Guess Who’s Not Coming to Dinner – and Why

Mealtime has become a minefield, with allergy and avoidance for the main course and anaphylactic shock for afters. But this is a very recent development. When I was growing up in the 1950’s no one had food allergy, and we all shared the same food.

Dinner parties were simple affairs because no one in my parents’ wide and international circle of friends was allergic to peanuts, fish or beef. Nobody carried an EpiPen because they had not yet been invented – and were not needed, as anaphylactic shock was almost unknown. Anaphylactic reactions to bee stings (1) and heterologous serum injection (2) had been reported in the medical literature, but such responses to ordinary food were unheard of.

Fast forward 70 years, and at any dinner party today someone will be (or claim to be) allergic to something on the menu. Multiple menus are de rigeur.

We have become so alienated from what we eat, so concerned about its allergenicity, origins, ethics and calorie count and so fractured by social media that the simple communality of breaking bread is disappearing in post-industrial society. This is good for the food business, which can sell more ultra-processed ‘single-serve snackables’ (3), but bad for humanity.

How did we get so out of kilter?

In 2013, the CDC reported a 50% increase in food allergies in children during the 14 years between 1997 and 2011 (4). In 2020, FARE and Northwestern University found one in four Americans avoid foods containing common allergens (5). If you add those people who don’t have a food allergy but buy food for family members who do, almost half of all Americans (5) are now avoiding foods that, back in the 1950’s, were eaten and enjoyed by all.

The problem is that these figures are self-reporting, and include the fashionably allergic. When the data are chewed more thoroughly, many ‘allergies’ disappear. In one study of 40,443 US adults (6), 19% believed they were food allergic but only 10.8% appeared to have a genuine allergy. Other researchers found similar disparity, with self-reporting just over 10% and proven allergy rates around 3% (7-10).

Children are similarly (un)-affected. About 20% are reported by their parents as having a food allergy (11) but after screening, only about 8% are found to have a genuine food allergy (12).

Part of the problem is the over-enthusiastic use of skin prick tests, which are taken as gospel by the alternative crowd but which have, clinically, a false positive rate as high as 85% (13, 14). Their false negative rate is probably less than 5% (15, 16), but many practitioners and most end-users fail to appreciate or utilize this information.

Notwithstanding, I believe there has been a real increase in food allergy. There have certainly been increases in other allergic conditions, from asthma through allergic conjunctivitis, rhinitis and dermatitis (ie 17-21). Coeliac disease, a gastro-intestinal autoimmune condition with an allergic component, is certainly increasing (22).

There is also good evidence for rising rates of eosinophilic gastrointestinal disease (EGID), which can be driven by food allergy (23). And there are plausible mechanistic explanations for the increase in both allergies and the auto-immune diseases.

1. The removal of 1-3, 1-6 beta glucans from the food chain would be expected to increase the risk of sub-clinical infection and to drive allergy, as it encourages increasing TH2:TH1 ratios (24-25). Conversely, supplementing with beta glucans damps allergy intensity (ie 26-27).
2. The oceans of plant oil poured into ultra-processed foods increase 6:3 ratios, chronic inflammatory stress and therefore the intensity of allergic reactions (28, 29). The parallel removal of polyphenols would be expected to have the same effects (30-32). Replacing these anti-inflammatory nutrients is protective (33-35).
3. The progressive removal of prebiotic fibers from the diet causes chronic inflammation in the walls of the gut (36, 37), damaging epithelial integrity; damage which may be exacerbated by modern food emulsifiers (38). This allows the entry of macromolecules into the body. These include pathogens, allergens, and foreign immunogenic antigens which then activate the autoimmune cascade (38, 40). Replacing the fibers protects against food allergy (ie 38-43), with the protection mediated by vitamin A (40).
4. Vitamin A depletion is now very common. Just over half of adults no longer achieve even the rather conservative EAR (44), and the near-universal burdens of chronic inflammatory stress and/or sub-clinical infection caused by the ultra-processed diet drag serum A levels down further (45-47).

The above mechanisms would largely explain why allergies and autoimmune diseases are increasing, particularly in developed nations where folks eat the ultra-processed, ultra-toxic diet (ie 22, 48, 52).

So there is a real problem, with real allergy. But the numbers of people incorrectly self-diagnosing with food allergy are staggering, and worth investigating in their own right. After all, they are self-diagnosing because in most cases they have symptoms.

One confounding problem is the dysbiosis that has become practically universal, due to the progressive removal of prebiotic fibers from the modern diet. The resulting chronic inflammation in the gut is a key characteristic of EGID, which presents with dysphagia, nausea and vomiting, heartburn, abdominal pain and diarrhoea.

If this sounds familiar, it might be because there is considerable overlap with the symptoms of food allergy – which include dysphagia, nausea and vomiting, heartburn, abdominal pain and diarrhoea. To complicate matters further, both EGID and allergy commonly occur in the same patient.

Tingling, itching or swelling in and around the mouth, hives and difficulty breathing are more accurate signs of allergy. Anyone with these symptoms, especially the respiratory ones, needs an EpiPen and antigen avoidance. The others mostly need to get over themselves, increase their intake of prebiotic fibers, omega 3 HUFA’s and polyphenols, and stop identifying as having special needs. They are merely collateral damage in the chemical warfare being waged by Big Phood against humanity.

We are hopelessly out-gunned. The food multinationals sell junk food that causes our health problems in the first place and then profit hugely from the public’s perception of unreality. They charge higher margins on gluten-free and all the other allergen-free and ‘clean’ products people think they need but which, in reality, are more likely to harm them (49).

Sadly, it doesn’t end there. This profitable but deranged dual strategy is likely to increase true allergy in the next generation via epigenetic and other routes (50, 51).

Meanwhile, Big Phood is busily exporting obesity, dysbiosis, dysnutrition, allergy and other problems to the developing world (50-52). This is a developing tragedy because children of East Asian or African descent appear to be at even higher risk of developing food allergy than Caucasian children (50-52). The frequency of food allergy in these groups is rising in parallel with their adoption of Western-style diets (52-55).

Big Pharma is in the game too. By over-selling antibiotics, antacids and laxatives (made necessary by our terrible diet) they contribute to dysbiosis. Their OTC arms, by over-marketing sanitisers and biocides, make matters worse again. Food, drug and supplement companies are still using TiO2 nano-particles in coloring for foods, pills and tablets. These exacerbate inflammation in the gut (56), especially when dysbiosis is co-present (57), and in other tissues also (58-60).

For those with EGID, cutting down on ultra-processed foods and whenever possible on medications will help many achieve better gut health. A blended prebiotic supplement is an invaluable second step, and combining these elements is often enough to restore normal gut function.

Genuine food allergy requires a different strategy, in terms of both prevention and treatment. Prevention is where we should start; allergy to food allergy and allergy in general is clearly largely preventable, as our recent history shows.

As many as 1 in 6 children today have asthma (61), which usually has an allergic component. British schools average 3 asthmatic children in every class (62). 1955 was very different. Those who have heard me lecture know that in my school of some 2000 pupils there was only one asthmatic, my classmate and friend Andrew G.

The 50’s diet contained relatively little ultra-processed food. It largely consisted of basic produce and therefore had low calorie density, high nutrient density, plenty of prebiotic and other fibres and trace amounts of 1-3, 1-6 beta glucans. With that nutritional configuration pets, pollen and house dust mites could only cause problems in a small number of individuals who carried genetic risk factors.

Conversely, today’s diet which is rich in ultra-processed food correlates substantially with both asthma and food allergy (52-55, 63, 64). Parents who want their children to have the best chance of growing up allergy free should return to the 1950’s, eschew ultra-processed foods and (re)-learn to cook with basic produce.

For anyone with an established and proven food allergy, avoiding foods known to contain trigger factors is often a necessary starting point. Switching to a pre-transitional diet will provide many further gains. Adding 1-3, 1-6 beta glucans, omega 3 HUFA’s stabilized with amphiphilic polyphenols, a blend of prebiotic fibers and vitamin A precursors such as alpha- and beta-carotene provides a final layer of defense.

To Zinzino clients: The Health Protocol is designed as a specific series of antidotes to the modern, post-transitional diet and for this reason is, amongst other things, TiO2-free.

Photo credit: foodbusiness.net

Next Week: Urinary urgency, and how to make it less urgent.

References

1. Müller U. Geschichte der Insektenstichallergie. Allergo J 2009;18:342-352.
2. Langerhans R. Tod durch Heilserum! Berl Wochenschr 1896;33:602.
3. Mintel ’19. Snacking Motivations and Attitudes – US – January 2019
4. Jackson KD, Howie LD, Akinbami LJ. Trends in Allergic Conditions Among Children: United States, 1997–2011. NCHS Data Brief 121, May 2013 https://www.cdc.gov/nchs/data/databriefs/db121.pdf
5. https://www.foodallergy.org/fare-consumer-journey-infographic
6. Gupta RS, Warren CM, Smith BM, Jiang J, Blumenstock JA, Davis MM, Schleimer RP, Nadeau KC. Prevalence and Severity of Food Allergies Among US Adults. JAMA Netw Open. 2019 Jan 4;2(1):e185630.
7. Boyce JA, Assa’ad A, Burks AW, Jones SM, Sampson HA, Wood RA, Plaut M, Cooper SF, Fenton MJ, Arshad SH, Bahna SL, Beck LA, Byrd-Bredbenner C, Camargo CA Jr., Eichenfield L, Furuta GT, Hanifin JM, Jones C, Kraft M, Levy BD, Lieberman P, Luccioli S, McCall KM, Schneider LC, Simon RA, Simons FE, Teach SJ, Yawn BP, Schwaninger JM. Guidelines for the diagnosis and management of food allergy in the United States: Report of the NIAID-sponsored expert panel.J Allergy Clin Immunol. 2010;126(6 Suppl):S1–S58.
8. Chafen JJ, Newberry SJ, Riedl MA, Bravata DM, Maglione M, Suttorp MJ, Sundaram V, Paige NM, Towfigh A, Hulley BJ, Shekelle PG. Diagnosing and managing common food allergies: A systematic review.2010;303(18):1848–1856.
9. Rona RJ, Keil T, Summers C, Gislason D, Zuidmeer L, Sodergren E, Sigurdardottir ST, Lindner T, Goldhahn K, Dahlstrom J, McBride D, Madsen C. The prevalence of food allergy: A meta-analysis. J Allergy Clin Immunol. 2007;120(3):638–646.
10. Zuidmeer L, Goldhahn K, Rona RJ, Gislason D, Madsen C, Summers C, Sodergren E, Dahlstrom J, Lindner T, Sigurdardottir ST, McBride D, Keil T. The prevalence of plant food allergies: A systematic review. J Allergy Clin Immunol. 2008;121(5):1210–1218. e1214.
11. Gupta RS, Springston EE, Smith B, Pongracic J, Holl JL, Warrier MR. Parent report of physician diagnosis in pediatric food allergy. J Allergy Clin Immunol. 2013b;131(1):150–156.
12. Gupta RS, Springston EE, Warrier MR, Smith B, Kumar R, Pongracic J, Holl JL. The prevalence, severity, and distribution of childhood food allergy in the United States.2011;128(1):e9–e17.
13. McGowan EC, Keet CA. Prevalence of self-reported food allergy in the National Health and Nutrition Examination Survey (NHANES) 2007-2010.J Allergy Clin Immunol. 2013;132(5):1216–1219.e5.
14. Verrill L, Bruns R, Luccioli S. Prevalence of self-reported food allergy in U.S. adults: 2001, 2006, and 2010. Allergy Asthma Proc. 2015;36(6):458–467.
15. Sicherer SH, Sampson HA. Food allergy.J Allergy Clin Immunol. 2010;125(2 suppl 2):S116–S125.
16. Scurlock AM, Lee LA, Burks AW. Food allergy in children.Immunol Allergy Clin North Am. 2005;25(2):369–388, vii-viii.
17. Lundbäck B, Backman H, Lötvall J, Rönmark E. Is asthma prevalence still increasing? Expert Rev Respir Med. 2016;10(1):39-51.
18. Rosario N, Bielory L. Epidemiology of allergic conjunctivitis. Curr Opin Allergy Clin Immunol. 2011;11(5):471–6.
19. Singh K, Axelrod S, Bielory L. The epidemiology of ocular and nasal allergy in the United States, 1988–1994. J Allergy Clin Immunol. 2010;126(4):778–83.
20. Brozek G, Lawson J, Szumilas D, Zejda J. Increasing prevalence of asthma, respiratory symptoms, and allergic diseases: four repeated surveys from 1993–2014. Respir Med. 2015;109(8):982–90.
21. Pelkonen MK, Notkola IK, Laatikainen TK, Jousilahti P. 30-year trends in asthma and the trends in relation to hospitalization and mortality. Respir Med. 2018 Sep;142:29-35.
22. Lionetti E et al. Celi Screen preliminary report. Presented at 6th World Congress of Paediatric Gastroenterology, Hepatology and Nutrition, Vienna 01-05 June 2021.
23. Pesek RD, Reed CC, Muir AB, Fulkerson PC, Menard-Katcher C, Falk GW, Kuhl J, Martin EK, Magier AZ, Ahmed F, Demarshall M, Gupta A, Gross J, Ashorobi T, Carpenter CL, Krischer JP, Gonsalves N, Spergel JM, Gupta SK, Furuta GT, Rothenberg ME, Dellon ES; Consortium of Eosinophilic Gastrointestinal Disease Researchers (CEGIR). Increasing Rates of Diagnosis, Substantial Co-Occurrence, and Variable Treatment Patterns of Eosinophilic Gastritis, Gastroenteritis, and Colitis Based on 10-Year Data Across a Multicenter Consortium. Am J Gastroenterol. 2019 Jun;114(6):984-994.
24. Chen Y, Dong L, Weng D, Liu F, Song L, Li C, Tang W, Chen J. 1,3-β-glucan affects the balance of Th1/Th2 cytokines by promoting secretion of anti-inflammatory cytokines in vitro. Mol Med Rep. 2013 Aug;8(2):708-12.
25. Burg AR, Quigley L, Jones AV, O’Connor GM, Boelte K, McVicar DW, Orr SJ. Orally administered β-glucan attenuates the Th2 response in a model of airway hypersensitivity. 2016 Jun 21;5(1):815.
26. Baran J, Allendorf DJ, Hong F, Ross GD. Oral beta-glucan adjuvant therapy converts nonprotective Th2 response to protective Th1 cell-mediated immune response in mammary tumor-bearing mice. Folia Histochem Cytobiol. 2007;45(2):107-14.
27. Kim IS, Lee SH, Kwon YM, Adhikari B, Kim JA, Yu DY, Kim GI, Lim JM, Kim SH, Lee SS, Moon YS, Choi IS, Cho KK. Oral Administration of β-Glucan and Lactobacillus plantarumAlleviates Atopic Dermatitis-Like Symptoms. J Microbiol Biotechnol. 2019 Nov 28;29(11):1693-1706.
28. Di-Nicolantonio JJ, O’Keefe JH. Omega-6 vegetable oils as a driver of coronary heart disease: the oxidized linoleic acid hypothesis. Open Heart. 2018 Sep 26;5(2):e000898.
29. Ahmed N, Barrow CJ, Suphioglu C. Exploring the Effects of Omega-3 and Omega-6 Fatty Acids on Allergy Using a HEK-Blue Cell Line. Int J Mol Sci. 2016 Feb 6;17(2):220.
30. Singh A, Holvoet S, Mercenier A. Dietary Polyphenols in the prevention and treatment of allergic diseases. Clin Exp Allergy (21001) 41:1346-59
31. Magrone T, Jirillo E. Influence of polyphenols on allergic immune reactions: mechanisms of action. Proc Nutr Soc. 2012 May;71(2):316-21.
32. Jurikova T, Mlcek J, Sochor J, Hegedusova A. Polyphenols and their Mechanism of Action in Allergic Immune Response. Glob J Allergy 2015. 1(2): 037-039.
33. Singh A, Holvoet S, Mercenier A. Dietary polyphenols in the prevention and treatment of allergic diseases. Clin Exp Allergy. 2011 Oct;41(10):1346-59.
34. Shakoor H, Feehan J, Apostolopoulos V, Platat C, Al Dhaheri AS, Ali HI, Ismail LC, Bosevski M, Stojanovska L. Immunomodulatory Effects of Dietary Polyphenols. 2021 Feb 25;13(3):728.
35. Brigham EP, Woo H, McCormack M, Rice J, Koehler K, Vulcain T, Wu T, Koch A, Sharma S, Kolahdooz F, Bose S, Hanson C, Romero K, Diette G, Hansel NN. Omega-3 and Omega-6 Intake Modifies Asthma Severity and Response to Indoor Air Pollution in Children. Am J Respir Crit Care Med. 2019 Jun 15;199(12):1478-1486.
36. Khoshbin K, Camilleri M. Effects of dietary components on intestinal permeability in health and disease.Am J Physiol Gastrointest Liver Physiol 2020;319:G589–G608.
37. Camilleri M. Human Intestinal Barrier: Effects of Stressors, Diet, Prebiotics, and Probiotics. Clin Transl Gastroenterol. 2021 Jan 25;12(1):e00308.: PMC7838004.
38. Lerner A, Matthias T. Changes in intestinal tight junction permeability associated with industrial food additives explain the rising incidence of autoimmune disease. Autoimmun Rev. 2015 Jun;14(6):479-89.
39. Pretorius R, Prescott SL, Palmer DJ. Taking a prebiotic approach to early immunomodulation for allergy prevention. Expert Rev Clin Immunol. 2018 Jan;14(1):43-51.
40. Tan J, McKenzie C, Vuillermin PJ, Goverse G, Vinuesa CG, Mebius RE, Macia L, Mackay CR. Dietary Fiber and Bacterial SCFA Enhance Oral Tolerance and Protect against Food Allergy through Diverse Cellular Pathways. Cell Rep. 2016 Jun 21;15(12):2809-24
41. Brosseau C, Selle A, Palmer DJ, Prescott SL, Barbarot S, Bodinier M. Prebiotics: Mechanisms and Preventive Effects in Allergy. 2019 Aug 8;11(8):1841.
42. Baxter NT, Schmidt AW, Venkataraman A, Kim KS, Waldron C, Schmidt TM. Dynamics of Human Gut Microbiota and Short-Chain Fatty Acids in Response to Dietary Interventions with Three Fermentable Fibers. 2019 Jan 29;10(1):e02566-18.
43. Bao R, Hesser LA, He Z, Zhou X, Nadeau KC, Nagler CR. Fecal microbiome and metabolome differ in healthy and food-allergic twins. J Clin Invest. 2021 Jan 19;131(2):e141935.
44. Fulgoni VL, 3rd, Keast DR, Bailey RL, Dwyer J. Foods, fortificants, and supplements: Where do Americans get their nutrients? J Nutr. 2011;141(10):1847-1854.
45. Ross AC. Vitamin A. In: Ross AC, Caballero B, Cousins RJ, Tucker KL, Ziegler TR, eds. Modern Nutrition in Health and Disease. 11^th Philadelphia: Lippincott Williams & Wilkins; 2014:260-277.
46. Tanumihardjo SA. Assessing vitamin A status: past, present and future. J Nutr. 2004;134(1):290S-293S.
47. Tanumihardjo SA, Russell RM, Stephensen CB, et al. Biomarkers of nutrition for development (BOND)-vitamin A review. J Nutr. 2016;146(9):1816S-1848S.
48. Dinse GE, Parks CG, Weinberg CR, Co CA, Wilkerson J, Zeldin DC, Chan EKL, Miller FW. Increasing Prevalence of Antinuclear Antibodies in the United States. Arthritis Rheumatol. 2020 Jun;72(6):1026-1035.
49. Vici G, Belli L, Biondi M, Polzonetti V. Gluten free diet and nutrient deficiencies: a review.Clin Nutr. 2016;35(6):1236–1241.
50. Baïz N, Just J, Chastang J, Forhan A, de Lauzon-Guillain B, Magnier AM, Annesi-Maesano I; EDEN Mother-Child Cohort Study Group. Maternal diet before and during pregnancy and risk of asthma and allergic rhinitis in children. Allergy Asthma Clin Immunol. 2019 Jun 22;15:40.
51. Gatford KL, Wooldridge AL, Kind KL, Bischof R, Clifton VL. Pre-birth origins of allergy and asthma. J Reprod Immunol. 2017 Sep;123:88-93.
52. Loh W, Tang MLK. The Epidemiology of Food Allergy in the Global Context. Int J Environ Res Public Health. 2018 Sep 18;15(9):2043.
53. Leung ASY, Wong GWK, Tang MLK.Food allergy in the developing world. J Allergy Clin Immunol. 2018 Jan; 141(1):76-78.e1.
54. Mahesh PA, Wong GW, Ogorodova L, Potts J, Leung TF, Fedorova O, Holla AD, Fernandez-Rivas M, Clare Mills EN, Kummeling I, Versteeg SA, van Ree R, Yazdanbaksh M, Burney P. Prevalence of food sensitization and probable food allergy among adults in India: The EuroPrevall INCO study. 2016;71:1010–1019.
55. Julia V, Macia L, Dombrowicz D. The impact of diet on asthma and allergic diseases.Nature Reviews Immunology. 2015;15:308–322.
56. Rinninella E, Cintoni M, Raoul P, Mora V, Gasbarrini A, Mele MC. Impact of Food Additive Titanium Dioxide on Gut Microbiota Composition, Microbiota-Associated Functions, and Gut Barrier: A Systematic Review of In Vivo Animal Studies. Int J Environ Res Public Health. 2021 Feb 19;18(4):2008.
57. Bianchi MG, Allegri M, Chiu M, Costa AL, Blosi M, Ortelli S, Bussolati O, Bergamaschi E. Lipopolysaccharide Adsorbed to the Bio-Corona of TiO₂Nanoparticles Powerfully Activates Selected Pro-inflammatory Transduction Pathways. Front Immunol. 2017 Aug 3;8:866.
58. Kim BG, Lee PH, Lee SH, Park MK, Jang AS. Effect of TiO₂ Nanoparticles on Inflammasome-Mediated Airway Inflammation and Responsiveness. Allergy Asthma Immunol Res. 2017 May;9(3):257-264.
59. Ihrie MD, Bonner JC. The Toxicology of Engineered Nanomaterials in Asthma. Curr Environ Health Rep. 2018 Mar;5(1):100-109.
60. Palmer BC, DeLouise LA. Morphology-dependent titanium dioxide nanoparticle-induced keratinocyte toxicity and exacerbation of allergic contact dermatitis. HSOA J Toxicol. 2020;4(1):019.
61. Simpson CR, Sheikh A. Trends in the epidemiology of asthma in England: a national study of 333,294 patients. J R Soc Med. 2010 Mar;103(3):98-106.
62. Essential Fact, stats and quotes relating to asthma. https://psnc.org.uk/services-commissioning/essential-facts-stats-and-quotes-relating-to-asthma/
63. Hancu A, Mihaltan F, Radulian G. Asthma and Ultra-Processed Food. Maedica (Bucur). 2019 Dec;14(4):402-407.
64. Melo B, Rezende L, Machado P, Gouvela N, Levy R. Ultra-processed products and asthma Associations of ultra-processed food and drink products with asthma and wheezing among Brazilian adolescents. Pediatr Allergy Immunol. 2018;5:504–511.