Food allergies are so confusing and becoming so prevalent in today’s society. At some point the question “why are food allergies so prevalent?”; needs to be further explored, but for now this is a brief overview of food allergy. What follows is some research I did on food allergy.
Brief Description and Classification
Food allergies are incredibly complex to define, due to this there are many variations on the definition. The definition I found cited in several studies originates from the (HHS, NIH) National Institute of Allergy and Infectious Diseases (NIAID) (2011), “A food allergy is an adverse health effect arising from a specific immune response that occurs reproducibly on exposure to a given food” (p.6). This definition seems slightly vague which may explain the many other variations on the definition. Food allergy is then divided into multiple categories, based on systems involved in the reaction and the length of time before the reaction. There are immunoglobin E (IgE) mediated allergic responses, which are an interaction between the allergen and the antibody IgE (NIAID, 2011). There are also non-IgE mediated reactions and mixed IgE and non-IgE mediated reactions (Chaudhry & Oppenheimer, 2012). Skypala (2011) includes the three above reactions and adds in a fourth reaction, cell mediated. Wang & Sampson (2011) state that non-Ige mediated reactions are “cell mediated reactions with more delayed symptoms” (p. 827). From here the definition gets a little bit stickier, Chaudhry and Oppenheimer (2012) state that IgE mediated reactions are characterized by acute onset of symptoms within two hours of allergen exposure (p. 312). Taylor and Hefle (2001) state that true food allergies can be dived into two categories, based on length of time before reaction, immediate hypersensitivity and delayed hypersensitivity (no reactions until 24 hours or longer). Zopf, Baenkler, Silbermann, Hahn and Raithel (2009) have three categories for reaction time, immediate symptom onset (less then two hours), intermediate reaction time (two to 24 hours) and delayed reaction (over 24 hours). The slight differences in definitions make it difficult when sorting through the literature to make sure that true comparisons are being made.
There are multiple ICD 9 codes for food allergies depending on the type of reaction and the type of food. For example, code 693.1 is for allergic dermatitis due to food taken internally and code 995.7 is for “other adverse food reactions, not elsewhere classified” (Howard, 2008). Anaphylactic shock is classified as code 995.6x, with the last digit indicating which food caused the reaction.
Mahoney, Veling and Mims (2011) classify food allergy as an acute and chronic disease. The Asthma and Allergy Foundation of America (n.d.)states that food allergy is a chronic disease. Based on my understanding of the terms, food allergy would be a chronic disorder and anaphylaxis due to food allergy would be an acute reaction.
Origin and History
Over 2,000 years ago Hippocrates wrote about the effect of cheese on man, there are some who do not bear it well, their constitutions are different, and they differ in this respect, that what in their body is incompatible with cheese (Hippocrates, n.d.). There appears to have been a bunch of interest in food allergy at the beginning of the 1900s. In 1905, Dr. Hare wrote a book called “The Food Factor in Disease” (Lundy, 2007). In 1906, Dr. Clemens von Pirquet recommended using the word “allergy” to describe an unusual reaction to food or other substances thought to be harmless (Lundy, 2007). The first report of oral immunotherapy was published in 1908 (Wang & Sampson, 2011). In 1911, allergen specific immunotherapy was introduced, it sounds very similar to current day allergy injections that are small amounts of the allergen in serum injected into the sensitive person.
Food allergies are on the rise in the United States, according to NIAID (2010) the prevalence of food allergy increased 18% from 1997-2007. Food allergies cause many adverse reactions in sufferers, which are in more detail below, including the potential for anaphylactic shock. As a sufferer of a food allergy, the hardest thing with the grocery store or even going to restaurants is the cross contamination in all of the processed foods. In addition, many of our foods contain more ingredients than are truly necessary. For example, even in cream cheese I have found vegetable starch most likely corn derived. Lack (2012) speculates that changes in diet, obesity related inflammation, increase in omega 6 consumption, decrease in antioxidant consumption and even vitamin D deficiency, can all be linked with the increase in food allergies. If he is correct on any of these, we can expect to see continued rise in food allergy in modern society.
The agent in food allergy appears to be whatever component, usually proteins (on occasion haptens) are the cause of an allergic reaction (Chaudhry & Oppenheimer, 2012). In the United States 90% of food allergies are caused by eight foods; milk, soy, eggs, wheat, peanuts, tree nuts, fish and shellfish (Wang & Sampson, 2011). These proteins only cause an allergic reaction in a sensitized individual.
The host is the person who is sensitized to the specific allergen.
Pre-clinical phase. When you are first exposed to a food allergen, your immune system makes IgE antibodies specific to that allergen. I understand this to mean that the first time you are exposed, similar to bee stings, most people do not react. The IgE antibodies move through your body and attach to specific cells, mast and basophils (NIAID, 2010). “Mast cells are found in all body tissues, especially in your nose, throat, lungs, skin, and gastrointestinal (GI) tract. Basophils are found in your blood and also in tissues that have become inflamed because of an allergic reaction” (NIAID, 2010). During this pre-clinical phase, it is when exposure to the allergen has occurred, but prior to symptoms there are conflicting reports on the ability to test. The ability of the two main tests, IgE food specific serum test and skin prick test, to detect a true positive are only 50-60% (Skypala, 2011). In addition, food allergy can begin in adults, which means that a person can be exposed many times before showing a reaction (HHS, NIH, NIAID, 2011).
Food allergy is not transmitted person to person, however there is evidence to show that a person is at an increased risk of developing food allergy if they have a parent or sibling with asthma, eczema, food allergy or hay fever (HHS, NIH, NIAID, 2011). Since food allergy is largely a reaction to an ingested food, the main portal of entry is through the mouth and the gastrointestinal tract. However, allergic reaction can also occur due to exposure through the skin or respiratory tract (Taylor & Hefle, 2001). Adults can contract food allergy as a result of inhaled respiratory exposure to the allergen. There are instances where a non food respiratory allergen can cause a food allergy reaction, due to cross reactivity with the food allergen (Bohle, 2004). For example, I am extremely allergic to ragweed, which is cross reactive with cucumber and melons, so my allergy doctors advised me to avoid those during ragweed season.
Clinical phase. Food allergy symptoms are extremely diverse in reaction type and in severity. Some symptoms are simply mild and annoying, while others are life threatening (Taylor & Hefle, 2001). IgE mediated reactions include, but are not limited to; itchy skin, hives, flushing, angioedema, tachycardia, hypotension, throat tightness, shortness of breath, gastrointestinal and anaphylaxis (Skypala, 2011). Symptoms can effect the skin, eyes, upper and lower respiratory systems, oral gastrointestinal tract, lower gastrointestinal tract, cardiovascular, and other parts of the body, including causing an “impending sense of doom” (HHS, NIH, NIAID, 2011, p. 10)
As I mentioned earlier food allergy can be tested for with an IgE food specific blood test or skin prick test (small amounts of allergens injected underneath skin), but they are not always accurate. The optimal test which has been called the gold standard by several articles, is the double-blind placebo controlled food challenge (DBPCFC) which is not always used due to cost and time to test (Taylor & Hefle, 2001). If DBPCFC is not an option, the other two options are the single blind food challenge or the open food challenge (OFC). In the OFC the patient and the health professional know which food is being tested (Taylor & Hefle, 2001). For me, I test positive to almost every skin prick test they give me and negative on all the IgE, I had to do an elimination diet with the top allergens to pin point exactly which ones caused symptoms when I added them back in. The current treatment for food allergy consists of avoiding trigger foods, carrying epinephrine to be prepared for anaphylaxis and wearing an allergy identification bracelet (Mahoney et al., 2011).
The environment for food allergy in the epidemiologic triad is the actual setting that brings the sensitized person in contact with the allergen. A study done in Denmark reported that 10-25% of the young adult population have pollen allergy and that 47-70% of the people with pollen allergy experience pollen related food allergy (Sicherer, 2011). In this case, the environment is exposing sensitized individuals to pollen allergens which are connected with the food allergens. Lack (2012) presents an hypothesis that address environmental factors, he states that low dose exposure to environmental food proteins on surfaces or in dust, can explain severe incidences of eczema in infants which is related to food allergy development. This hypothesis provides some evidence for why food allergens differ throughout the world, in a society where a food is not consumed there is no environmental exposure and therefore an allergy to that food will not occur.
The age group that has the highest IgE proven allergenic reactions are the 20-39 year olds, while the highest rate of the non-IgE mediated food allergy reactions occur in the over 60 age group (Skypala, 2011). One study shows statistically significant food allergies in females compared to males, 11.4% of females self reported food allergy compared to 6.5% of males and 7.6% of females reported a doctor diagnosed food allergy compared to 2.7% of males (Chaudhry & Oppenheimer, 2012). Sicherer (2011) reports that there is an increased risk for boys and possibly women, and that non-white may be at risk (p.599). Sicherer (2011) further states that in “telephone surveys, shellfish allergy was reported at a significantly higher rate among black/African American subjects than white subjects (3.1% vs 1.8%)” (p. 600). Additionally African ancestry is a risk factor for increased chance of peanut allergy (Lack, 2012). In the National Health and Nutrition Examination Survey, non-hispanic blacks reported an increased risk of having positive blood tests for food allergy, reported at a 3:1 odds ratio (Sicherer, 2011, p. 600).
I mentioned earlier how sensitization to certain foods may be linked to geographic location based on foods that are consumed locally. For example, bird’s nest soup in Singapore, royal jelly in Hong Kong and mustard seed in France are all known geographically linked allergens (Lack, 2012). Peanut allergies are more common in North America than in any other part of the world (Taylor & Hefle, 2001). Peanut sensitization in the U.S is 9.3% compared to only 1.5% in the United Kingdom (Sicherer, 2011). According to Wang and Sampson (2011) the higher peanut allergy rate in the US may be due to roasting the peanuts at high temperature. When the peanuts are roasted the allergen becomes more potent. In other countries like China, peanuts are boiled or fried and allergy rates are lower.
I did not find anything time specific, however I would speculate that as some food allergies are linked to pollen that increased food allergy reactions would be seen during higher pollen times of year.
Incidence. Data from the US National Electronic Injury Surveillance System from 34 emergency departments in August and September 2003 collected on food adverse reactions shows that there were 20,281 ER visits, 2333 episodes of anaphylaxis and 520 hospitalizations (Sicherer, 2011). (I did not find any specific information on incidence most likely due to the inability to accurately test for and define food allergy. To calculate the incidence rate, the entire population could be part of the denominator which may further complicate calculating incidence. Unfortunately I do not know which ED’s reported this data or what the at risk population was or if there were multiple visits from the same people counted in those numbers.)
Prevalence. There is slightly more information available on the prevalence of food allergy, but it is very limited and vague. The studies that I read reported an abundance of different information. Zopf et al. (2009) report that more than 20% of the population in industrialized countries suffer from food intolerance or allergy, but immunologically mediated reactions are only 2-5%. Wang and Sampson (2011) report food allergy effects 3-4% of adults. Skypala (2011) reports IgE mediated food allergy effects 1-4% of adults. A 2010 study by Rand Corporation states that food allergy affects more than 1-2%, but less than 10% of total population (Chaudhry & Oppenheimer, 2012). The most concrete numbers I found were from the National Health and Nutrition Examination Survey from 2005-2006 which states that the overall prevalence of food allergy is estimated at 2.5% (Chaudhry & Oppenheimer, 2012).
The Asthma and Allergy Foundation of America (n.d.) states that food allergies account for over 200 deaths per year, which is another vague not very useful bit of information. I did not find any specific information on mortality or case-fatality rates, since there is so little data on how many people have food allergy. Sicherer (2011) reports that “no studies address directly the prevalence of fatal food-allergic reactions” (p.599).
There is some data that suggests that early oral exposure to leads to tolerance of food (Lack, 2012). There is evidence to suggest that food allergy can be delayed but not prevented (Taylor & Hefle, 2001). Nothing else suggests that there is any way at all to avoid food allergy development.
A person becomes sensitized to the food allergen before the allergy develops, this doesn’t always occur on the first exposure to the allergen, but can occur at any point in the future when the person is exposed (Taylor & Hefle, 2001). At that first sensitization the person is not symptomatic, but it is highly unlikely that a person would be identified at this point. Without symptoms there is no reason for a doctor to run tests for food allergy.
Sometimes food allergies are outgrown on there own, for example milk, egg and soybean allergies can be outgrown, where peanut allergy is almost never outgrown (Taylor & Hefle, 2001). The number one way that most articles and websites recommend is complete avoidance of the allergen. Once a person has an initial allergic reaction there is no way to determine if the next reaction will be more or less severe, due to this the only way to safely deal with food allergy is to not eat the allergenic food (HHS, NIH, NIAID, 2011). In addition, epinephrine should be carried by individuals with food allergy in the event of anaphylaxis (Mahoney et al., 2011). Some researchers have proposed use of oral immunotherapy as a way to slowly build up tolerance to allergenic foods, however there is a high rate of adverse reactions (Wang & Sampson, 2011). Based on my readings, until a safer alternative to oral immunotherapy is available or another treatment is proposed, I think that the avoidance diet is the best option for those with food allergy.