Not to be confused with an intolerance or food sensitivity, the presence of a food allergy means there was a glitch in the system. Somewhere, somehow, a simple food protein makes its way into our blood stream and stimulates the production of protein-specific Immunoglobulin Epsilon antibodies, a.k.a. IgE antibodies. It is not fully understood how this mechanism called “sensitization” works, and why for example, one person may mount a response to one protein, but not other protein. Or why some people are sensitized to certain foods, and others are free to eat them. When a person is sensitized to an allergen, the allergen-specific IgE antibodies travel throughout the body and attach to mast cells, and wait for the allergen to return. The next time the allergen makes its way in through the mouth, or lungs, or touches the skin, the immune system kicks into gear and releases histamine, which is the allergic reaction we all dread: itching, scratching, sneezing, swelling, vomiting. Blood pressure lowers, airways tighten, which leads to anaphylaxis.
Normally, food proteins that we consume stimulate IgG antibodies (memory antibodies, because like a good door man, they remember the food) and something called “oral tolerance” develops with frequent grazing of those foods. IgG antibodies are a good thing, for they suppress the immune system from making IgE antibodies toward those foods. This is why we aren’t allergic to everything, and why someone with an IgE-mediated allergy can eat other allergens, just not “their” allergen.
So what is the Deal with Food Allergies?
Once just a phenomenon, food allergies that cause anaphylaxis have been increasing steadily every year all over the world, it is officially a global epidemic. Every scientist and researcher agree the cause for this rise is both genetic and environmental. Genetics by themselves don’t cause epidemics. Because allergies show up in the first few years of life, this is where more research is needed. It is now estimated that 8% of kids have a food allergy, but in some countries like Australia, it is estimated to be closer to 10%. Contrary to what you may think, the increase is not the result of better diagnostics or overly zealous parents–plain and simply, more and more kids are developing severe allergies.
7. Food Allergies are a Global Epidemic
The hygiene hypothesis just doesn’t work when you consider that all countries are being burdened by food allergies. We noted the trends first in the United States, when food allergy hospital admissions for children under 18 went from 2,615 in 1998-2000 to nearly 10,000 by 2004-2006. That’s a threefold increase in less than a decade. From 1997 to 2011 food allergies increased by 50% in the United States alone. Australia experienced a 350% increase in hospital admissions for food-related anaphylaxis episodes between 1994 and 2005, mostly in the 0–4 age group. While it’s curious that children born outside of the United States have half the prevalence of allergic disease–including asthma, eczema and food allergies–than children born in the United States. If a foreign born child lives in the United States for more than 10 years their incidence of allergic disease is three times that of a child who lives in the US for less than two years. But confirmed food allergies have been cropping up and exponentially growing all over the world in the last decade. Morocco, Nigeria, Ghana, Korea, Chile, Singapore all document growing food allergies. Look at it this way, the EpiPen went from $200 million a year in revenue in 2007 to $1 billion a year in 2015. Not too bad for a product that contains $1 worth of the hormone epinephrine. Well the question is of course–what do all these countries have in common? Besides just being a market for EpiPen sales.
6. Natural Infection Protects Against Allergies
Right after the varicella vaccine started unrolling out into pediatric vaccine schedules (licensed in 1995), a group of medical researchers wanted to assess the allergic tendency of kids who contracted wild chickenpox vs. kids who got the vaccine. They compared two groups of kids (ages 1-18) who either caught wild chickenpox before age 8, or who got the vaccine, and what they observed was a decrease in overall atopic disorders–like asthma, allergic rhinoconjunctivitis, atopic dermatitis and decreased total serum IgE levels–for the kids that caught wild chickenpox. Puzzling to me, including all birth years, they found an overall increase of food allergies in the wild chicken pox group. Stratifying by year of birth, however, offered the information I was missing. Kids born before 2002, who caught wild chickenpox had a lower rate of food allergy than the children born after 2002. For these people, year of birth offers more protection than the natural infection. What happened around 2000? Well in 1998 folic acid fortified foods became a mandatory law. Also, a slurry of new vaccines were added to the pediatric schedule during that time: rotavirus added in 1998, hepatitis A in 2000, pneumococcal in 2001 and influenza in 2002.
Chickenpox isn’t alone: This study found natural measles infection was inversely associated with “any allergic symptom” and “any diagnosis of allergy by a physician.” As for pertussis, this study found higher incidence of atopic disorders only in the vaccinated kids who also contracted pertussis infection, despite their vaccination status. These kids had higher rates of asthma (2.24 times higher than pertussis non-vaccinated), hay fever (2.35 times) and food allergies (2.68 times).
5. There is More to the Meat Allergy Story
Allergy to red meat, also known as mammalian meat, is a very new thing. First described in 2007, there has since been confirmed cases all over the world of a severe anaphylactic food allergy to red meat they think is triggered by a tick bite. Researchers isolated the allergen present in both red meat and tick saliva: carbohydrate Alpha Gal. Curiously, we all have IgG antibodies to alpha gal (called anti-gal) circulating normally in our blood, which is why for example we can’t successfully put a pig heart in our body. IgG is a normal response to something that isn’t “self.” But for some people with sensitive immune systems, a bite from the Lone Star tick sends their immune system into IgE overproduction. Just eating red meat and being exposed to the a-gal epitope from gut bacteria does not signal IgE production, scientists noted. It’s the “bite” that allows the allergen to get under the skin, and the nearby lymph node alarms the immune system toward IgE production. But the story doesn’t end here: alpha-gal is one of the major allergens in gelatin, which is made from mammalian animals like cows and pigs. Scientists actually know that gelatin in vaccinations can trigger anti-gelatin IgE, and they published their finding nearly two decades ago in 2000. And yet the CDC is still scratching their heads as to why food allergies are rising? Gelatin (alpha-gal allergen) is an ingredient in vaccines against influenza; measles, mumps, and rubella (MMR); varicella; yellow fever; zoster; rabies; Japanese encephalitis; and diphtheria, tetanus, and pertussis (DTaP).
4. Babies are Not Born Allergic
While it is often thought that hereditary plays a role in allergic disease, it is widely agreed it is not the only factor. While identical twins have a 60% chance of sharing a peanut allergy, there is still quite a bit of wiggle room for the environment to take its hold. Even through the study of epigenetic changes (how our gene expression is influenced by outside or environmental factors without changing our DNA code), simple interventions or lack of interventions could switch on or off genes that take effect in our children, or our children’s children. For example, in 2008 these researchers fed folic acid to pregnant mice, and found that changes in their DNA methylation caused by folic acid (which is a methyl donor: Look up MTHFR polymorphism), promoted allergic airway disease that was inherited by the second generation of mice. In a nutshell, this is epigenetics.
Some studies find around 15% of babies have detectable levels of IgE at birth in the cord blood. The allergen-specific antibodies detected often matched specific IgE of the mother, and were found to dissipate by six months, not being predictive of future allergy. In other studies, no detectable levels of IgE-specific antibodies were found in the cord blood of babies who later developed peanut allergy.
After birth, there seems to be a lot of environmental interventions that do however have an impact on the development of food allergy. Diaper creams applied to an infant’s skin containing peanut oil (arachis oil) in the first six months of life accounted for 84 percent of children who were allergic to peanuts and 91 percent who had a positive peanut challenge test in this study.
Breastfeeding also has protective abilities over formula to prevent the onset of allergy. This study found that mothers who followed certain interventions of their lifestyle reduced their children’s allergic disease significantly over the mothers who followed no interventions. For example, breastfed babies has less total IgE than non-breastfed or partially breastfed babies. Some of the factors that increased allergic outcomes included: formula implementation begun in the first week of life; early weaning (< 4 months); feeding beef (< 6 months); early introduction of cow’s milk (< 6 months); and parental smoking in the presence of the babies and early day care admission (< 2 years of life).
3. A Diverse Gut Flora Is Important in Preventing Food Allergies
It is estimated that sixty percent of immune system cells live in the gut. The intestinal flora is integral to the development of a strong immune system. When a baby is born by cesarean verses vaginal birth they are exposed to a completely different microbiome. Instead of getting the vaginal and intestinal flora necessary for a developing immune system, they are picking up the bacteria of the skin. This can have lasting effects on their own establishment of gut flora, which is protective against food allergy and intestinal issues. It was found, that in mothers who were allergic, being born by c-section made that child 7 times more likely to have a perceived (not confirmed) allergy to eggs, fish and nuts than vaginal birth babies. There was a 4-fold increased risk of confirmed egg allergy in this group. Amazingly, it can take up to 6 months for a baby born by c-section to establish the same healthy gut flora of a baby born via vaginal birth at one day old.
Beyond mode of birth, other actions or choices in one’s life can have an impact on intestinal flora. This study found that there was more microflora diversity in infants who were breastfed, whose mothers were vegetarian and ate fermented foods, and practiced a holistic lifestyle that “restricted” the use of antibiotics, anti-pyretics (like Tylenol) and vaccinations. The children of families who practiced a more holistic lifestyle had just a little over half of the IgE antibodies (confirmed via skin-prick tests and blood tests) of children whose families did not follow that lifestyle, resulting in a lower prevalence of atopy in general.
Looking more closely at these Swedish Waldorf children, researchers gained a lot of invaluable information, but information we don’t hear about often: for example, the use of antibiotics during the first year of life was associated with increased risks of rhinoconjunctivitis, asthma, and atopic eczema. Early use of anti-pyretics was related to an increased risk of asthma and atopic eczema. Children who received the MMR vaccination had increased risk of rhiniconjunctivitis, whereas measles infection was associated with a lower risk of IgE-mediated eczema.
2. Antacid Medication Impairs Digestion Enough to Cause Food Allergy
It turns out the stomach needs acid to digest food properly. Who knew?! Pepsin (not to be confused with Pepsi Cola, but that’s where they got their name from) is an important enzyme (made of amino acids) that breaks down proteins in our food into smaller peptides. This is crucial to digestion. When researchers were studying the way antacids impair digestion in mice, they noticed that the group of mice who were given antacids (Zantac) along with Caviar proteins and parvalbumin, a fish allergen, they had significant levels of IgE, T-cell reactivity and elevated counts of gastrointestinal eosinophils and mast cells. Food allergy was proved in oral provocation tests and positive immediate-type skin reactivity. They found that the antacid medication impaired gastric digestion enough to develop IgE synthesis toward novel proteins.
Antacids are also in things like vaccines, which sounds to me like an awful place for antacids. Oral vaccines like Rotarix and RotaTeq, against the rotavirus, as well as DTaP (Infanrix), DTaP-Hep B-IPV (Pediarix), Td, Hepatitis A (Havrix), Hep A-Hep B (Twinrix), Tdap (Boostrix)–all contain antacids in them, like aluminum hydroxide, calcium carbonate and amino acids like glycine. Along with food proteins from the top eight allergens and antigens and adjuvants that disrupt and elicit an immune response, no one can rule out that vaccines aren’t contributing to immune system error fostering this food allergy epidemic.
1. Food Proteins Through the Skin Cause Food Allergies
It shouldn’t be a paradigm shattering revelation that food proteins can cause allergic sensitization without having to be ingested. We are exposed to all sorts of food proteins or allergens in our every day products, well, every day. Things like diaper creams, shampoos, lotions, sunscreens, nipple creams, medications, vitamins, vaccines–all contain allergens.
In 2004, medical researchers wanted to see if epicutaneous (meaning on the skin with a shallow prick) exposure to food protein through the skin may interfere with oral tolerance and promote food allergies. The researchers found that the mice with the epicutaneous exposure to peanut protein (without the aid of an adjuvant) induced a potent Th2-type immunity with high levels of IL-4 and IgE, which prevented oral tolerance, or got rid of any oral tolerance that the mice had developed. Clearly, rubbing a cream or medicine on eczema with potentially allergenic proteins should be thoroughly researched.
Ever wonder why only 8 foods make up 90% of the world’s main allergens? These eight foods–eggs, milk, peanuts, tree nuts, fish, shellfish, wheat and soy–are most often the culprits behind allergic reactions. But what makes them the bad guys? In addition to these things being staple parts of many people’s diets, they may very well be in your baby’s diaper cream or your baby’s first round of vaccines.
The food proteins themselves are not intrinsically more allergenic. For example, the mice in this study had no discernible allergic response from being exposed with an adjuvant to wheat, soybeans, coffee, carrots, and white potatoes. Whereas, they reacted much more strongly to peanuts, almonds, hazelnuts, sweet potatoes, cherries, and spinach. Researchers noted that the mice had stronger reactions to almonds and spinach than peanuts.
Food allergens masquerade as many names and as ingredients in many every day products. Some things, like highly refined peanut oil is on the “Generally Recognized as Safe” list and does not need to be listed as an ingredient in products. Some people think only proteins cause food allergies, but refined peanut oil is high in oleic acid, which incidentally, is an acid found in vaccines under the name Polysorbate 80. How do we know that oleic acid is not contributing to food allergies? Or other amino acids like glycine? Could the oral vaccines against rotavirus be damaging the intestinal microbiome of tiny two-month old infants, who really need all the immune system protection of that flora. As Heather Fraser pointed out in her book “The Peanut Allergy Epidemic”, in 70% of infants who react to peanuts, it represents their first known exposure. Something is happening from birth to that first reaction. Whether these allergens are in children’s vaccines, medications, formulas, food, lotions or diaper creams–we need to collectively get to the root of what is transforming babies and children’s immune systems, and enabling them to turn a novel food protein into an allergen.