ABSORBING THE COSTS
INGREDIENTS: ALUMINUM, FOOD PROTEINS, AND MORE
Vaccination was the elephant in the room. Researchers glanced at it, knew it was there, but were reluctant to get too close. Only a handful of doctors through the late 1990s looked directly at pediatric injections and asked whether a reduction of common childhood diseases through a policy of mass vaccination (and other injections) was worth the price of a higher prevalence of allergy and other adverse outcomes.1
Vaccines are a complex blend of antigens, stabilizers, adjuvants, preservatives, antibacterials, antifungals, suspending fluids, gels, and more. While manufacturers, government, and doctors are not obliged to reveal the precise ingredients of vaccines, the CDC offered a limited list.2 The common childhood vaccine DtaP-IPV/Hib (Pentacel), for example, contains aluminum phosphate, bovine serum albumin, formaldehyde, glutaraldehyde, MRC-5 DNA, and cellular protein, neomycin, polymyxin b sulfate, polysorbate 80, 2-phenoxyethanol. MRC-5 (Medical Research Council 5) is a cell line developed in 1966 from lung tissue taken from a fourteen-week-old fetus aborted for psychiatric reason from a twenty-seven-year-old woman, and more. Bovine serum albumin (BSA) is blood protein from cattle. Neomycin is an antibiotic. Aluminum phosphate is part of an antigen sparing adjuvant.
Adjuvants, as already discussed, stimulate the immune system to respond to just a small amount of antigen. They reduce the cost of a vaccine and increase its efficacy measured in antibodies specific to the disease being addressed. However, they can be dangerous. The choice of adjuvant (or even whether to use one or not) in any vaccine by a maker or government reflects a compromise between immune stimulation and invariable side effects that would be produced in a percentage of consumers. One of the invariable and guaranteed side effects engendered by vaccine ingredients is the production of IgE antibodies.3 The more effective a vaccine is, the greater the risks of allergies and other adverse effects.4
The question about vaccination has never been whether there would be damage but rather how much and what kind in relation to the established vaccination goals. Risk management for the five remaining vaccine manufacturers in the United States was an ongoing concern as the millenium approached. While the FDA had statutory responsibility for licensing vaccines, it appeared to lack the resources to fully grasp all safety issues. In 2004, researchers identified the need for an independent safety risk assessment system.5 The system of post-licensure vaccine assessment was insufficient and hampered by perceived conflicts of interest.
Before 2000, doctors were beginning to admit that there was an uncomfortable unpredictability in combining different vaccine products in the same syringe.6 Doctors knew that iatrogenic conditions were being caused by vaccinations, and yet, without comparative data on unvaccinated children, officials were not compelled to reduce the pediatric schedule. In fact, it increased. The possibility of multiple vaccinations causing immune dysfunction was reviewed by the Institute of Medicine in 2002. The researchers admitted that they were unable to reach a satisfactory conclusion on the question. The primary obstacle to resolving the question was that they could not find research on an appropriate control group of unvaccinated children.7 And the IOM had no authority to conduct its own scientific study.
In 2000 at a meeting of American adjuvant experts fatefully dubbed “thimerosal 2,”8 doctors admitted that they did not know enough about the absorption, distribution, and excretion of an adjuvant’s aluminum from the body especially in infants. “Storage” of aluminum salts that can stimulate autoimmunity and allergy was a problem for some children, they agreed.9 Birth dose of aluminum, followed by regular doses of aluminum were excreted mostly by the kidneys although in a follow-up study, 4% of the aluminum was still present over three years later.10 One of the meeting’s speakers observed that somewhere in virtually every vaccinated child there remains a depot of the metal that the body does not want to release. Aluminum has an affinity for bone, kidney, brain, and muscle.11 The hugely provocative nature of aluminum in vaccines was an obvious problem to researchers in a 1978 study who observed that it resulted in a prolonged synthesis of specific IgE in animals: “It is hypothesized that the regular application of aluminium compound-containing vaccines on the entire population could be one of the factors leading to the observed increase of allergic diseases.”12
Another common vaccine ingredient is gelatin. Gelatin is made from collagen derived from bovine (beef) or porcine (pork) hide and bones. It can also be made from tuna skin.13 Starting in 1994, a rising prevalence of gelatin allergy in children startled doctors. Children were reacting to many foods that contained gelatin such as marshmallows, fruit gums, yogurt, and vitamin capsules.
A rare admission by Japanese doctors confirmed that there was a causal link between the outbreak of gelatin allergy and the gelatin contained in a new diphtheria-tetanus-acellular pertussis vaccine (DTaP).14 Japanese doctors acknowledged that an outbreak of gelatin allergy in children was indeed caused by pediatric vaccination. In 1994, changes to the vaccination schedule 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 it was given before the live virus MMR vaccine that also contained gelatin. A significant rise in anaphylactic reactions to the MMR vaccine given to children at two years of age peaked in 1995 and 1996 after which time vaccine makers removed gelatin from the DTaP. In Japan, discontinuation of gelatin in the DTaP, the MMR, and most other vaccines reduced the rising prevalence of anaphylaxis to the MMR vaccine in children.15 However, gelatin continued to be used in vaccines in the United States and other Western countries. Doctors admitted that these vaccines were also causing allergies to gelatin in children.16
It was perhaps more difficult to conceive of peanut allergy in the same light. The idea that hundreds of thousands of children since the late 1980s had been sensitized to peanut or a reasonable corollary to peanut by ingredients in one or more of the routine pediatric injections was an incredible idea. Doctors seemed surprised that peanut had been used as a solubilizing excipient for decades in oral and injected formulations. “Did You Know This Medicine Has Peanut Butter in It, Doctor?”17 the title of this 2007 medical journal article highlights the fact that prescribing doctors did not always know that food products were contained in pediatric medicines.
But the real clue is in the sudden rise in severe allergies to peanut, other foods and bee venom following the significant changes to routine pediatric injections. While contaminant proteins in injections have been proven to sensitize children to foods, it is equally possible that the effect of pediatric injections on the integrity or functioning of the GI system has also contributed to the rise of peanut allergy. No meaningful research has been done into the rise of allergy and the impact of the pediatric schedule on the gut—a system responsible for about 70% of immune function.
SLIPPERY LABELS BUT NO SMOKING GUN
As the peanut allergy epidemic grew, doctors and the government expressed concern regarding the allergenicity of refined peanut oil in processed foods and pharmaceuticals. They debated whether or not it should be labeled. Label reading had become something of a pastime for parents of food-allergic children. If any product listed peanut oil as an ingredient, refined or not, those parents would not purchase it. There were negative financial implications related to manufacturing with peanut oil.
At the same time, demand for the refined oil had increased in the manufacture of processed foods due to concerns over consumption of trans fats. Refined, bleached, and deodorized (RBD) peanut oil was used in fried products, baked goods, and as a flavor carrier.18 It was considered a healthy alternative to other oils.
But the oil had been shown to cause both sensitization and reactions in a small number of people.19 The most highly refined peanut oils contain trace levels of intact proteins, up to 0.2–2.2 µg/ml.20 Lower-quality refined peanut oils could contain 3–6 µg/ml of protein. Thus, in 2004, the European Food Safety Authority (EFSA) investigated the safety of the oil and concluded that “fully refined peanut oil and fat” in foodstuffs could indeed cause allergic reactions in peanut-allergic individuals.21 The EFSA established a guideline that peanut oil must appear on food labels whether the oil is crude or refined.
In contrast, the WHO Codex Alimentarius Committee on Food Labeling in 2000 had expressed similar concerns but did not render a conclusion: refined peanut and soybean oils in foodstuffs did not necessarily need to be labeled.22 While this too was a guideline only, the fact that it was laid down by a panel of experts from around the world implied that it was reliable information. Laws would be made based on such on-the-fence guidelines.
The US FDA also acknowledged the presence of trace peanut proteins in the refined oil. However, they chose to grant the oil GRAS (generally recognized as safe) status since they believed no reactions had occurred from its consumption.23 In the United States, it was not and is not mandatory to label refined peanut or soybean oil in foodstuffs.
But what of the peanut oil used in injectable drugs? Where refined peanut or soybean oil appeared as excipients in parenteral drugs used in Europe, the labeling of these products as of 2001 was required on package leaflets. It was expected that manufacturers should warn users that if one was allergic to peanuts, one should not use this medicinal product.24 These guidelines were produced by the Committee for Medicinal Products for Human Use (CHMP) at the European Medicines Agency (EMEA). The EMEA helps formulate vaccine package insert statements. Again, these were guidelines with an expectation of compliance and not laws. Deviations from the guidelines, according to the agency, may be allowed if justified on a case-by-case basis. However, in the case of refined peanut or soybean oil, an agency representative confirmed that the consequences of ignoring the labeling guidelines could be serious. Allergic reactions to injected peanut oil in sensitive individuals can occur, stated an EMEA representative: “Patients have a right to know this information, and it is also their right to have it presented to them in a clear, simple, and unambiguous manner.”25
In the United States, labeling the oil in injected drugs remained voluntary. However, the FDA indicated that inactive ingredients that present an increased risk of toxic effects should be noted in the contraindications, warning, or precautions sections of drug labels.26 In fact, this labeling option for these ingredients in the United States and Canada was supported by law. Trade secrets that include exact ingredients of pharmaceutical products are exempted under freedom of information legislation in the US, Canada and Britain.
The guidelines and the moral obligation to provide a full list of ingredients were in conflict with laws protecting trade secrets. Again, full disclosure of excipients that included adjuvants, food proteins, and potential side effects was not and continued not to be general practice in the United States or Canada. Thus, labeling became a matter of least legal exposure within carefully worded vaccine product monographs. Whether parents were offered and read the monographs or not was another matter. A search for granted vaccine patents will certainly reveal all manner of vegetable oils including peanut as an ingredient, that may or may not be used. But there are scores of patents that never make it to manufacturing. There is, again, no way for a parent to know precisely what is in a vaccine. To be clear, the author has found no evidence that peanut oil is used in any of the vaccines in the pediatric schedule.
HOMOLOGY OF PEANUT AND HAEMOPHILUS INFLUENZAE TYPE B
Further complicating the outcome of routine vaccination was the apparent homology of the proteins of H. influenzae b in the Hib vaccine and the proteins of peanut.
Homology simply refers to the similarity in the structure and the weight of protein molecules of different substances. Homology of molecules leads to cross-reactivity. This phenomenon explains why a person allergic to peanut proteins may also react to nuts, even though they are from different plant families. The protein molecules of peanuts and those of tree nuts are homologous.27
The success of any vaccine design is in part built around the molecular weight(s) of the antigen. For example, studies indicate that protein conjugates made with low molecular weight dextran (polysaccharide) were more “immunogenic” than those made with dextrans of higher molecular weight.28 In fact, molecules liable to bind more readily with blood serum are those with low molecular weight. Researchers have pointed to the low weight of drugs that must bind to carrier proteins in the body to elicit sensitization (less than 1,000 Da) whereas high molecular weight molecules (larger than 5,000 Da) can act as complete antigens and bind covalently on their own.29
It occurred to some researchers that Hib proteins, bound to their diphtheria or tetanus toxins or free floating and circulating in the blood stream, could result in an allergy to Hib. Once sensitized to these proteins, there would exist the potential for cross-reactivity to foods of homologous molecular weights: foods such as peanut.
The peanut protein Ara h 1 has a molecular weight of between 20 kDa and 63.5 kDa.30 A similar range exists for proteins of the Hib outer membrane—between 39 kDa31 and 98 kDa.32 While there is a potential for cross-reactivity between the Hib and peanut, there were no apparent formal studies on this relationship.
VACCINE ANTIGENS AS AN ADJUVANT IN CREATING PEANUT ALLERGY
A 1959 study that found mice inoculated with a killed pertussis vaccine easily became allergic to grass pollens. In other words, the vaccination created a life-threatening allergy to a substance in the environment.33 A similar study took place in the late summer of 1973. Mice vaccinated again with a killed pertussis vaccine became sensitized to ragweed pollen that happened to be in the air at the time.34 Subsequent intravenous injection of the mice with pollen extract resulted in an anaphylactic reaction. And in several peanut-allergy studies, mice were made allergic to peanuts by inhaling or eating the food mixed with a toxic bacterium.35
Thus, the antigens and other toxins used in the vaccines, including the Hib vaccine—diphtheria and tetanus—were also causes for concern. These antigens promoted allergies to the environment and foods consumed following vaccination or injection.
TOXICITY OF HIB-DPT IN CREATING ALLERGY
Anaphylaxis to the Hib vaccine itself, including tetanus and diphtheria toxins it contained, was surprisingly common. The natural bias of the infant immune system toward the Th2 response may have increased this allergic potential within an expanding and intense pediatric vaccination schedule.36 In fact, by 2000, anaphylaxis following vaccination had notably increased. Doctors admitted that this increase had “complicated” what used to be a routine procedure.37
Margie Profet elucidated the purpose of allergy in the vaccination event—whether the serum sickness of the early twentieth century, postwar penicillin allergy, or the massive rise in food allergy in children since 1990, the purpose of allergy is to protect the body against acute toxicity.38
Already it was well known that toxins from tetanus and diphtheria bacteria in the conjugate Hib vaccine frequently produced high levels of IgE and anaphylaxis in children.39 Indeed, bacterial toxins were well-known adjuvants. It was possible, again, that these toxins, which adjuvanted the Hib or other ingredients in the combined vaccines, also enhanced the risk of allergic sensitization to foods in the diet or food proteins in the vaccine.
A 1999 study hammered home this potential. It was found that pertussis bacteria had the ability to induce intestinal hypersensitivity and to prolong sensitization to foods in a mouse model. A mouse injected with ovalbumin (egg) showed IgE in jejunal segments that disappeared by fourteen days. However, pertussis toxin with ovalbumin resulted in long-lasting sensitization present eight months after primary immunization. Bacteria when administered with a food protein resulted in long-term sensitization to the food and the antigen and altered intestinal immune function.40
In fact, medical literature was replete with examples of “how to” make an animal anaphylactic to foods by injecting it with toxic pathogens and peanut proteins. For example, mice were made anaphylactic to peanut through injections of heat-killed listeria and peanut,41 a “cocktail” of measles vaccine and peanut,42 and mycobacteria and peanut.43
But when both Hib and its toxic conjugates were combined with a highly stimulating DPT vaccine, the immune response was even more pronounced. The Hib polysaccharide in a combination vaccine with DPT resulted in a more than twentyfold increase in antibody levels over the Hib alone.44 This overstimulation of the immune system tipped the scales too far in favor of iatrogenic conditions including allergy.
Again the challenge in vaccine research was to gain potency while minimizing toxicity.45 Many doctors saw toxicity and allergenicity as an acceptable compromise in the use of vaccine adjuvants. This compromise, for some doctors, was an “accepted principle in the search for adjuvants suitable for use in human vaccines because one of their functions is to stimulate antigen presenting cells.”46 Doctors seemed unaware, however, that the risk-benefit ratio had shifted.
The countries in which the peanut allergy first emerged were those that first paired the Hib with the DPT vaccine. In 1997, Hib was not used in Russia, India, China, the Philippines, Romania, Korea, Iran, Singapore, and other countries where peanut allergy was virtually unknown at that time.
Singapore provided a poignant illustration of the impact of Hib-DPT combination when it was first introduced after 2001. In this country where full immunization of children was enforced by fine and imprisonment, Hib was optional, available for a fee. Since Hib was uncommon in Singaporean children, doctors suggested that the universal Hib vaccination program was not needed.47 And yet in a surprising turn of events, many Singaporean parents had actually chosen and preferred to vaccinate with the convenient and combined acellular-pertussis-inactivated polio-Hib vaccine (DPTa-IPV/Hib).48
This combination had been approved for use in Singapore after 2001. At that time, sensitivity through skin prick tests to peanut showed that the allergy existed in Singapore, but there were no reports of actual reactivity.49 By 2007, a three-year study revealed a “worrying trend” of peanut reactivity in Asian children living in Singapore (identifying with Chinese, Malay, Indian, and Eurasian ethnic groups).50 Researchers there underscored the importance of examining environmental factors in this development, but lack of exposure to peanuts was not one of them.
And doctors in Africa were puzzled by the high levels of IgE to peanut in children living in Ghana. Children there had received the five-in-one shot containing DPT and Hib starting in 1992. In 2000, the Global Alliance for Vaccines and Immunization (GAVI) set a goal to fully vaccinate children under the age of one by 2010 in that country.51 The hyporeactivity of the children was explained by the problematic prevalence of helminths. These parasitic worms depressed immune system reactivity. By 2011, however, 2.5% of children were allergic and reacting to peanut.
But reactions to peanut were virtually nonexistent in Indonesia and seemingly rare in western Siberia, Russia.52 As of 2005, children were not vaccinated for Hib in Russia.53 It was set to be introduced after 2010. And as of 2010, a probe study for future use of the Hib vaccine was being conducted in Indonesia.54
And in India, where peanut allergy was also not reported, doctors did not vaccinate for Hib. However, a proposal to introduce the vaccine in a pentavalent vaccine was made in 2008. Its proponents claimed it had become cost effective to do so.55 A sharp rise in the prevalence of peanut allergy might then be expected to occur in India and other countries where a combination vaccine includes the Hib vaccine and there are high coverage rates.
THE AUSTRALIAN EXAMPLE
The history of changes to the pediatric schedules in Tasmania and the Australian Capital Territory provided yet another provocative illustration of how and when peanut allergy emerged.
In a 2001 study, none of the 456 Tasmanian children aged seven to eight years reacted to a peanut skin prick test.56 By 2009, one in ninety children or 1.11%57 was allergic to peanuts. Changes in the vaccination schedule and the increased rate of children vaccinated in Tasmania correlated to this development.
In 1997, Tasmanian children were the least likely to be vaccinated at 27% of children according to the Australian Bureau of Statistics.58 Vaccination rates were dramatically low and declining on this island of about five hundred thousand people. In 1998, only 21% of children were vaccinated by their first year.59
In 1998, the Australian government established a General Practice Immunization Initiative that intensified the pediatric schedule and national coverage for preschool children, including those in Tasmania. The goal was to have over 90% of the children vaccinated. In 2001, the Australian government implemented their strategy60 and surpassed their goal by vaccinating 94% of Tasmanian children by age one. Tasmania became the highest vaccinated population in the country.61 By 2009, 1.11% of Tasmanian children were allergic to peanuts.
In contrast to the sudden growth of the allergy in Tasmanian, peanut allergy in children living in the Australian Capital Territory (ACT)62 grew steadily. By 1995, 0.5% of ACT children were peanut allergic.63 By 2001, 0.71% of ACT children were allergic, and by 2009 2% of “school entrant” ACT children were confirmed as peanut allergic.64 Children living in this national political center were the most likely to be fully immunized at 48% in 199565 according to the Australian Bureau of Statistics. Changes to the pediatric schedule of ACT were similar to but made less rapidly than those in the United States and the United Kingdom. The changes to the schedules for ACT and Tasmania were, of course, the same. But again, the primary difference between Tasmanian children and those living in ACT was vast differences in rate of vaccination. Government programs attempted to harmonize this rate in 2001.
THE VITAMIN K1 PROPHYLAXIS
Most peanut-allergic patients also have IgE antibodies against other legume proteins, including soybean and also oil seed proteins such as castor. However, “fewer than 15% of such patients react to other members of the legume family.”66 As suggested in the broken-skin hypothesis, soybean sensitization can lead to peanut sensitization through subsequent environmental exposure to peanut but with reactivity only to the peanut.
As discussed in chapter 5, since the mid-1980s the United States, the United Kingdom, Canada, Australia, and many other Western countries have routinely administered a prophylactic injection of a vitamin K1 to virtually all newborn babies. The use of vitamin K as of 2002 was not consistent in China, by contrast.67 The purpose of this prophylactic is to help prevent hemorrhagic disease of the newborn (HDN) also known as vitamin K–deficiency bleeding (VKDB) (K for koagulation). This injection has commonly contained castor seed oil.
The administration of an oral vitamin K1 formula began in many Western countries during the 1950s and ’60s. However, there were side effects. This oral dose was suspected of causing hemolysis (destruction of red blood cells). This problem was addressed by the introduction of an intramuscular or subcutaneous vitamin K1 (phytomenadione) injection that appeared to reduce the prevalence of hemolysis. However, routine use of this product did not begin until the mid-1980s following several reported cases of HDN in Britain.
The injectable vitamin K1 (phytomenadione) prophylaxis known as Konakion by Roche also contained Cremophor EL, a polyethoxylated castor oil. Seven hundred twenty-eight million children were injected with Konakion or Konakion MM between 1974–95, 95% with Konakion.68 Aquamephyton by Merck is a synthetic petrochemical derived from 2-methyl 1,4-naptha-quinone also in a polyethoxylated castor seed oil base. In the studies, Konakion was shown to induce anaphylaxis and was linked to a rise in leukemia.69 Konakion MM that replaced the ubiquitous Konakion in 2006 was made with lecithin E322 derived from soybean and egg.
While the food products used in these pharmaceuticals were refined to reduce the sensitizing proteins in them, it was and continues to be impossible to remove them all. And it is well known that antibodies to castor seed bind to proteins of other oilseed plants such as peanut and soy. A 1987 study in Plant Physiology confirmed that antibody to the castor bean glyoxysomal lipase (62 kDa) also binds to a 62 kDa protein in extracts from peanut.70
The injected ingredients of the vitamin K1 shot remain as a depot71 in the child for an extended period of time. This depot is metabolized gradually, the ingredients released into the body over the course of a few months. Little is known about the fate of the ingredients, but this metabolizing process overlaps with the vaccination schedule. When the child receives his first vaccinations at birth (Hep) and/or at two months of age (DPaT-IPV Hib), the vitamin K ingredients that include seed or legume proteins are still being released.
There was a real potential that resulting IgE to castor or soy could cross-sensitize a child to similar dietary proteins such as peanut and nuts. Adding weight to this potential is the presence of aluminum in some of the vitamin K brands.72 Aluminum is a well-known IgE stimulating adjuvant, 4% of that injected also remains indefinitely in the body.
IDIOSYNCRASIES: THE ABILITY TO DETOXIFY
But if the schedule of pediatric injections was somehow sensitizing children to peanut or homologous proteins, why were all children not allergic? Why, even in the same family, was one vaccinated child peanut allergic and another one was not?
Allergy is designed to defend against toxins that escape general detoxification. This being true, the potential for allergic sensitization to drugs and the ability to detoxify those drugs are inversely related, suggested Profet.73 The ability of peanut-allergic children to eliminate toxins, including those from the pediatric injections, would have been challenged at the time they were administered and afterwards.
Bock pointed to four catastrophic changes that have contributed to the rise of allergy as well as asthma, autism, and ADHD: toxins have proliferated, nutrition has deteriorated, vaccinations have increased, and children’s abilities to detoxify have dwindled. Methylation and sulfation, two important detoxification processes responsible for removing mercury and other toxins, have been damaged, suggested Bock.74
Children with severe allergy exhibit an immune system overload75 caused by antibiotic overuse, fungal overgrowth, overactivitiy of the Th2 cells, childhood vaccinations and injections, and more. The fungal infection that began in the gut was made worse by poor eating habits and deficiencies in nutrition, probiotics, essential fatty acids, stomach acid, and digestive enzymes. Further challenging the child was maternal health. Fungal infection was passed to unborn children. Birth by cesarean that delayed the introduction of healthy digestive flora would only have exacerbated the condition.
Gender also played an enormous role in who developed the peanut allergy. The allergy appeared more often in boys than girls—the ratio greater than 2:1.76 A male predominance of peanut and tree nut allergy was reported in children younger than eighteen years—1.7% versus 0.7% males to females.77
While there was no clear explanation for this disparity, a parallel phenomenon had occurred in the prevalence of autism where boys were affected more than girls in a 4:1 ratio. This gender gap was as high as 10:1 for Asperger’s syndrome. In 1964, Bernard Rimland observed that boys tended to be more vulnerable to “organic damage” than girls whether through hereditary disease, acquired infection, or other conditions.
The rate of autism and peanut allergy in children increased within the same window of time starting around 1990 with a concomitant sex ratio difference. The rate of autism in the United States was believed to be one in one thousand in 1970.78 In 2009, it was more than one in one hundred children in the United States by 2014 this number was believed to be 1 in 68 children with 1 in 25 boys being affected. Peanut allergy had a small but growing profile prior to 1990. In 2008, an estimated 1.4% of US children were allergic to peanuts. And 2 years later, this number had jumped to 2% (see Appendix).
And so, children with an extant immune overload caused by various deficiencies and impaired detoxification processes responded adversely to the new and intense schedule of injections launched in the late 1980s and early 1990s. It was a final straw. And within this scenario it is possible that all the four A conditions may, in fact, exist to some degree in every child who has reacted adversely to vaccination. For example, the child with food anaphylaxis also has a “touch” of ADHD and struggles with fine motor skills; the child on the autism spectrum has a food intolerance and often anaphylaxis; the child with ADHD has food intolerance and a touch of asthma but only when he gets a cold—in short, although perhaps undetected one of the As may not exist without the presence of the others in a tragically rounded dissonance to a variety of substances inside and outside of the body. The four As are not parallel phenomena but may coexist within an umbrella condition precipitated by vaccination.
Screening children before vaccination would have been a way to reduce risks of injection but was not common practice before the terrific increase in allergies that has occurred. Even with the few questions posed to parents prior to vaccination, no inquiry was made into the child’s sulfation and methylation processes, kidney health, mitochondrial function, or whether mother and child had fungal infections.
A vetting process based on idiosyncrasy was antithetical to the aims of mass and routine vaccination. A thorough screening would also challenge the cost effectiveness of vaccination. Vaccination was alleged to save money otherwise lost should working parents have to stay home to care for their sick children. This affected the national economy. And if many children were found to be at high risk of adverse reaction, they would have to be exempted from these injections. How would society manage this scenario?
Conversely, what was the financial cost of peanut allergy to society? Since the parents and allergic children absorbed the damage, there was little or no financial burden on government or society although it challenged the peanut industry—that appeared to fight back with a genetically modified and impossibly “hypoallergenic” peanut or helping fund a study offering an unsteady conclusion that we might need to eat more peanuts to help prevent allergy. Peanut-allergy families coped through avoidance strategies, and school communities modified their behavior to accommodate the growing problem. Alternatively, revenues were being generated through peanut- and other food–allergic children in the United States—almost six million children in 2008 but that number probably being much higher and with a bullet—fueled a burgeoning food allergy industry through the purchase of drugs and free-from foods.