, ; Metcalfe et al., ; Taylor and Hefle, a).

If a gene is transferred from a known allergenic source, the potential allergenicity of the expressed novel protein can be assessed with reasonable certainty by evaluating its reactivity by specific serum screening with serum containing IgE antibodies from individuals with well documented allergies to the source material. This assessment approach was demonstrated to be effective when it was sure that a Brazil nut protein transferred into soybeans to correct the inherent methionine deficiency of soybeans was the heretofore unidentified major allergen from Brazil nuts (Nordlee et al., ).

The company involved abandoned further commercial interest in these transgenic soybeans as a result. It should be emphasized that genes are not often obtained from known allergenic sources in the development of commercial transgenic varieties. However, when genes are transferred from known allergenic sources, it must be assumed that the gene encodes for an allergenic protein unless proven otherwise.

More typically, genes are obtained from sources with no history of allergenicity. In these situations, a decision-tree approach is advocated for the assessment of the potential allergenicity of the novel protein.

While no single test can perfectly predict the potential allergenicity of a specific novel protein from a source with no history of allergenicity, the application of a series of tests provides reasonable assurance that the novel protein is not likely to become an allergen. Several decision-tree approaches own been developed (FAO/WHO, ; Metcalfe et al., ; Taylor and Hefle, a). These approaches rely upon evaluation of the source of the gene and its history of allergenicity, the sequence homology of the novel protein to known allergens, the immunoreactivity of the novel protein with serum IgE from individuals with known allergies to the source of the transferred gene, the immunoreactivity of the serum IgE from individuals with known allergies to sources that are broadly related to the source of the novel gene (e.g., grass pollen allergic individuals in cases where the gene is obtained from monocot sources), the pepsin resistance or digestive stability of the novel protein, and the immunogenicity of the novel protein in validated animal models (Fig.

3). Other factors especially the level of expression of the novel protein in the food are also likely to be significant since allergies are generally elicited by food proteins where dietary exposure is comparatively high.

Foods produced through agricultural biotechnology including corn, soybeans, canola, and potatoes are already reaching the consumer marketplace. The potential allergenicity of the novel proteins expressed in these commercial products has been assessed using the approaches indicated above.

The novel proteins in these approved transgenic varieties are not obtained from known allergenic sources, are not structurally homologous to known food or environmental allergens, and are sensitive to digestive proteolysis. Furthermore, the novel proteins are expressed at extremely low levels in the edible portions of these modified crops. Thus, the likelihood of allergenicity from this current generation of crops produced by agricultural biotechnology is virtually nil.

Considerable publicity has surrounded one specific transgenic variety, the so-called StarLink™ corn. StarLink corn was never approved for human use, but was unfortunately approved for animal feed use.

When segregation failed, some StarLink corn residues were found in corn-based food products intended for human consumption. Although the gene inserted in StarLink corn was obtained from a source with no history of allergenicity and the novel protein was not structurally similar to known food or environmental allergens, the novel protein was comparatively more resistant to digestive proteolysis than other novel proteins that had been approved for other genetically modified crops.

For this reason, StarLink corn was never approved for human consumption. However, given the extremely low level of exposure to the novel protein in StarLink corn in corn-based food products, the likelihood of allergic sensitization to this specific novel protein is low. Despite that and due to the concerns about the potential allergenicity of this transgenic variety, it has been withdrawn from the marketplace, although traces may remain for one or more growing seasons. This episode emphasizes the importance of assessing the potential allergenicity of transgenic varieties as part of the overall safety evaluation process.

Agricultural biotechnology can also be used to decrease the inherent allergenicity of foods.

The proteins in specific foods that are responsible for allergic reactions could be removed or altered through agricultural biotechnology. While no commercial examples exist yet of the application of this possibility, it is an athletic area of research with peanuts.

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Non-IgE Cell-Mediated Reactions
As noted earlier, cell-mediated allergic reactions, also known as delayed hypersensitivity reactions, own an onset time of 6–24 hours after ingestion of the offending food. The reactions develop slowly, reaching a peak at approximately 48 hours and then slowly subsiding over 72–96 hours.

Cell-mediated food allergies involve the interaction between specific antigens or allergens from the food and sensitized, tissue-bound T cells that release inflammatory mediators when sensitized (Sampson, ). The role of cell-mediated reactions in food allergies remains somewhat uncertain. Compelling and mounting evidence has accumulated, however, indicating that celiac disease occurs through a T cell-mediated mechanism (Ferguson, ; Strober, ).

Celiac Disease.

Also known as celiac sprue or gluten-sensitive enteropathy, celiac disease is a malabsorption syndrome occurring in sensitive individuals upon the consumption of wheat, rye, barley, triticale, spelt, and kamut (Ferguson, ; Lemke and Taylor, ). The role of oats in celiac disease has recently been questioned. Apparently, oats and oat products that are totally free of wheat, rye, and barley, are safe for celiac sufferers to consume (Janatuinen et al., ).

What is a food allergies definition

After consumption of the offending grains or products made from these grains, the absorptive epithelial cells in the little intestine are damaged by an inflammatory process (Ferguson, ). As a result, absorption of nutrients through the epithelium is compromised. The loss of absorptive function along with the ongoing inflammatory process results in a severe malabsorption syndrome characterized by diarrhea, bloating, weight loss, anemia, bone pain, chronic fatigue, weakness, muscle cramps, and, in children, failure to acquire weight and growth retardation (Lemke and Taylor, ; Skerritt et al., ).

A part of wheat, the gliadin part, and related part in barley and rye are associated with initiation of celiac disease in susceptible individuals (Skerritt et al., ).

Celiac disease is an inherited trait, but the inheritance is complicated and poorly understood. Celiac disease occurs in about 1 of every individuals in the U.S. (Kasarda, ). In some other parts of the world, celiac disease occurs more frequently. The highest prevalence occurs among individuals in certain regions of Europe (Greco et al., ; Kasarda, ). Celiac disease seems to happen more frequently among Europeans than among Americans of European descent for unexplained reasons. Celiac disease rarely occurs among individuals of Chinese or African descent (Ferguson, ).

The treatment of celiac disease involves the avoidance of wheat, rye, barley, triticale, spelt, kamut, and oats and products of these grains (Hartsook, ). The threshold dose of gliadin and related protein fractions needed to provoke celiac disease in sensitive individuals is not precisely known, but symptoms can be elicited by ingestion of little amounts of these grains (Lemke and Taylor, ). If a gluten-free diet is followed, the symptoms of celiac disease will resolve and the absorptive function of the little intestine will be restored.

Most celiac sufferers adhere to extremely strict gluten-free diets. In the absence of information on the safety of products made from the offending grains, affected individuals often select to avoid products that contain remarkably little amounts of protein from these sources including rye alcohol, wheat starch, malt extract, and vinegar. The wisdom of such severely restricted avoidance diets remains to be established.

Food Intolerances
In contrast to true food allergies, food intolerances happen through non-immunological mechanisms. However, love true food allergies, food intolerances affect some individuals in the population but not every.

Individuals suffering from food intolerances can generally tolerate little amounts of the offending food or food ingredient in their diet without ill effects. Food intolerances can be divided into three categories: anaphylactoid reactions, metabolic food disorders, and idiosyncratic illnesses.

Anaphylactoid Reactions. In IgE-mediated food allergies, the release of histamine and other mediators from the mast cells and basophils is mediated by the interaction of IgE with proteinaceous allergens, as described earlier. In contrast, anaphylactoid reactions are caused by substances that bring about the release of the same mediators from mast cells without the involvement of IgE (Lemke and Taylor, ).

Some substance in the implicated food is presumed to destabilize the mast cell membranes allowing for the spontaneous release of histamine and the other mediators. However, no such histamine-releasing substance has ever been isolated or identified in foods, although this mechanism is well established with certain drugs. Strawberry sensitivity is generally cited as the best example of an anaphylactoid reaction. Although strawberries are known to cause adverse reactions (frequently urticaria) in susceptible individuals, there is little evidence for the existence of an IgE-mediated mechanism.

Strawberries contain little protein, and no evidence has been found for the existence of a strawberry allergen. Furthermore, there is no evidence for the existence of strawberry-specific IgE in the sera of strawberry-sensitive individuals. Spontaneous histamine release is thus a plausible mechanism. However, if a substance exists in strawberries that destabilizes mast cell membranes, that substance has yet to be identified. The possibility that strawberry sensitivity is a form of oral allergy syndrome has not yet been excluded, and is an equally plausible mechanism.

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Metabolic Food Disorders.

Metabolic food disorders result either from inherited defects in the ability to metabolize some component of food or from a genetically sure, enhanced sensitivity to some foodborne chemical that occurs through an altered metabolic pattern (Lemke and Taylor, ). Lactose intolerance is an example of an illness that occurs when a genetic deficiency affects the host’s ability to metabolize a food component (Kocian, ). In lactose intolerance, an inherited deficiency occurs in the quantity of the enzyme, β-galactosidase, leading to an impaired ability to digest lactose. Favism is an example of a genetic deficiency that enhances the sensitivity to a foodborne chemical.

In favism, a genetic deficiency in glucosephosphate dehydrogenase in the erythrocyte results in an enhanced sensitivity to several hemolytic substances that happen naturally in fava beans (Mager et al., ). These two metabolic food disorders are the most common and best understood illnesses in this category of food intolerances.

Lactose Intolerance. Lactose is a dissaccharide and the principal sugar in milk. Normally, lactose is hydrolyzed into its constituent monosaccharides, galactose and glucose, in the little intestinal mucosa.

These monosaccharides can then be absorbed and used as metabolic sources of energy. In lactose intolerance, the activity levels of β-galactosidase, the key hydrolytic enzyme that exists in the mucosal membranes of the little intestine, are diminished (Houts, ; Suarez and Savaiano, ). Since lactose cannot be absorbed in the little intestine unless it is hydrolyzed to glucose and galactose, the undigested lactose passes into the colon where it encounters large populations of bacteria. The colonic bacteria metabolize the lactose to CO2, H2, and H2O (Lemke and Taylor, ).

Abdominal cramping, flatulence, and frothy diarrhea are the predominant symptoms of lactose intolerance (Bayless et al., ) and are the direct result of the action of the colonic bacteria on lactose. The symptoms vary in intensity in concert with the individual level of activity of β-galactosidase in the little intestine and the quantity of lactose ingested.

Lactose intolerance is a fairly common metabolic food disorder. Lactose intolerance is especially prevalent among some ethnic groups in the world including Greeks, Arabs, Jews, black Americans, Hispanics, Japanese, and other Asians (Houts, ; Suarez and Savaiano, ).

Only about % of Caucasians are affected (Suarez and Savaiano, ). Lactose intolerance can own its onset at any age, occurring as early as the age of three (Simoons, ). However, lactose intolerance tends to worsen with advancing age and is often more common and more severe among the elderly (Houts, ; Simoons, ). The level of intestinal b-galactosidase is generally sufficient at birth to permit digestion of lactose in mother’s milk, but susceptible individuals suffer as a result of decreased activity of this enzyme as life progresses. Lactose intolerance may also happen on a more transitory basis on occasion, secondary to another intestinal illness or infection such as a bout of viral gastroenteritis (Metcalfe, b).

Secondary lactose intolerance tends to subside rather quickly after the original illness is resolved.

Individuals with lactose intolerance are capable to control their symptoms through the avoidance of dairy products containing lactose (Lemke and Taylor, ). However, numerous lactose-intolerant individuals can tolerate some lactose in their diets. The degree of tolerance for lactose is individualistic and variable among such individuals. Yogurt, sour cream, and acidophilus milk that contain athletic cultures of bacteria with b-galactosidase activity, are better tolerated by lactose-intolerant individuals than other dairy products (Kolars et al., ).

Lactose-hydrolyzed milk is also available in the marketplace (Paige et al., ). And, lactose-intolerant individuals can add b-galactosidase to milk just before consumption, and this seems to be an effective practice (Barillas and Solomons, ). Certainly, the level of tolerance for dairy products is much higher with lactose intolerance than it is with IgE-mediated cows’ milk allergy (Taylor, ).

Favism. Individuals with an inherited deficiency of the enzyme, glucose phosphate dehydrogenase (G6PDH), in their erythrocytes are susceptible to favism.

Symptoms happen after consumption of fava beans or the inhalation of pollen from the Vicia faba plant (Mager et al., ). Fava beans contain vicine and convicine, naturally occurring oxidants that are capable to damage the erythrocyte membranes of G6PDH-deficient individuals causing hemolysis and the symptoms of hemolytic anemia (Marquardt, ). G6PDH is a critical enzyme in erythrocytes because it helps to maintain adequate levels of the reduced form of glutathione (GSH) and nicotinamide adenine dinucleotide phosphate (NADPH). GSH and NADPH assist to avert oxidative damage to erythrocytes. In individuals who are G6PDH-deficient, this protective mechanism is nonfunctional and the oxidants in fava beans can exert their hemolytic effects.

In rare cases with repeated exposure, more severe symptoms can happen including hemoglobinuria, jaundice, and renal failure. The onset time after ingestion of the fava beans ranges from 5 to 24 hours. The illness is self-limited, however, with symptoms resolving promptly and spontaneously upon avoidance of further exposure.

G6PDH deficiency is extremely common and affects approximately million individuals on a worldwide basis (Mager et al., ). The prevalence is highest among Oriental Jewish groups in Israel, Sardinians, Cypriot Greeks, African Americans, and certain African populations.

This inherited trait is virtually absent among Caucasians, North American Indians, and Eskimos. Despite the high prevalence of G6PDH deficiency, favism is an unusual occurrence because fava beans are not frequently eaten except in Mediterranean and Middle Eastern locales.

Idiosyncratic Illnesses
Some individualistic adverse reactions to foods are idiosyncratic in that the mechanism for these illnesses is unknown. Numerous reports, mostly anecdotal, own occurred regarding illnesses in certain individuals attributed to certain specific foods or food ingredients.

Conceivably, a large number of diverse mechanisms could be involved in these idiosyncratic reactions.

What is a food allergies definition

The symptoms involved in idiosyncratic reactions range from unimportant to severe, life-threatening reactions (Taylor et al., b).

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The role of specific foods or food ingredients in the causation of these idiosyncratic reactions remains to be sure in numerous cases. The cause-and-effect relationships can only be established through carefully controlled DBPCFCs (Taylor et al., b). A positive DBPCFC would definitely confirm that the specific food or food ingredient is involved in the specific adverse reaction.

The mechanism of the adverse reaction, however, cannot be sure from the positive DBPCFC alone. A negative DBPCFC indicates either that foods are not involved in causation of the reaction or at least that the specific food or food ingredient used in the challenge was wrongly incriminated. Unfortunately, DBPCFCs are rarely performed to establish convincingly that a specific food or food ingredient is associated with a specific idiosyncratic reaction.

The role of specific foods or food ingredients are firmly established in a few of the numerous alleged foodborne idiosyncratic reactions.

Sulfite-induced asthma is perhaps the best example (Bush and Taylor, ). In the case of sulfite-induced asthma, numerous clinicians own documented the role of sulfites in the provocation of asthma in dozens of patients using DBPCFC protocols (Bush and Taylor, ). Aspartame has been identified as a causative factor in two subjects using DBPCFC (Kulczycki, ). However, other cases of aspartame-induced urticaria own not been identified so this may be a rather rare phenomenon.

For numerous other alleged idiosyncratic reactions to specific foods or food ingredients, the association with the specific food or food ingredient has not been conclusively documented through DBPCFCs.

Examples would include the role of chocolate or aspartame in migraine headache; the roles of BHA, BHT, tartrazine, benzoates, or parabens in chronic urticaria; the role of tartrazine in asthma; the role of monosodium glutamate (MSG) in asthma or MSG Symptom Complex; and the role of sugar in aggressive behavior (Bush and Taylor, ). A thorough critique of the numerous studies that own been conducted on the role of these foods or food ingredients in the causation of these idiosyncratic reactions is beyond the scope of this specific review.

However, extremely few of the clinical studies own used double-blind and placebo-controlled trial designs. Furthermore, numerous of the studies own involved individuals with chronic, episodic symptoms such as chronic urticaria or asthma and the clinical investigators own removed critical medications from the patients before initiating the challenge trials. In such cases, the observed symptoms might be due either to the challenge substance or to the withdrawal of medications that controlled the condition. With such critical clinical design flaws, the role of these specific foods and food ingredients in  these specific idiosyncratic illnesses remains unproven. Furthermore, psychological disorders may be involved in perceived reactions to specific foods or food ingredients (King, ; Selner and Staudenmayer, ).

In a few cases, the role of specific foods or food ingredients in idiosyncratic reactions has been disproven by careful clinical investigations.

However, consumers may persist in their belief that such reactions happen. The outstanding example of such a reaction is the role of artificial food colors in hyperkinetic behavior in children. Several decades ago, Dr. Benjamin Feingold implicated artificial food colorants as causative factors in hyperkinesis on the basis of poorly controlled trials and anecdotal experiences (Feingold, ). The resulting publicity on the Feingold hypothesis was considerable, and, consequently, numerous consumers became convinced of a relationship between ingestion of artificial food colorants and provocation of hyperkinetic behavior in children.

Subsequently, several double-blind, placebo-controlled challenge trials own been conducted with artificial food colorants and own demonstrated convincingly that few, if any, hyperkinetic children are adversely affected by the ingestion of these food colorants (Harley et al., a). Despite this evidence, numerous consumers persist in their belief regarding the role of artificial food colorants in hyperkinetic behavior.

A similar situation exists with honor to monosodium glutamate where the involvement of MSG intake in the so called Chinese Restaurant Syndrome, now more appropriately called MSG Symptom Complicated, has been alleged so often that it is now accepted as fact by numerous consumers.

However, the role of MSG in MSG Symptom Complicated has not been corroborated in carefully controlled clinical challenge studies (Kenny, ; Tarasoff and Kelly, ). More recently, MSG intake has been linked to asthma (Allen et al., ). However, the role of MSG in provocation of asthma seems questionable at best when patients are evaluated using a DBPCFC protocol (Bush and Taylor, ). The alleged role of tartrazine, also known as FD&C Yellow #5, in asthma and chronic urticaria is also extremely questionable in the light of DBPCFCs (Bush and Taylor, ; Stevenson et al., ). Yet, undeclared tartrazine remains the basis for a large number of FDA recalls.

Sulfite-Induced Asthma.

Sulfiting agents allowed for use in foods include sulfur dioxide, potassium metabisulfite, sodium metabisulfite, potassium bisulfite, sodium bisulfite, and sodium sulfite. Sulfiting agents own been used as food ingredients for numerous years, because they own numerous significant technological benefits (Taylor et al., b). Sulfites also happen naturally in some foods, especially fermented foods (Taylor et al., b). However, residual levels of sulfites in foods vary from a few ppm arising mostly from natural sources, to less than 10 ppm to >1, ppm as a result of additive usage.

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Although sulfites own been used for centuries, they own been implicated as triggers of asthma in some sensitive individuals only in recent years (Bush and Taylor, ; Stevenson and Simon, ).

The reactions generally happen within a few minutes after the ingestion of a provoking dose of sulfite. The reactions can be fairly severe on occasion and deaths own been attributed to sulfite-induced asthma (Bush and Taylor, ). The role of sulfites in the causation of asthma in susceptible individuals has been well documented by DBPCFC (Bush and Taylor, ; Stevenson and Simon, ). Other symptoms own also been alleged to happen as a result of sulfite sensitivity but these reports own been largely anecdotal and unverified by DBPCFC (Bush and Taylor, ).

Sulfite-induced asthma affects only a little percentage of every asthmatic individuals (Bush et al., ).

The prevalence among severe asthmatics who are dependent upon steroid-based drugs for control of their symptoms appears to be in the range of 4–7%, while mild asthmatics do not seem to be extremely susceptible to sulfite ingestion (Bush et al., ). Thus, the overall prevalence of sulfite-induced asthma is estimated at –% of the entire asthmatic population (Bush et al., ).

Sulfite-induced asthmatics display thresholds for sulfites (Bush and Taylor, ; Taylor et al., ). While the ingestion of high doses of sulfite in highly sulfited foods and beverages can be fairly hazardous for susceptible individuals, the ingestion of sulfited foods with lower levels of residual sulfite (< ppm as entire SO2) seems to present little risk (Taylor et al., ).

Thus, sulfite-sensitive asthmatics must be alert to the presence of sulfites in foods at levels that are required to be declared on the ingredient statement, but are at no risk from ingestion of sulfites from foods that own levels of residual sulfite under the detection limit of current assay procedures (<10 ppm as entire SO2).

The mechanism of sulfite-induced asthma is not known. Several diverse mechanisms own been proposed including IgE-mediated reactions, hypersensitivity to inhaled SO2 from ingestion of acidic foods and beverages, and sulfite oxidase deficiency (Bush and Taylor, ).

However, none of these mechanisms has been proven, so sulfite-induced asthma remains an idiosyncratic illness.

Implications for Food Manufacturing

Erin Spain: This is breakthroughs, the podcast from Northwestern University Feinberg School of Medicine. I’m Erin Spain, executive editor of the Breakthroughs newsletter. There’s been an uptick in childhood food allergies in recent years, and new evidence from northwestern shows that food allergies are also becoming more common in adults.

Numerous of the reactions to these allergies are life threatening. Why is this increase happening and how can we hold people affected by food allergy safe? Dr. Ruchi Gupta is trying to answer those questions. She’s dedicated her career to food allergy and asthma research here at Northwestern and the Ann & Robert H. Lurie Children’s Hospital of Chicago where she’s an attending physician. Her work is debunking myths and shaping policies around food allergy. Thanks for joining me today.

Ruchi Gupta: So happy to be here. Thank you.

Erin Spain: You’re an expert on childhood food allergies and asthma.

Leading much of the current research on this topic, but your most recent paper and JAMA Network Open focused on adults with food allergies. Why the shift to adults?

Ruchi Gupta: That’s a grand question. As I am a pediatrician, you know, over the years we’ve been studying, love he said, pediatric food allergy and that’s where the emphasis has been, but now a lot of those kids are growing up and they’re becoming adults and they’re going to college and they continue to own their food allergy and then you know, at meetings with other physicians, you start hearing about how numerous adults seem to be developing food allergies as adults.

Since we had the expertise in doing large scale prevalence studies, we thought we would modify our pediatric study for adults and really understand how numerous at people in the United States are affected by food allergy and what that looks like.

Erin Spain: So we really didn’t own excellent data on how numerous adults?

Ruchi Gupta: No, no. We own extremely little data on adults with food allergy. For some reason we’ve every really focused on the kids.

Erin Spain: So this paper that came out did make some headlines. You found that almost half of adults, they developed adult-onset food allergies.

And was that surprising to you?

Ruchi Gupta: So surprising. I mean, we knew, love I said, you hold hearing it right? Anecdotally in clinic and you start hearing and seeing more and more adults talking about how they’re developing these food allergies, but the number we found was extremely surprising. I mean, we really found that about half, 48 percent said they developed at least one new food allergy as an adult that they didn’t own as a kid. So those numbers were a little astonishing. Additionally, about one in four adults said they developed an allergy as an adult and never had a food allergy as a kid. So that’s, that’s a lot of adults developing new allergies.

Erin Spain: And the allergies are similar to what we see in children.

There’s milk, peanuts, tree nuts, fin fish, egg, wheat, soy and sesame. Those are among the most common. But for some reason shellfish is at the top of the list for adults. Do we know why that is?

Ruchi Gupta: That is such a excellent question. I ponder my favorite thing about doing research is once you do a study, it opens up love more that you can do and answer new questions. You’re absolutely correct, the top eight, we used to call it, now we call it the top nine because sesame is becoming the ninth most common allergen. Those are the same in kids and adults, but the adults own a extremely diverse order with shellfish being way beyond other foods.

I ponder % of adults reported having a shellfish allergy. It was the most common allergen in adults by far because after that it was milk and peanut around % — %. What is it about shellfish? I’ve heard from so numerous adults «Oh my gosh, I love shellfish and I can’t eat them anymore» and that is really hard for a lot of people. I ponder we now need to explore what is it about the proteins and shellfish and what’s so unique about the specific food that is causing so much adult-onset allergy?

Erin Spain: Well, the exciting thing about this study is it was a survey. It’s a survey you said that you’ve used for children before and it’s self-reported. So people, you know tell, well I ponder I own a food allergy or I own a food allergy.

Well, tell me about that because 20% of the adults reported having a food allergy, but you sure that it was only actually half of them that seem to own a genuine allergy. It was more love a sensitivity from how they reported that they reacted to the food. Tell me about that.

Ruchi Gupta: Yeah. I really appreciate you asking this question because I ponder this has been one of the most confusing questions that’s come up in the media and how people take it.

So, love you said it’s a survey. So people were asked, adults were asked do you own a food allergy? Then if they said yes, it went into what food allergies. So it would enquire specifically. So tell you said you own peanut milk and wheat. Every correct. Then it would take you through each food, it would tell «For peanut allergy, what are your most severe symptoms that you’ve had?» And then you would list them and you could record in or you could select from the list. And then it would enquire you things about diagnosis and about emergency department use and about epinephrine use, right?

So it asks you a series of question, then it would go into milk and would enquire you the same series of questions and then it would go into wheat. So you had to be specific for each food. Now what we did with that data, because there are so numerous food related conditions, right? You can own so numerous diverse things that looked love a food allergy but may not be. So what we did is we tried to do our best. We had an expert panel go through and attempt to clean the data so that if there were things that may be something else. So tell said you own a milk allergy, but you said you just get stomach cramps and some diarrhea. Okay. Then we would tell, well, we’re not completely certain that’s a food allergy that might be lactose intolerance.

So we would put it aside. Okay. So when people tell they were incorrect, that’s not true. So let’s go back to food allergies. The problem is that food allergies can impact any organ system, correct, so you can own GI symptoms. In fact, it’s one of the most common ones. Vomiting is one of the most common things that happen as an allergic reaction. You can own skin symptoms so you can get hives, you can own oral symptoms, you can get tightening of the throat and tingling, swelling of your mouth.

You can own respiratory symptoms, you can own trouble breathing, wheezing, tightness in the chest. You can even own cardiovascular, right? The drop in blood pressure. The problem with food allergies is you can own these mild symptoms or you can own them progressed to severe symptoms with the breathing difficulty and tightening of the throat and that can be life threatening. When people report only GI symptoms — we take them out. Or they only report oral symptoms because sometimes you can own something called oral allergy syndrome where you’re actually allergic to the pollen.

So if you eat a fruit and you only get tingling and a little swelling and itching in your mouth, that’s not a food allergy. But those could also be symptoms of a food allergy. So endless tale to tell you that what we really did was attempt to take a people who had symptoms that could glance love an intolerance or oral allergy syndrome and take them out and that was about half of the people. So whether they own a true food allergy, we are not certain. Whether they own an intolerance, we’re not certain. But, what it told us was that can you believe that one in five adults ponder that they own a food allergy and do potentially own some food related condition.

That’s a huge number.

Erin Spain: And it underscores the importance of getting that diagnosis and going into your doctor and really determining is this a food allergy?

Ruchi Gupta: And that was our goal by saying, glance, there’s one in five, but then of the convincing there’s only one in 20 that are getting diagnosed. I understand this as an adult, you know, a lot of times what happens is you eat a food, you own a negative reaction, and you’re love, well I just can’t eat that food and you don’t necessarily ponder, oh, let me go get it checked out by a doctor and I desire this to assist people ponder, let me go get it checked out by a doctor.

Because avoiding foods in your diet is so hard, right?

What is a food allergies definition

Trying to take out milk from everything you eat. I ponder for me the goal was, you know, let’s attempt to figure out what every these food related conditions are so that you’re not having to avoid a food unnecessarily and if it is a true food allergy, you need to know how to manage it because that can be life threatening and you need to know what type of reactions can happen and you need to carry your epinephrine with you.

Erin Spain: You touched on it a little bit with the shellfish. What is it about the shellfish, the protein?What are some of the hypothesis out there about why more kids and adults are developing food allergies?

I know there’s some theories. You’re one of the experts. What do you say?

Ruchi Gupta: I know, and this is what’s so exciting because we every know that genetics plays a role, right? But we would not own this epidemic and this huge increase if it was just genetics. So we need to better understand what is it in the environmental component that has changed over beautiful much a generation that has caused this incredible increase. So some theories are, of course, the hygiene hypothesis, right?

Love, are we becoming too clean?

Erin Spain: The hand sanitizers the soap?

Ruchi Gupta: Correct. It could extremely well be because our bodies are not exposed to things that are not fighting things they should. They’re fighting things they shouldn’t. There’s a couple of other really exciting hypotheses that are somewhat related. The microbiome, you’ve probably heard that that’s really boiling correct now. What is it about our gut bacteria and how much of a role does that frolic and what are we doing to it? You know, the whole thought of getting antibiotics early in life and that first year every the antibiotics infants are getting or mothers are getting during pregnancy, other hygiene related things.

You know, C-section births are up and so they’re not going through the normal vaginal canal and then they’re not getting that natural bacteria. Is that hurting them? Is that part of that whole hygiene piece and the microbiome that is in their gut and how do we eat, what are we eating these days? You know, are we eating locally grown food love before? No. Are eating from every over the world. What helpful of pesticides are used? You know, the ideas of GMOs. There are every these question marks that we haven’t fully understood yet.

Erin Spain: You’re interested in looking into those?

Ruchi Gupta: Yeah, I mean, you own to.

I would love to better understand what these factors are. Chances are they’re not one factor. We’re not going to tell, oh, it’s every about this. It’s going to be a group of factors and how our lifestyles own changed. The one large breakthrough that’s happened is there was a large study done in London called the LEAP Study and they found that if you feed infants, high risk infants, peanut products early in life, that you may be capable to prevent peanut allergy.

So that exposure through the gut early could be preventive. This was a really large breakthrough because for the first time we own a way to potentially prevent it. Because before that we told pediatricians to tell families to avoid peanut products until age three, which is what I did with my daughter and she has a peanut allergy. It was a extremely, extremely large finding to ponder that, okay, maybe by waiting we may be hurting.

Erin Spain: Now parents are giving those babies in the first six to 12 months, a little bit of peanut butter.

Ruchi Gupta: They should. They should absolutely. I mean, I ponder that is a extremely significant finding and every parents of infants should initiate peanut products watered below peanut butter.

Early in life, by that, you know, not the first food, but in that first group of foods, love around six months for sure.

Erin Spain: You’re a pediatrician as you mentioned and this is your focus — children and allergies. How did you start below this path? You mentioned that your daughter has a peanut allergy.

Ruchi Gupta: So it’s an exciting tale because I am a pediatrician and I came to Northwestern and Lurie Children’s 14 years ago to really study asthma disparities and to work with one of the leaders in the field that was here at that time and I met a family with two young children with extremely severe food allergies.

Been to the ER and hospitalized and they really wanted research to be done in this area. I was junior faculty, «Hey, you desire to come in, you desire to work on this?» I knew extremely little about food allergies back then, but what I found was compared to asthma, which I had been studying, there was a huge hole. We didn’t even know how numerous, as you know, we talked about. We didn’t know how numerous kids had it, how numerous adults had it. We didn’t know the basic prevalence or types of foods people were allergic to or what kinds of symptoms.

Every that data was not in the literature. I was trained in health services research and had my MPH and I was unused and ready to start. I thought, you know, this may be an area that I could make a difference and own an impact because so little is known. So that’s how I started. As I was studying it, three years into it, I believe, my son who loves peanut butter and jelly sandwiches, was playing with my daughter and touched her, I guess every over her face because she just broke out in hives.

Erin Spain: And you knew what it was immediately?

Ruchi Gupta: Oh yeah.

I’m love, wow, you know, what helpful of present is this? It’s really had such an amazing influence on my life and my career because there is a large difference just studying a condition and then living with a condition and every the things I go through every day in my life with her really do assist influence the research. By having her I know so numerous others with food allergy and then these support groups and listening to what their needs are. Right? Listening to that patient and that whole patient centeredness. It just really brings that home because they know what they need. We as researchers need to hear to them and answer their questions.

So, it’s been a blessing in some ways. But yeah, extremely difficult.

Erin Spain: How ancient is your daughter now?

Ruchi Gupta: She’s

Erin Spain: She’s still working through the peanut allergy? Because I know at some point a lot of people outgrow it.

Ruchi Gupta: She is working through it. Only about 10 to 20 percent outgrow peanut allergy. She’s got peanut and tree nuts and she used to own an egg which she has outgrown.

It’s a challenge every day because, you know, we don’t own a severity spectrum for food allergies, which I ponder a lot of parents, it really affects their life because if you don’t know my kid is mild or moderate. You know, people enquire you, «Oh, how severe is it?» and we own nothing to tell them and so everyone’s severe, right? Everyone could own a life threatening reaction. It’s a lot of anxiety and fear for families because food is a part of everything kids do.

Even adults.

Erin Spain: You’re doing so much to bring knowledge into the scientific community and build the literature. In , you led a study that, found that eight percent of kids in the US own at least one food allergy. This was new information as you said, we didn’t know before, and 40 percent of those kids had experienced a life threatening reaction already in their lives. How significant was this when you were capable to actually put some numbers out there?

Ruchi Gupta: It was really incredible to see what happened after that because after that study, people had numbers that they could hold onto and tell schools and see it in their classrooms.

You know, 8% is about two in every classroom. It’s about one in 13 kids. When you picture it love that, you’re love, oh yeah, that’s true. You know, there are about two kids in the class that own a food allergy and you realize how realistic this is and how prevalent. By being capable to list the foods and talk about the reactions I ponder it made more sense and it increased awareness and people started to get it and we actually repeated that study that was published in pediatrics again in December of What was exciting, the numbers are beautiful comparable, but we asked this time about emergency department visits and one exciting thing we found was of kids with food allergy, about 1 in 5 go to the emergency department every year for their food related reaction.

Erin Spain: So these are severe reactions?

Life threatening reactions?

Ruchi Gupta: Yeah. They are having them and so people would tell, «Okay, you own a food allergy, but how much does it impact your life?» So, for the first time we were capable to quantitate that and tell, you know, 1 in 5 are going every year. It’s a large deal. It’s something that we own to take seriously and assist protect these kids.

Erin Spain: And what is it, about children, they actually die from the reaction and that’s something that you were trying so hard to prevent through education and awareness.

Ruchi Gupta: Every time that happens, love every of our hearts are broken and we desire to prevent that from happening so badly and not only the deaths but even the severe reactions because they throw you off course.

You know, when you own one of those shut calls, it messes you up. It’s hard to then go out to eat and do normal things. But what’s so grand, I feel love, you know, in the 14 years I’ve been in this field, I’ve never seen a field change so much. So the quantity of research that’s happening now, we actually own treatments that will be coming out this year.

Erin Spain: Wow.

Ruchi Gupta: Yeah, so a lot of the researchers at Lurie Children’s are working on them. There is oral immunotherapy. Eating little amounts and increasing the dose and that’s going to hopefully be out later this year. It’s already in phase filed five clinical trials.

It feels extremely, extremely likely that it’ll be on the market. There’s a patch epicutaneous immunotherapy for peanut that’s coming out and then these companies are working on the next set of foods, the next most common foods. There’s a couple other treatments that I’ve heard of and that are in diverse phases of trials. So I feel love in the next five to 10 years we’ll own grand treatments for food allergy. The other grand thing that I’ve seen change over time in this 14 year period, as the awareness has been picked up, schools and Chicago Public Schools where one of the first to join us building policies, having stock epinephrine in case of an emergency.

Unfortunately, this every was sparked by, as you said, a young kid dying in school after an anaphylactic reaction and there was no epinephrine. After that CPS said, we’re not going to ever let this happen again. They passed a law to own stock epinephrine in every CPS school. And then every through the country, I ponder, every state now has a law or a policy around stock epinephrine in school. To see policies developed, to see the community coming together to protect kids and adults with food allergy so quickly is so inspiring.

Erin Spain: You said kids are sometimes the biggest advocates, classmates, they desire to assist protect their friends.

Ruchi Gupta: Yes, and to that, you know, we do three areas of research that epidemiology, that we’ve talked about, we do a lot of the clinical care, helpful of that early introduction stuff that we talked about.

The third large pail we own is community. We work extremely closely with the schools and we’ve actually developed videos that are free on our website and for schools to use around how to teach a classroom about food allergies and how to own your peers be supportive. What we found is that is the number one thing to protect these kids — is if they own that peer support and not the bullying. Bullying is also extremely common, but if we can take it to developing more peer understanding and peer support and it could change these kids’ lives.

Erin Spain: We’ll make certain to put links to those videos on the podcast website so people can glance them up and share them. (Watch Gupta’s food allergy peer-to-peer educational videos.)

Ruchi Gupta: That would be great.

Erin Spain: Well this is fascinating.

The past 14 years, as you mentioned, so much has changed, but it sounds love we are now at a point where there’s going to be some genuine treatments and we’re really looking forward to see what’s coming up.

Ruchi Gupta: Thank you. Yeah, I am too. You know, I own a little cartoon on my wall at work and it is what I hope to see. It’s an adult talking to a kid and the adult is saying, «You know, in my day there were no food allergies», because this is what you hear every the time.

Then that kid grows up and as an adult talking to a kid and saying, «You know, in my day there were food allergies». So hopefully that’s where we’re headed and hopefully I can assist be a part of that.

Erin Spain: Well, thank you so much Dr. Ruchi Gupta for coming and sharing your research with us today.

Ruchi Gupta: My pleasure. Thank you.

Erin Spain: A note for physicians who hear to this program, you can now claim continuing medical education credit just by listening to this podcast. Go to our website and search for «CME» for more details.

On Monday, based on a detailed review of every available evidence on the topic, the American Academy of Pediatrics published updated guidance on what works and what doesn’t when it comes to the prevention of food allergies and other allergic conditions.

The new guidelines continue to liberalize the introduction of what are thought to be highly allergenic foods such as peanuts, fish and milk.There is no convincing evidence that delaying the introduction of allergenic foods beyond 4 to 6 months of age works in preventing food allergies, the report says. In addition, there is strong evidence that purposeful, early introduction of peanuts as early as 4 months may prevent the development of a peanut allergy in infants at high risk, defined in this report as those with a shut relative with a history of an allergic condition. «There is no reason to delay giving your baby foods that are thought of as allergens love peanut products, eggs or fish,» Dr.

Scott Sicherer, a co-author of the report, said in a statement. «These foods can be added to the diet early, just love foods that are not common allergens, love rice, fruits or vegetables.»The gastrointestinal tract is home to a unique set of immune system cells, and when these cells are given a taste of the allergenic proteins in diverse foods, they take up these proteins and become tolerant to them. Dr. David Stukus, a pediatric allergist and associate professor of pediatrics in the Division of Allergy and Immunology at Nationwide Children’s Hospital, said that’s true «as endless as it’s introduced early and in an ongoing fashion,» meaning there is a critical window of time during which being introduced to these foods may lead the body to become tolerant.

And early means as soon as 4 months to 6 months of age, said Stukus, who was not involved with the new guidelines.The report also looked at whether breastfeeding protects against eczema, wheezing, asthma and food allergies. Exclusive breastfeeding for the first three to four months of life was found to be protective against eczema, the authors concluded. Any quantity of breastfeeding beyond that time, even if not exclusive, was found to be protective against wheezing in the first two years of life and asthma in the first five years and even later. The report says no conclusion could be made when it came to breastfeeding and its effect on the prevention of food allergies.

No evidence was found that avoiding allergenic foods during pregnancy or during breastfeeding worked in the prevention of allergic conditions. Neither did the use of special hydrolyzed formulas, even in kids who were at high risk. «I really appreciated the comprehensiveness of this clinical report,» said Dr. Wendy Sue Swanson, a general pediatrician and chief of digital innovation at Seattle Children’s Hospital. Swanson, who has endless advocated for the early introduction of a diversity of foods in young children, described feeling grateful for the guidance, given the ongoing changes in the understanding of allergy prevention.

In , the American Academy of Pediatrics recommended delaying the introduction of cow’s milk until children were 1 year ancient, egg until 2 years and peanuts, tree nuts and fish until 3 years. «Recommendations were to avoid allergenic foods until children were older,» Stukus said. «The thought process at the time was, well, if we avoid any exposure, maybe the allergic response won’t develop.»In , after a review of the available literature, the organization issued a report saying there was no convincing evidence that delaying allergenic food introduction prevented food allergies.

The report did not give specific guidance as to when these foods should be introduced. Almost 10 years later, after a study was published in the New England Journal of Medicine, the academy recommended that babies at high risk of developing peanut allergies be introduced to peanuts as early as 4 months. Infants considered at high risk included those with eczema and/or an egg allergy. This study — known as the Learning Early About Peanut or LEAP trial — showed that children at high risk of developing peanut allergies who are introduced to peanuts at 4 months to 6 months ancient had a significantly lower risk of developing a peanut allergy than those who waited until they were 5 years; % of the kids who had peanuts early developed an allergy, compared with % of the kids who waited.

The LEAP trial formed the basis for Monday’s new recommendations, which urge the early introduction of peanut products in infants at high risk for allergies.But most babies are not at high risk, and peanuts are just one of the eight culprit foods; the others are milk, eggs, fish, crustacean shellfish, wheat, soy and tree nuts, according to the US Centers for Disease Control and Prevention.

The evidence for other foods and children

The latest report explains that the same mechanism that protects infants at high risk is likely to protect infants at low or standard risk of developing food allergies. A study that examined these other foods, known as the Enquiring About Tolerance or EAT trial, recruited 1, 3-month-olds and randomly assigned them to get six allergenic foods — peanut, cooked egg, cow’s milk, sesame, whitefish and wheat — at that age or to wait until 6 months.

The team then measured whether these infants developed food allergies between 1 and 3 years ancient. Only 40% of parents were capable to hold up with the diverse food frequency that the study protocol recommended. When researchers looked at the data from every of the children in the study, no difference was found in the rates of food allergies. When they looked at only the children whose parents had been capable to hold up with the foods, there was a significantreduction in peanut and egg allergies.

«The EAT study provides some evidence but is less strong than the LEAP trial evidence,» said Dr. Elizabeth Matsui, pediatric allergist and chairwoman of the American Academy of Pediatrics Section on Allergy and Immunology, comparing the trial that included the diverse foods to trial that involved peanuts. When the risk of an illness is relatively low, proving that it can be decreased even further is extremely hard, she added. An significant takeaway from the trial is that introducing a variety of foods as early as 4 months is safe, Stukus explained.

Overwhelmingly, the data is pointing toward the benefit of early food introduction, Swanson said. «I don’t desire kids to delay introduction. Stop medicalizing this and let babies eat,» she added.

The bottom line for parents

«It’s not just early introduction. It’s routine feeding. It’s habituating. We need to make a habit of eating extremely diverse foods,» Swanson said. «It’s a grand habit to own your whole life, because 50% of people who develop a food allergy develop it in adulthood.»In his practice, Stukus has started to recommend early introduction — between 4 and 6 months of age — of allergenic foods for every babies, no matter their individual risk.

He encourages parents to continue to give these foods several times a week for babies who are tolerating them. «I ponder the benefits far outweigh the risks in this situation,» he said. The most serious risk is anaphylaxis, a severe allergic reaction that can be life-threatening. But in most young infants, Stukus explains, anaphylaxis manifests as vomiting and hives, without the difficulty breathing and the closing airways that can be seen in older children. Parents who spot vomiting or hives — especially together — should still seek medical attention. But pediatricians and parents same can relax assured that these foods can be introduced freely at home, reversing decades of fear in the introduction of new foods, he added.

«We come from a put of restriction and medicalization,» Swanson said. Pediatricians were strong in telling parents to be cautious, and now they must be strong in telling parents not to be cautious. «No, I don’t desire you to be cautious. In fact, waiting might cause harm,» she said.

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