Why are cases of food allergies in developed countries on the rise?

Abstract

Allergic diseases have increased by over 50% in the last two decades. To raise awareness, education to children about their management and prevention is urgently needed. This is of rising importance as the number of people dying from food allergies, anaphylaxis and allergic asthma continues to rise at a shocking rate. In case this happens to you, contact a personal injury lawyer because you might be entitled for a compensation.

This report discusses the evidence highlighting reasons responsible for accelerating the allergy epidemic, including nutrition, the Hygiene Hypothesis, behavioural changes and genetics. Described are simple food allergies, sensitisation, tolerance, and anaphylaxis. Future directions to prevent further growth of the number of allergic patients are briefly mentioned and comparisons of allergic inflammation to the COVID-19 pandemic have been outlined.

Introduction

Cases of allergic diseases have shown a clear acceleration over the last two decades, with increasing evidence drawing attention to reasons responsible for accelerating the allergy epidemic ^[1][2]. In 2016, anaphylaxis killed a 15-year-old, who had consumed a baguette lacking allergy warnings on the packaging ^[3]. Despite similar cases noted previously in the media amidst many companies, the Department for Health have only now added allergy warnings to food labels ^[4] (Natasha’s Law). In late 2019 there was also a push to form Owen’s Law to ensure restaurants to clearly label allergenic foods in meals ^[5].

Food allergies are medical conditions accounting for emergency room admissions every 3 minutes ^[6]. Around 15 million Americans and 17 million Europeans suffer from allergies ^[1], while in Western countries 0.003% annually get bacterial meningitis ^[7]. The late Professor William Frankland pioneered research of seasonal allergies ^[8] , but despite 100 years of research and the huge numbers affected, allergy related research still lacks the acknowledgement it deserves. The National Health Service (NHS) states that “for reasons unclear, rates of food allergies have risen sharply in the last 20 years” ^[9] ,and much research over the past decade has investigated factors causing this escalation, outlined herewith.

The Extent of This Issue

Many professionals believe allergies are increasing globally ^[10][11][12]. Allergies, the most common chronic disease in Europe, affect more than 20% of the United Kingdom (UK) population ^[13]. The Centres for Disease Control & Prevention reported from 1997-2008, peanut/tree nut allergies tripled in US children. In a US nationwide, cross-sectional telephone survey it was found the prevalence of peanut/tree nut allergy in children was 0.6% (1997), 1.2% (2002), 2.1% (2008) ^[24].

Hospital records provide strong evidence; there was a 615% increase in the rate of hospital admissions in the UK for anaphylaxis from 1992-2012 ^[13], highlighting the rise of pressure on the NHS.

Allergies can cause disruption to daily tasks like sleeping, eating out and socialising ^[15]. Studies show children with food allergies are more likely to be bullied ^[6], further leading to a negative impact on a child’s emotional and physical health ^[15]. Dr Rebecca Knibb, health psychologist, found having a food allergy causes greater distress and 40% of children and teens use avoidance strategies, avoiding events where food is present ^[16].

There is a large economic impact for those living with or caring for someone with a food allergy, especially without universal healthcare systems. It costs US families $25 billion annually ^[6], ($4184 per child per year) including medical costs, special food and absence from work ^[17]. Consequently, there are adverse effects on the financial stability of families and the welfare of individuals.

Another issue, highlighted by the Royal College of Physicians, is the “gulf” between the need for advice and treatment, and services available, partially fuelled by the lack of training in this field and a struggling NHS budget ^[18]. Further upskilling of the workforce and students, especially at degree level, is imperative to raise awareness.

Science and Mechanisms

In 1906, Clemens-von-Pirquet created the term “allergy” for symptoms of hypersensitivity disorders in the body when it’s exposed to certain allergens, before overreacting from adaptive immunity ^{[19] [20] [21]}. Food allergy is an antigen-specific immunologic disease ^[22]. An antigen is a molecule that can trigger an immune response if foreign to the body. Undigested proteins travel the gut by the mucosal barrier of the gastrointestinal tract ^[23]. Especially in weaning infants, increased permeability of the intestine raises the chance of allergens crossing epithelial borders (figure 1) ^[24]. Non-self-antigens initiate acute (rapid) or chronic (delayed) immune responses (allergic reactions) ^[24]. The rapid immune response is IgE mediated and delayed immune response is Non-IgE mediated food allergy.

In the first category, sensitised subjects produce inflammation after exposure ^[19] (protective response) ^[24] according to the Th1/Th2 hypothesis. T lymphocytes (a type of white blood cell) can be T helper (Th) cells, regulating the allergic response ^[26]. Th2 cells (another category of Th cells) promote immunity, regulating antibody production to fight extracellular organisms or food proteins ^[26]. An antibody is a protein that can help destroy the appropriate antigen. They produce cytokines, soluble mediators ^[26], IL-4, IL-5, IL-6, IL-13 contributing to Immunoglobulin (IgE)^[27] production – a type of antibody ^[21] made by B cells (also another type of white blood cell) (see figure 1) ^[19]. IgE destroys the allergen, producing chemicals, including histamine ^[22]. After a sudden acute reaction, the specific antibodies created remain as memory cells, ready for the next allergen exposure ^[9]. If the same protein is eaten again it will trigger the same rapid response ^[28]. Persistent allergen exposure causes chronic allergic inflammation development (allergic disorders); the down-regulatory mechanisms of Th1 cells, producing tolerant mediators IL-10 and IFN-Y ^[19], are imbalanced by inflammatory factors (see figure 3) ^[21]. In the second category, there are Non-IgE mediated food allergies, but it is difficult to diagnose as symptoms appear much later and are delayed in their presentation.

[32] Figure 1 – Diagram showing the difference of T-cell independent activated and T-cell dependent activation of the allergic response. Courtesy of E. Crompton MRes thesis (2019). 

Chemicals released during allergic responses cause specific symptoms: mouth and throat itchiness, urticarial, angioedema ^[21] and diarrhoea ^[33]. Severe reactions harm the skin (flushing), the respiratory tract (inability to breathe), gastrointestinal tract (diarrhoea/vomiting/blood in faeces) and cardiovascular system (palpitations/drop in blood pressure) ^[34]. Over 40% of children with food allergies have experienced ^[6] the life-threatening ^[35] condition of anaphylaxis. This rapid response to allergens impairs breathing and causes sharp drops in blood-pressure, affecting heart rate ^[34] due to histamine tightening muscles of the airway and walls of blood vessels. This leads to cardiac-arrest ^[34]. Over 170 foods are known to cause an allergic reaction ^[36]. Common triggers include cow’s milk protein, eggs, peanuts, tree nuts and shellfish ^[21]. For treatment, antihistamine relieves rapid symptoms ^[21]. Anaphylaxis must be treated with adrenaline through a pre-filled device or injection ^[34]. Adrenaline opens up airways by narrowing blood vessels to maintain blood pressure ^[9. .Figure 3 shows that many allergic diseases are not outgrown through a person’s life and form their allergy march.

[37] Figure 2 – The Th2 Allergic Inflammation March. It shows the interaction between all the Th2 Allergic Inflammation hypotheses. Infants develop eczema as a genetic tendency. Sensitisation then occurs through the skin, and also nose, gut and lung if mucosal barriers are ‘leaky’ (figure 1) initiating further IgE and Non IgE allergic disease and other allergic comorbidities. In this diagram allergic diseases then become long term and are not outgrown due to issues such as a constant breached skin barrier, immune dysfunction, dysbiosis, low iron, low vitamin D and the use of polypharmacy. Courtesy of F. Johnson MRes thesis (2020).  (Original figure adapted from LJ Michaelis 2019). 

Do the principals of the Dual Allergen Hypothesis prevent allergies?

Professors Gideon Lack and George Du Toit wondered why peanut allergy was more common in the UK compared to Israel and why avoiding nuts may increase allergy. A cross-sectional investigation of Israel and the UK, with 5000 Jewish children in each cohort, found peanut allergy to be 10 fold higher in the UK. The research revealed that this was due to peanuts being introduced eight times more/in larger quantities in Israeli in early infancy as a weaning food (Bamba snack), with the median monthly infant consumption of 7.1g compared to 0g ^[38].

Their results formed the basis of the Dual Allergen Hypothesis, which suggests early exposure to food proteins absorbed by the skin through disrupted skin barriers leads to allergic sensitisation. Contrastingly, early oral exposure during infant weaning induces tolerance ^[38] . The skin, a complex, self-renewing barrier, plays a fundamental role ^[23]. Disrupted skin barriers can allow for increased permeability, allowing allergen penetration ^[38].

A study by Saloga et al showed that ovalbumin applied to abraded skin of BALB/c mice (Bagg Albino mice bred in a laboratory)^[38] caused increased anti-ovalbumin IgE levels, which revealed that sensitisation occurred through damaged, not normal skin ^[23].

An interesting study by Fox et al, “Household peanut consumption as a risk factor for the development of peanut allergy”, using household questionnaires, showed children with peanut allergies had been exposed to more peanut allergen “dust” in their first year, compared to children who had allergy to egg ^[40]. This further promoted the idea that environmental factors render the risk of food allergy.

The final paper was published after the “learning about peanut” (LEAP) study (discussed later), showing whether early consumption of peanuts by infantsallows their immune system to tolerate them better in life ^[41].

Is there a damaging effect of the New World’s nutrition- The Microbiome, Anti-oxidant and Dietary Fat Nutritional Hypothesis?

A microbiome (a microorganism community) ^[42] in the gut affects allergy risk. Symbiosis describes the state of mutual benefit/dependence between different species ^[43] . A healthy microbial balance is Eubiosis. A community with low biodiversity or microbial imbalance is dysbiosis, promoting IgE production and possibly pro-inflammatory responses ^[44] .

The developed world’s altered diet may have a microbial effect in altering the gut flora and non-microbial mechanisms through altering the intake of the nutrients ^[45] .

The antioxidant hypothesis suggests a western diet contains a lower quantity of fruit ad vegetables showing that a lack of nutrients are critical in determining a high risk of allergy. It is thought specific antioxidants (eg-vitamin C/B-carotene) have anti-inflammatory effects useful in counteracting allergic diseases ^[22]. The ISAAC (International Study of Asthma and Allergies in Childhood) questionnaire, an international survey in several phases of investigation, involving 306 research centres, 105 countries with 2 million children, supports this proposal ^[46]. Phase one found populations consuming more plant-based foods had lower allergic symptoms; phase 2 discovered a protective effect from consuming fruit, vegetables, fish (Mediterranean diet) ^[46]. However, the lack of an accepted biological mechanism could cause this to be seen as correlation and not causation.

The dietary fat hypothesis claims increases in consumption of unsaturated fats, coupled with a decrease in saturated fats, cause food allergies ^[22]. This is because fatty acids from plants cause the production of prostaglandin E2, which decreases IFN-y, (anti-inflammatory cytokine), production by T lymphocytes, leading to increased IgE production by B cells. Alternatively, fatty acids from animal fats inhibit prostaglandin E2 ^[22]. ISAAC Questionnaire European analysis revealed man-made fatty acids had a positive correlation with the prevalence of allergic conditions, proving as a risk factor ^[46].Yet, some guidelines recommend avoiding sources rich in saturated fats, thus causing a contradiction between preventing allergy and other health risks such as heart disease.

The modern diet has higher levels of food additives and preservatives(e.g. tartrazine and MSG (Monosodium Glutamate)), and there is unsupported evidence that many may exacerbate intolerances due to their ability to sometimes cause symptoms of an allergic reaction ^[47]. The Food and Drug Administration states tartrazine can cause hives in less than 1 in 10,000 people ^[48]. The Food Allergy and Anaphylaxis Meeting in 2016 noted that of 1460 cases of anaphylaxis, it was found that of these 843 cases occurred from non-packed foods and 617 from pre-packaged foods ^[48]. Contrastingly, lots of food additives are synthetic and testing is not reliable. Thus, whilst evidence based literature remains unhelpful; the multitude of additives is a large concern for increasing food allergies for children ^[41].

Does the Vitamin D Hypothesis influence the risk of food allergy?

Vitamin D, a vital nutrient for calcium absorption that aids the maintenance of healthy bones, plays a functional role in the immune system ^[49]. It is absorbed through exposure to sunshine or consumed through supplements and food (oily fish is the richest dietary source) ^[49]. Stored in the body’s fat cells, hydroxylation by the liver and kidneys forms calcitriol ^[50]. The nutrients relation to food allergy, includes two contradicting arguments: vitamin D excess and vitamin D Deficiency hypothesis ^[22] .

Vitamin D excess hypothesis claims that an increase in Vitamin D levels leads to increases in food allergies ^[22]. Milner conducted a study showing children, who had vitamin D supplementation, were higher risk ^[51] . On the other hand, a study by Kull et al found that regular fish consumption for the 1^st year links to lower risks of sensitisation to foods by age 4 ^[52]; this may not be relevant in terms of effects of having nutrient excess.

Vitamin D deficiency hypothesis claims western lifestyles include less outdoors-time, causing reduced sunlight exposure and lower vitamin D production ^[52]. In the western world, 50% are vitamin D insufficient and 10% are vitamin D deficient ^[49]. In Melbourne, southern Australia, blood samples showed infants with low vitamin D, due to less sun exposure, sunscreen use and diet, had a higher risk of egg or peanut allergy and a higher probability of multiple food allergies compared to those with normal levels ^[53]. Epi-Pen prescriptions in the USA also provide strong evidence; northernmost states had 8-12 per 1000, while in southernmost states there was 3 per 1000, with the south having the most sunshine ^[54].

The contradicting evidence leads to unsolved answers. However, when applying theories to real life the Vitamin D Deficiency hypothesis is stronger, due to the multitude of evidence and lifestyle changes in developed countries; it is more likely populations have more time indoors. The above pro-con debate is further supported by the multitude of hypotheses discussed in this paper.

Does the Principles of the Hygiene Hypothesis Lead to An Increase In Food Allergies?

In the 1980’s, Professor P. Strachan (Professor of epidemiology in the BMJ) discovered children in larger households had less allergic rhinitis (hay fever), an allergic disease of the nose, due to exposure to germs by older siblings ^[55]. He created the Hygiene Hypothesis, arguing “fundamental changes in lifestyle led to reductions in exposure to pathogens, important for the development of immunoregulatory mechanisms”^[22]. Therefore, “hygiene and a westernized, semi-sterile diet may facilitate atopy by influencing the stimulation of gut-associated lymphoid tissue”^[22]. The US Food and Drug Association is of the opinion that a child must be exposed to germs so the immune system can develop and strengthen ^[55] but this shall include an avoidance of serious infections. Changes in industrialised countries may have had a part to play and include decontamination of water supplies, pasteurisation and sterilisation of milk, vaccinations, and wide use of antibiotics ^[56].

In the 1990s, Dr Erika von Mutius compared rates of allergies in Germany, finding East Germany’s children, who lived in dirtier cities, had lower allergic reactions than children in the West ^[55]. More infections in the East may promote normal development of the immune system, with a bias for non-allergic Th1 cells rather than allergic inflammatory Th2 cells ^[10], reducing the risk of allergy.

Generally positive correlations between Gross National Product and incidence of allergic disorders ^[56] exist, with wealthier individuals demanding more cleaning products. From 1969-1988, consumption of hard surface cleaner quadrupled and dishwashing detergents tripled (see table 1) ^[22], increasing cleanliness, and inflammation of the skin, further allowing an allergen to enter.

Products	1969	1977	1988	1994
Hard Surface Cleaners	0.730	1.794	2.977	2.060
Dishwashing Detergents	1.183	2.272	3.794	3.120
Fabric Washing Detergents	6.957	7.951	8.376	8.890

Table 1 – Per Capita Consumption (Kg) of Soaps and Detergents.

[45] Bloomfield.SF, “Too Clean or Not Too Clean ; The Hygiene Hypothesis and Home Hygiene”, US National Library of Medicine National Institutes of Health, (2006) (Accessed 6/12/2019)

Studies show immigrant children born outside the USA, who lived in the USA over 10 years, had more risk of developing allergic disorders compared to those who had lived in America for less than two years ^[57]. Others showed immigrant’s offspring acquire the same incidence as the country they occupy ^[56]. This highlights environmental factors that influence risk, supporting the Hygiene Hypothesis, and the country\’s diet (nutritional hypothesis).

Antibiotics kill a large proportion of gut bacteria ^[58], affecting how we digest food, fight infection plus risk of allergy. Dr Christina West, found “a reduction in potentially immune-modulatory bacteria (Ruminococci) is associated with aberrant innate immune responses and increased risk of atopic eczema” ^[44]. It’s believed composition of gut microbiota may disrupt the development of the immune system ^[59] .Lab mice studies show antibiotic-induced changes in the gastrointestinal tract affect immune systems responses to common allergens ^[22] . Furthermore, ISAAC Questionnaire (Phase 3) showed antibiotic use in the first year had an increased risk factor of 1.70 for allergic conditions ^[44] .

Evidence against this theory is prominent: i) A decline in infections, e.g.- Cholera/Typhoid, caused by the improvements in sanitation, hygiene, and water quality occurred from the 19^{th to} 20^th century in developed countries; and ii) Introduction of antibiotics and vaccines for infections, like measles, occurred 1940s onwards ^[22]. These changes are too early to be a direct cause for the sharp increase in food allergies in the past 20 years. Additionally, while cleaning product usage rises, evidence shows minimal effect as the re-colonisation of surfaces occurs rapidly by well-adapted species, meaning our microbial exposure has not greatly decreased ^[22] .

Additionally, in Maputo, Mozambique (economically poor) with half the city covered by sewer systems ^[60], self-reported prevalence of food allergy was 19.1% ^[61], indicating allergy is also prominent in less hygienic conditions.

Overall, the Hygiene Hypothesis is contributing to rises in food allergies, but the evidence reveals it does not act solely alone to progress the epidemic.

The effect of common behavioural changes and practices in the developed world on food allergy prevalence

In the developed world, birthing and feeding of infants has drastically changed, a suspected force catapulting the rise in allergy prevalence.

Significant numbers of USA caesarean births are carried out due to maternal request/convenience, causing this type of delivery to rise 48% since 1996 ^[62] . Caesarean risks include neonatal depression, foetal injury, and respiratory hypoglycaemia (drop in blood glucose level) leading to breast feeding complications ^[62], and now there is evidence for food allergies ^[19] .

During vaginal delivery, the baby has contact with intestinal and vaginal flora of the mother. The infant passes through the vaginal introitus, an important source of microbes that begins colonisation in the infant’s intestine where the baby swallows the uterine fluid during delivery. They play fundamental roles in training and strengthening the immune system. Within year-one, the ecosystem of microbes has developed towards characteristics of the adult gastrointestinal tract. During caesarean, direct contact is absent, non-maternally derived bacteria from the environment begin colonisation inside the infant. This is known as the Bacterial Baptism Hypothesis ^[63]. It suggests babies born vaginally were predominantly colonized by Lactobacillus, whereas babies born by caesarean were colonized by bacteria from skin and hospitals like Staphylococcus and Acinetobacter ^[62]. Figure 3 shows how incidence of allergic diseases can occur at such a young age.

Gronlund’s study showed gut flora in caesarean-born infants may be disturbed for 6 months ^[62], leading to a delay and alteration of the full intestinal colonisation ^[65] and thereby causing an abnormal immune system ^[62]. In a large study (2803 children) delivery method and antibiotic use was recorded from the Norwegian Birth Registry. It was discovered for children born by caesarean whose parents were allergic, had a 7-fold increased risk of egg/fish/nut allergy ^[65]. Conflictingly, a UK research team discovered differences in microbiome had largely disappeared by 6-9 months implying that the babies’ gut bacteria came from their mother’s gastrointestinal tract, instead of from the vagina during delivery ^[66] .

Allergy prevention via birthing method is difficult as many caesarean deliveries are necessary to reduce mortality. An alternative is vaginal seeding, the transfer of vaginal microbiota to the baby to aid the development of a normal microbiome. Safety of this is questionable; it carries serious infection risks and no clinical body currently recommends it ^[63] .

Antibiotics are common practice with caesarean deliveries, and carry the same risks as discussed in the Hygiene Hypothesis.

Mothers who have a caesarean are often highly sedated post-delivery prompting the first 2-3 infant feeds being fed with formula milk rather than breast milk. Plus, it is suggested that formula milk may be given in the first 72 hours of birth for low blood sugar levels, as an alternative to sugar drops which was previously practiced. A study by Osborn and Sinn found no evidence hydrolysed formulas prevented allergy compared to breast-feeding ^[67] . Breastfeeding is recommended for the first 6 months of life ^[68], providing the infant with bioactive factors, including maternal antibodies ^[67] and tolerogenic properties ^[43] , helping the gut microbiome ^[59] . The ISAAC questionnaire found breastfeeding helped protection against allergic or atopic diseases ^[46] . However, a Cochrane review’s study concluded at least 4 months of exclusive breastfeeding did not protect against food allergy at age 1 ^[60] . Overall, there is a general lack of consistent evidence ^[38] which weakens this argument and shows that more long-term evidence is needed.

A change in weaning pattern suggests many parents used an exclusion diet-avoiding feeding infants common allergic food (whole nuts) during weaning due to choking concerns ^[12] . Evidence for this is minimal compared to early weaning.

The LEAP study, the first large study to investigate if early allergen introduction can prevent food allergy ^[41], studied 640 high-risk UK children ^[38]. One group consumed 6g of peanut butter weekly, others avoided peanut butter until 60 months. It provided evidence that, for high-risk infants, regular peanut consumption for the first 11 months of life, causes a large reduction in the incidence of peanut allergy at 60 months and an 81% fall in risk ^[41] . When published in 2015, there was a mass review of many recommendations [38]. This is also supported by the results of the Early Allergen Tolerance (EAT) study involving representatives of the UK population, which concluded that introducing allergenic foods from 3 months of age could prevent food allergy in infants ^[70].

Overall, the change in behaviours is one of the largest factors determining food allergy prevalence with strong evidence – especially for early weaning –highlighting a well-documented link between the two.

The evolution of genetic change – effect of epi-genetics?

The specific genetic loci modulating risk of food allergy is unidentified, and there is a limited number of gene association studies ^[71]. At present, the roles of genetic x genetic and genetic x environmental interactions includes promising research with focus on genes, such as FOXP3 effect on T-cells ^[71] and whether this renders risk of allergic diseases. Future Investigations could allow scientists to discover the relationship between the two.

Food allergies may be caused by genetic variation. Allergies tend to run in families ^[34]; a child with a parent or sibling with peanut allergy has a 7-fold increased risk of atopy ^[22], because family members often have the same exposure to environmental factors (e.g. diet). Atopy is the presence of an allergy, often with hereditary predisposition.

An active investigation is Epigenetics ^[72] (changes in inherited gene expression patterns are independent of changes in DNA sequences) ^[71].. These alterations happen in developmental periods due to environmental factors, a reason why early exposure affects the risk of food allergy ^[71] . Mechanisms include DNA methylations, which is an addition of CH₃ (a methyl group) to genes ^[73].

Evidence suggests genetics may pass the risk of food allergies through generations and epigenetics could provide a possible mechanism supporting practices like early weaning. Professor Harold Renz stated that “the development of chronic inflammatory diseases are the result of gene-environment interactions” ^[74]. There’s low support for the theory that genetics solely has caused the rise in food allergy in the past 20 years. It is too short a time frame to explain by a genetic shift or human evolution ^{[38] [45]} in developed countries. Future studies may discover the specific genes influencing food allergy.

COVID-19 and Food Allergy

With COVID-19 being the largest healthcare challenge in a lifetime, the pandemic’s interaction with the allergy epidemic should be carefully considered to allow scientists to learn about the link and conclude the best approach.

Unprecedented times of the COVID-19 pandemic can cause concern for those with existing health conditions. Risk factors include older age, chronic lung disease, cardiovascular disease, diabetes, hypertension, obesity, male gender, ethnicity, behavioural eating habits and Th2 inflammatory states. ^[75]

The European Academy of Allergy and Clinical Immunology (EAACI) has reviewed the evidence and discussed advice. Presently there is no evidence that food allergies are a direct risk factor, but caution should be taken as some allergies may worsen an individual’s asthma, which is a risk factor for more severe effects of a COVID-19 infection. Additionally, face-to-face hospital services are limited, so remote communication is being used for healthcare professionals to provide guidance and support. Current evidence shows that most allergy treatments do not increase risk, and so guidelines remain the same. However, allergists should be flexible as new research is constantly being carried out and the pandemic is still very new ^[76].

In the UK, statistics are highlighting a disproportionate effect of COVID-19 on Black Asian Minority Ethnicities (BAME), with around a third of patients in intensive care units being BAME even though they form only 14% of the UK population ^[77]. Social factors such as racism, increased levels of poverty and a higher probability of chronic diseases, which make people more susceptible to the virus, may render this. Contrastingly, 90% of doctors who have died due to Covid-19 were of BAME ^[78] ,highlighting it may be other factors besides income, such as genetics.

Some of the risk factors, such as vitamin D and diet, which can render the severity of COVID-19 side effects, are also involved in the hypotheses discussed above. A link to consider is that for allergy sufferers, an avoidance diet can often have a high content of sugar due to unhealthy alternatives to allergic foods. This increases the risk of obesity. Obesity can lead to Th2 inflammation which can affect the ability of the immune system to fight the COVID-19 virus ^[82], leading to more severe symptoms. So, it is likely that someone with an allergy is at a higher risk, not directly because of their food allergy, but because of the other factors involved that promote inflammatory states.

The link is yet undiscovered, but during this pandemic there has been a rise in children showing symptoms, such as inflamed blood vessels, from paediatric multi-system inflammatory syndrome (PMIS), similar to those of a patient with Kawasaki disease ^[79]. Many show acute gastrointestinal symptoms, haemodynamic instability, and myocarditis, making this a potentially fatal illness where patients need intensive care. In Paris ,57% of these patients are of African ancestry ^[80], further supporting a genetic link or immigrant environmental link.

In terms of considering long-term effects, the recent surge in cleanliness to reduce the spread of the virus could result in increased allergy cases in the future according to the Hygiene Hypothesis. This could especially show in this generation of infants, where this period is crucial to immune system development and training.

By reflecting upon this event in the future we shall be able to see the full effect on the incidence of allergy and consolidate the hypothesis discussed.

Conclusion

Overall, it is a collection of factors which are as a result of evolution as to why food allergy prevalence is increasing in developed countries (see figure 4). Changes in nutrition, hygiene, vitamin D exposure, alterations to weaning and birthing practices have contributed to the rise whilst being common adjustments in lifestyles. Although different levels of impact exist for each factor, e.g. the hygiene improvements may have had a smaller effect with developments in sanitation occurring before the sharp increase. Rises in caesarean deliveries are a more recent trend that has a stronger positive correlation with the allergy epidemic. In the future, more clinical prospective trials are needed to provide more clarity and form a precise and comprehensive picture of the factors contributing to the rise in prevalence. Furthermore, with the help of healthcare professionals, changes to lifestyles need to be driven to prevent further damage caused by the allergy epidemic.

[81] Figure 4 –Suspected factors rendering the risk of allergic disease. Courtesy of Chee Hwai Lim MRes thesis. (2019). 

What Future Directions Do We Have to Prevent Allergy? 

Figure 5 illustrates the range of what is needed to combat the allergy epidemic and aid those already suffering. As mentioned in my introduction, through up-skilling students, the public and healthcare professionals, we can become more equipped to control the escalation in allergy prevalence.

Acknowledgements

This work was supported by Dr Louise Michaelis, who I also interviewed to help guide my research. I was very kindly granted use of the diagrams by Chee Hwai Lim, Freya L Johnson, and Esther Crompton. No funding/finance was involved. Dr Louise J Michaelis has lectured on her research and supervised, as a Principle Investigator, clinical commercial research trials with Industry (Nurticia, Regeneron).

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Biography

 Jessica is a student in Sixth form at Queen Elizabeth High School in the North East of England. She holds a passion for learning about the interaction between the body and food, and enjoys reading about new scientific developments. In the future she hopes to pursue a career in healthcare and to be part of implementing life changing treatments.