The Peanut Allergy Epidemic: What’s Causing It and How to Stop It
Excerpted with permission from The Peanut Allergy Epidemic: What’s Causing It and How to Stop It by Heather Fraser. Copyright 2018 by Skyhorse Publishing, Inc.
Why is the peanut allergy an epidemic that only seems to be found in western cultures? More than four million people in the United States alone are affected by peanut allergies, while there are few reported cases in India, a country where peanut is the primary ingredient in many baby food products. Where did this allergy come from, and does medicine play any kind of role in the phenomenon? After her own child had an anaphylactic reaction to peanut butter, historian Heather Fraser decided to discover the answers to these questions.
The Peanut Allergy Epidemic
The Problem of Peanut Allergy
By 2012, as many as 2.3% of Canadian children under 18 and 2% to 3% of children in the US, the UK and AU were allergic to peanut. (See Appendix). And as children born during the first wave of the epidemic in the early 1990s have aged, the statistic of adults with peanut allergy is increasing. In 2008, an estimated 1% of the US population was allergic to this one food, about 3 million people. Four years later by 2012, that number jumped to an estimated 4 million living with a life threatening allergy to peanuts.
Peanut allergy began as a phenomenon largely affecting children living in Western countries, the US, Canada, Australia and the UK. The alarm sounded for Americans when between 1997 and 2002 the number of peanut allergic children doubled and then tripled reaching an astonishing one million in 2008. In 2010 one study put that number at 2%, an additional 500,000 children in just two years. As this book unfolds it will become evident that there is a pattern in the way in which the peanut allergy in Western and now non-Western countries has emerged—epidemic levels of peanut allergy in children are now also documented in mainland China, Hong Kong, Singapore, Israel and parts of Africa.
While the exact numbers are a matter of debate, it is clear through statistics, scientific inquiry, and simple anecdotal evidence (the parental refrain “no one had a peanut allergy when I was at school”) that the prevalence of the allergy among children has increased at an alarming rate.1 This development has altered the fabric of societies now forced to accommodate life-threatening allergies to common foods.
Families with children allergic to peanuts (or any of the other top 8 allergenic foods—tree nuts, fish, shellfish, wheat, soy, dairy, egg)2 live in a state of constant tension. If these families eat at restaurants, they do so with extreme caution. Not knowing the severity of the allergy, parents are vigilant about smears of peanut butter left on tables or on grocery cart handles. Trace amounts on the skin or lip or even the scent of the food could trigger a reaction. Parents, the child, caregivers, and teachers are fearful.
Children are segregated in school cafeterias at designated tables or left out of play because friends have peanut butter in the house. Every school now tackles the peanut question, whether to ban peanut butter sandwiches and how to educate staff and students about the deadly nature of this ubiquitous childhood food.
Public awareness of peanut and other severe food allergies has impacted education systems and social norms, provoked legal reform, and made billions of dollars for those active in the food-allergy industry. This industry’s infrastructure consists of many overlapping allergy awareness groups, international allergy associations, medical researchers, pharmaceutical companies, allergy doctors, “free from” food makers, and government regulators, all of which support or are supported by the growing legions of food-allergic children.
The inherent inertia of this industrious leviathan, however, has pushed the salient questions into the background: How has the peanut allergy epidemic developed, and why is it continuing?
It is difficult to accept the startling increase in peanut allergies in children in just the last twenty years as a coincidence or to chalk it up to genetic fluke. The challenge for any concerned medical professional has been to unearth the precise practical mechanism of sensitization common to these children—how did they become sensitized to peanut in the first place? And while there are a limited number of proven ways of “how to” make someone anaphylactic—ingestion, inhalation, through the skin, injection—no hypothesis of mass sensitization has yet connected any of these functional mechanisms to all the specific characteristics of the peanut-allergy epidemic.
Researchers have considered skin creams that contain peanut oil, peanut consumption, parasite burden, and more without satisfactorily explaining why there has been a rise of the allergy in children. Why peanut? Why has it happened so suddenly, and why just in certain countries, most of them Western?
Risk factors for developing the allergy have been explored without conclusion. These include the following: maternal age, mode of delivery, levels of intestinal flora, heredity, and even birth month and socioeconomic status. Confusing matters further is a debate over the basic concept of allergy: Is allergy the outcome of a roulette-style genetic predisposition to immune dysfunction, or is allergy an innate, purposeful immune defense?
An important and clear distinction must be made between sensitizing someone to peanut and launching the allergic reaction. Sensitization is believed to occur when a protein bypasses the detoxifying process of the digestive system and becomes bonded with blood serum. This prompts specific blood cells to create antibodies that are then programmed to recognize the threatening protein—in this case, peanut protein. The launching of an allergic reaction, on the other hand, occurs when the body is subsequently exposed to the protein and the antibodies trigger the biochemical players in the allergic reaction. Lack of a standardized definition of anaphylaxis has hampered some studies where categories of “true” anaphylaxis mediated by Ig antibodies are compared with non-Ig anaphylaxis. This is less of a concern with peanut allergy where apparent consensus is that it is almost always Ig mediated.
Immunoglobulins epsilon (called IgE) are sentries of the body. The job of the IgE is to patrol the fortress walls—mucous membranes—looking for peanut protein intruders. When they detect one of the many peanut protein epitopes (strings of amino acids that are numbered 1 through 8 and all called Ara h after Arachis hypogea, Latin for peanut)3 they alert the body, which in turn lets loose the army—the body’s immune system. A biochemical cascade is deployed that is damaging and potentially dangerous. It is typically characterized by coughing, shortness of breath, itchy skin hives, systemic leaking of blood vessels that causes swelling and potential asphyxia, vomiting, and diarrhea. In severe reactions, blood pressure drops, draining vital organs and causing the heart to stop.
Scientists have shown that the anaphylactic condition in all mammals can be achieved by inhaling peanut protein if it is combined with a toxic additive. For example, doctors have created anaphylaxis in lab animals that inhaled a mixture of peanut and cholera.4 The toxic bacteria functions as an adjuvant, an additive that excites the immune system to form antibodies. It is suggested that the toxin and benign food can become in this way linked and both remembered by the immune system.5 One wonders then at the idea of an allergy to bacteria and the toxins produced by them. Allergy to bacterial toxins has been acknowledged for many years and can result in inflammation of the tonsils and adenoids and anaphylaxis.
Researchers have not explored the role of adjuvants in peanut sensitization. They have preferred to focus only on the peanut proteins, their allergenicity, and the ingestion of them as the most obvious elements in sensitization. They seemed to think that if they could simply pinpoint the initial oral exposure to these proteins, they could stop the epidemic. To this end, they have considered the ways in which peanuts are prepared (boiled versus roasted), age when they are introduced to the child’s diet, maternal diet and breast milk, and even peanut oil used in nipple creams. Although it is possible to create the condition through simple ingestion, it is difficult. A healthy digestive system will neutralize any potentially sensitizing protein.
In fact, a 2006–2007 study stated that it did not matter whether mothers ate peanuts or not—the same percentage of children developed the allergy. Some children whose mothers did not eat peanuts before, during, or after pregnancy still developed a peanut allergy. Kids who had never been exposed to peanuts exhibited anaphylaxis on their first or second taste of it—suggesting that they were already sensitized either to peanut proteins or to proteins similar enough to them leading to cross-reactivity. Adding to the allergy mystery is the fact that Sweden, which has a low level of peanut consumption, has a higher prevalence of the allergy than the United States. Israel, which has a high level of peanut consumption, has a low prevalence of peanut allergy in Jewish children at .6% in 2012 (but a high prevalence of sesame allergy) and a high prevalence of peanut allergy in Arab children (2.6%) living in the same country.
Another puzzling feature of the epidemic is the sudden emergence of peanut allergy in non-Westernized countries like Ghana, China and Singapore. It was suggested previously by Sampson et al in 2001 that children living in China did not have peanut allergy because their peanuts are boiled which partially destroys and reduces sensitizing peanut proteins. However, the sudden and increasing prevalence of food allergy in children living in mainland China and peanut allergy Hong Kong upends this theory and deepens the seeming mystery of this allergy.
Today, thousands of research articles by doctors on the biology of the allergic reaction, clinical observations, and allergy management are available in prestigious periodicals. From this mound of information, doctors have developed and tend to favor two explanations for the current epidemic of peanut-sensitized children. They are the helminth hypothesis and the hygiene hypothesis.
Helminths are worms that live in the human intestinal tract. It surprised researchers in the 1980s to discover that people heavily infected with worms had few allergies. One study confirmed that most Venezuelan Indians living in the rainforest had worms but no allergies while very few of the wealthy Venezuelans living in the cities had worm infections, but many had allergies.
From this observation, researchers developed an explanation for all allergies: because parasites and humans have coevolved, they have an apparent symbiotic relationship in which parasites suppress allergic reactions while enjoying their human host. Without worms, the theory states, humans are unable to achieve homeostasis. In other words, immune dysfunction occurs due to lack of worms.
As an explanation for peanut allergy, the helminth hypothesis is inadequate. It cannot explain why there has been a rise of peanut allergy just in children. And given that Western countries have been largely unburdened by major helminth infections for decades, it does not explain the sudden increase of food allergy that shocked school systems in the early 1990s.
Another popular explanation for the rise in childhood allergies grew from an apparent correlation between this rise and the general decline in family size. It was proposed that unhygienic contact in large families—lots of siblings bringing illness home from school—was important for the development of a healthy immune system. The greatly expanded and much-touted hygiene hypothesis suggests that overzealous cleaning, germ-killing products, chlorinated water, antibiotics, (vaccination is specifically avoided by researchers) have “protected” Western children unnaturally. And as a result, the immune systems of First World children, in particular, are sheltered from a natural microbial burden. Their immature immune systems are understimulated, dysregulated, and therefore prone to random allergic sensitization. This malfunction is a product of an unburdened lifestyle.
The hygiene hypothesis is problematic in explaining peanut allergy. It does not consider the possibility that the immune systems of these children are not understimulated but rather overstimulated by Westernized approaches to toxic chemicals, drugs, and vaccinations. In addition, the theory does not indicate a practical mechanism of mass sensitization that would explain the sharp rise in food allergy just in children that was first noticed in the early 1990s in specific countries when a flood of affected children arrived for kindergarten. This is a primary clue to causation that researchers have either missed or dismissed altogether.
In addition, these two favored explanations for the epidemic assume that allergy is a dysfunction, that the body has made a mistake in attacking a benign substance. And yet, the opposite may be true. Some suggest that allergy has an evolved purpose seen before the twentieth century but provoked increasingly today by drugs and noxious pollutants in our air, water, and food.
American researchers Rachel Carson (1907–1964) and Theron G. Randolph (1906–1995) and evolutionary biologist Margie Profet (b. 1958) proposed that allergy is an evolved protective response. In 1991, Profet stated in The Function of Allergy that allergy is a final and often risky natural defense against toxins linked to benign substances. The IgE antibody is not, as it is generally characterized in medical literature, a rogue immune factor. It is more akin to a hero provoked by toxins the body has deemed a deadly threat. The scratching, vomiting, diarrhea, and sneezing are desperate attempts to eject a toxin as fast as possible. It is a risky reaction but one the body is programmed to unleash as a last-ditch effort to protect itself. This event occurs when the general defenses have been insufficient in preventing a specific toxin from accessing the bloodstream for a second time.
This is a provocative concept. However, because it was developed before the rise in peanut allergy, it lacks specificity—again, why peanut and why the sudden increased prevalence in children?
Conspicuous by its absence from current theories is the one mechanism that has an actual history of creating mass allergy—injection. Injection is examined in this book in some detail since it was the means by which the founder of anaphylaxis, Dr. Charles Richet, stumbled on alimentary (food) anaphylaxis in humans and animals over one hundred years ago. Richet concluded in 1913 that food anaphylaxis was a response to proteins that had evaded modification by the digestive system. Using a hypodermic needle, he was able to create the condition in a variety of animals—mammals and amphibians—proving that the reaction was not only universal but also predictable using the method of injection followed by consumption or another injection.
There are two lines of thought in the medical literature regarding injection as a mechanism of sensitization. The first is that injection, in the form of vaccination or other injections such as the neonatal vitamin K1 prophylaxis, merely unmasks genetic predispositions or tendencies to allergic disease. In short, there is something wrong with the child and not the injection(s).
The second line of thought is that there is a causal relationship between the injected ingredients and allergy—and although the proven allergenicity of vaccines is widely acknowledged, medical literature carefully avoids the question of what kinds of allergies vaccines can and do create to substances that are coincidentally or subsequently inhaled, ingested or injected. One exception to this unwritten rule was an unusual admission by Japanese doctors that an outbreak of gelatin allergy in children starting in 1988 and continuing through the 1990s was caused by pediatric vaccination. In that year, changes to the vaccination schedule in Japan meant that the DTP was replaced by an acellular version containing gelatin, the age at which it was administered to children was dropped from two years to three months, and this new vaccine was given before the live virus MMR vaccine that also contained gelatin. When children began reacting with anaphylaxis to the MMR vaccine as well as gelatin-containing foods (yogurt, Jell-O, etc.), doctors investigated. Finally, they concluded that the aluminum adjuvant in the DTaP had helped sensitize children to the “minute amounts” of proteins in the refined gelatin in the vaccine. Removal of gelatin from the DTaP vaccines was “an ultimate solution for vaccine-related gelatin allergy.” Subsequently, new cases of gelatin allergy in Japanese children dropped.
Quantities and qualities of adjuvant and other vaccine ingredients injected into children changed dramatically between 1989 and 1994 in ‘mature markets’ for vaccines including the United States, United Kingdom, Canada, and Australia. During those years, at least five new vaccine formulations for the same bacteria, Haemophilus influenzae type b (Hib) were introduced within an expanded and intense vaccination schedule. Like the gelatin allergy that emerged from a changed schedule of pediatric injections, was there some mix of ingredients that included powerful aluminum additives in the new Western schedule that was sensitizing children to peanut? The fact that refined peanut oil was a documented vaccine ingredient in the past is a subject of concern equal to the potential of sensitization to body tissues or even of cross-reactivity between dietary peanut and homologous injected proteins. These cross-reactive proteins may include those in the Hib cellular membrane or legume oil in a popular brand of the vitamin K1 prophylaxis. Cross-reactivity explains why a person who is allergic to peanuts, legumes like soy and castor beans, may also react to nuts or citrus seeds, which belong to different plant families—their proteins have similar molecular weights and structures.
As ingredients changed, the number of shots increased for kids in their first eighteen months of life from ten to as many as twenty-nine. The increase meant inconvenience to parents who would have to make more trips to the doctor and discomfort to the children who would have to experience multiple injections. To overcome these obstacles to compliance with the new schedule, the vaccines for diphtheria, pertussis, and tetanus (DPT); polio (OPV); and H. influenzae b (Hib) were administered to children in a single visit with two injections and an oral polio dose starting around 1988. By 1994 starting in Canada, these five were rolled into a single needle. Few parents realize that by design immunization provokes both the desired immune response and allergy at the same time. These natural defenses are inseparable and the more potent the vaccine, the more powerful the two responses. This is an outcome of vaccination the medical community has understood at least since Charles Richet won the Nobel Prize (1913) for his research on anaphylaxis. Anaphylaxis, Richet observed, is one of three outcomes of vaccination.
Paul Offit, chief of Infectious Diseases at Children’s Hospital in Philadelphia in 2008, dismissed concerns that the vaccination schedule was overwhelming children. To Offit, this was just not good science. Other doctors disagreed. In respected medical journals such as The Journal of the American Medical Association and Allergy: European Journal of Allergy and Clinical Immunology, doctors expressed concern over the long-term effects of early vaccinations. Some doctors state that excessive vaccination is ineffective and dangerous.
But vaccination is a complex subject, and its role in the food-allergy epidemic is difficult to address because of the heated political, social, and economic implications. It is a subject doctors avoid. And so, despite the continuing intense attention given to the peanut allergy in children, an answer to its cause(s) has not yet been found. What has emerged, instead, is a robust economy of doctor fees, nut-free foods, ongoing medical research, and pharmaceutical sales. Peanut and other food allergies have become enormously profitable. It is so much so that one market analyst has suggested that an “autoimmune index” would be a great tool for investors. This index, tagged as “save the children and make money,” would monitor the profitability of pharmaceutical stocks relative to the continued rise in peanut allergy and other childhood epidemics.
Peanut allergy began as a mere idiosyncrasy after World War II. Today, its epidemic proportions help fuel a multibillion-dollar food-allergy industry.
Bio: Heather Fraser is a Canadian author, speaker, and natural health advocate and practitioner. She is the mother of a child who suffers from peanut allergies. Fraser lives in Toronto, Canada.