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Allergies are a global public health menace (Pawankar 2011). More than 500 million people worldwide suffer from food allergies. More than 300 million, or about 5% of the global population, now suffer from asthma (Chang 2011). Allergic rhinitis, a risk factor for asthma, affects up to 30% of adults and 40% of children (Wallace 2008).

Some scientists theorize that a potential cause of allergies in the modern world may be over-sanitation. Excess utilization of antibiotics and less frequent exposure to microbes like bacteria and viruses during childhood may impair development of balanced immunity, causing hyper-reactivity to allergens later in life, a phenomenon known as the “hygiene hypothesis” (Fishbein 2012; Jedrychowski 2011).

Relieving allergy symptoms in hopes of improving quality of life is the primary goal of treatment. However, patients often report that their conventional medications fail to provide relief (Li 2009; Metcalfe 2010). Also, corticosteroids and beta-2-agonists, drugs frequently used to treat allergic asthma, are fraught with potentially deadly side effects over the long-term.

Reliable allergy testing methods allow for a more guided treatment approach that includes identification and avoidance of troublesome allergens, as well as targeted immunotherapy with allergy shots, or via sublingual immunotherapy – an effective method underutilized in the United States, but which has been employed in Europe for decades (Lin 2011).

When you read this protocol, you will learn what causes allergies, how medical treatment can help relieve allergic reactions, and how allergy testing strategies can empower you to significantly reduce your allergic symptoms by identifying and avoiding the dietary or environmental culprits driving them. You will also read about several natural compounds with immunomodulatory properties that quell allergen-induced inflammatory responses to provide symptom relief.

What is an Allergy?

An allergy occurs when your immune system responds aggressively to a harmless environmental substance.

Common inhaled allergens include tree and flower pollen, animal dander, dust, and mold. Ingested allergens include medications (penicillin, for example) and foods such as eggs, peanuts, wheat, tree nuts, and shellfish. Nickel, copper, and latex can also cause allergies (AAAAI 2011; Kasper 2005).

These allergens can affect various parts of the body and elicit symptoms in the nasal passages (such as itchy, stuffy and/or runny nose, postnasal drip, facial pressure and pain); mouth area (tingling sensation, swollen mouth and lips, itchy throat); eyes (swollen, itchy, red eyes); respiratory (wheezing, coughing, difficulty breathing, shortness of breath); skin (hives, rashes, swelling); and gastrointestinal (stomach cramps, vomiting, diarrhea). Symptoms can occur within minutes to days after exposure and can range from mild to severe.

The most severe form of allergic reaction is called anaphylaxis. It is a potentially deadly condition that results in respiratory distress and swelling of the larynx, often followed by vascular collapse or shock (Kasper 2005). Anaphylaxis should be treated rapidly because death can occur within minutes or hours after the first symptoms appear. Many people prone to anaphylaxis carry self-injecting epinephrine pens in case of emergencies.

What Causes an Allergic Response?

The immune system normally functions to protect the body against viruses, bacteria, fungi, and other pathogens by targeting these substances for destruction upon recognition. However, an allergic response arises when your immune system mistakes harmless substances as potential pathogens and attacks them.

Th1 and Th2 Immune Responses in Allergies

T lymphocytes are immune cells that recognize foreign pathogens and also produce cell-signaling cytokine proteins, which facilitate immunological communication. The two main subsets of T cells – Th1 and Th2 – complement one another to produce a comprehensive immune response against invading pathogens.

Th1 cytokines trigger the destruction of pathogens that enter the cells (such as viruses). They are also responsible for cell-mediated immune response and can perpetuate autoimmune reactions. Th2 cytokines destroy extracellular pathogens that invade the blood and other body fluids. As will be described below, an imbalance within the Th1-Th2 paradigm favoring Th2 underlies the increased susceptibility to allergies, called atopy, that some individuals experience (Berger, 2000).

A Closer Look at the Immunology of an Allergic Response

According to the Th2 hypothesis of allergy, atopy results from an overproduction of Th2 cytokines in response to allergens. The atopic individual is genetically predisposed such that he is more likely to over-produce Th2 cytokines and muster an insufficient Th1 response; the result of this imbalance is production of antibodies against normally innocuous environmental substances (Bellanti, 1998).

The first time an allergen is encountered, the Th2 cytokines interleukin-4 (IL-4) and/or IL-13 alert B cells (components of the immune system responsible for antibody generation) to produce a particular type of antibody called immunoglobulin E (IgE); this process is called “sensitization”.

Next, circulating IgE alerts other immune cells (basophils in the blood and mast cells in the skin and mucosal lining) that they should be ready to destroy the antigen in question if they detect it. IgE also triggers the formation of “memory” T-cells, which are able to react much more quickly to future recognition of the same antigen.

Upon subsequent exposure to the same antigen, an atopic individual will have a dual response characterized by an immediate, or acute reaction within minutes, and a delayed, or late-phase reaction within the next 4-8 hours after exposure (Hansen, 2004).

Acute Response

During an acute immune reaction, IgE antibodies, upon binding (crosslinking) a previously categorized antigen, provoke release of allergic mediators including histamine, prostaglandins, and leukotrienes from mast cells and basophils; these chemicals are responsible for the classic symptoms we think of in association with “allergy” (e.g. itchy skin, runny nose, etc.).

This immediate IgE reaction responds to antihistamines and decongestants (Bellanti, 1998).

Late-phase Response

After the acute response subsides, late-phase reactions can occur and produce long-term effects. The late-phase reaction manifests when an antigen is presented to a T-cell (especially those already “primed” by IgE specific to that antigen) that then releases cytokines (primarily IL-5), which induce degranulation (release of allergic mediators) from another type of immune cell called an eosinophil.

For example, the pathogenesis of allergic rhinitis, atopic dermatitis and asthma, are thought to be influenced more by the late-phase immune reactions. In general, late-phase allergic reactions respond to anti-inflammatory agents such as corticosteroids.

Together, allergic mediators including histamine, leukotrienes and interleukins cause a typical “allergy attack”. In the skin, they cause itchy hives, rashes and swelling. In the nasal cavities, these chemicals cause runny nose, tearing, burning or itching eyes, itching in the nose, throat, roof of the mouth and eyes. The release of histamine and other mediators in the lungs cause muscles of the bronchial wall to tighten, become inflamed and produce excessive mucus. This causes the symptoms of asthma — wheezing, difficulty breathing and coughing. In the digestive system, histamine can cause vomiting, diarrhea and stomach cramps.

Allergic Disorders

Epidemiological studies revealed that the prevalence of allergic diseases has increased worldwide over the last few decades (Gupta, 2004; Yuksel, 2008; Asher 2006; Björkstén, 2008). Allergic diseases include atopic dermatitis, allergic rhinitis, asthma, food, drug and insect allergy, urticaria (hives) and angioedema (swelling beneath the skin).

Atopy, the genetic predisposition to producing IgE antibody in response to allergens, increases the risk of developing allergic disorders (Zheng 2011; Johansson 2004). Having one allergic disorder significantly increases the risk of developing other allergic disorders (Simpson 2008). Atopy is the strongest predisposing factor of asthma in children. Epidemiological and experimental studies have shown that atopic disorders typically follow a natural history of manifestation or a progression of clinical signs, beginning with atopic dermatitis in infants and developing to allergic rhinitis and asthma in children (Spergel 2003). This progression, called atopic march, may be influenced by shared genetic and environmental risk factors (Spergel, 2010).

Atopic Dermatitis

Atopic dermatitis (AD) is a chronic inflammatory skin disorder that affects at least 15% of children and up to 10% of adults (Pawankar 2011). Studies among children reveal that AD develops very early in life. In fact, around 45% of affected children develop AD in the first 6 months of life, 60 % develop it in the first year, and 85% before their 5th birthday. Further, more than half of affected children will continue to have AD beyond 7 years of age, and more than 40% will experience it through adulthood (Pawankar 2011).

Atopic dermatitis is often the first manifestation of allergic disease and many patients may develop allergic rhinitis and asthma later in life (Spergel 2010). Eczematous rashes are dry, scaly and itchy, and can become infected if left untreated. In infants and young children, the rashes appear on the face, neck, cheeks and scalp. In older children and adults, eczema may appear on the folds of the forearms, the inner elbows and behind the knees. Factors that make the symptoms worse include temperature, humidity, irritants, infections, food, inhalant and contact allergens and emotional stress (Hoare 2000). Atopic dermatitis can affect development, personality, and quality of life of patients and their families.

Patients with atopic dermatitis have reduced skin barrier function. When vital skin lipids are lost, moisture escapes from the skin epidermis (top layer of the skin) and the skin becomes dry, causing cracks and microfissures to develop through which allergens and microbes can easily enter (Pawankar 2011). Soaking baths followed by an application of emollient (moisture-retaining lotion or salve) can help retain moisture and give the patient relief.

Topical corticosteroids are the standard treatment for atopic dermatitis. Low-potency corticosteroids help keep the symptoms under control and high-potency corticosteroids are used in severe flare-ups. Because of their potential adverse effects, high-potency corticosteroids should be used over short periods of time and topically only in areas that are lichenified (areas in which the skin has become leathery and thickened) (Leung 2004).

Allergic Rhinitis

Allergic rhinitis is an IgE-mediated inflammation of the nasal mucosa in response to outdoor and indoor allergens, the most common of which are pollens, dust mites, molds and insects. Sensitization and subsequent exposure trigger a release of symptoms that include sneezing, runny or stuffy nose, teary eyes and itchy nose, throat or skin (Meltzer 2009). The nose becomes primed and hyper-reactive on repeated exposure to the allergen, and over time, the amounts of allergen needed to mount an immune response decreases (Pawankar 2011).

Allergic rhinitis is a major respiratory health problem that affects between 10 to 30 percent adults and more than 40% of children worldwide. The prevalence of this disease is increasing. Allergic rhinitis negatively affects the patient’s quality of life, school/work performance and social interaction, and creates financial burden (Pawankar 2011). Allergic rhinitis is a risk factor for asthma (Choi 2007), and many patients with it also suffer from atopic dermatitis and conjunctivitis, and co-morbidities that include sinusitis, nasal polyps, upper respiratory infections, sleep disorders and impaired learning in children (Craig 2010). It can also develop 3 to 7 years later among patients with non-allergic rhinitis (Rondón 2009).

Based on frequency and severity of symptoms, allergic rhinitis may be classified into (1) mild intermittent; (2) mild persistent; (3) moderate/severe intermittent; (4) moderate/severe persistent (Bousquet 2008). Based on type of allergen, rhinitis is classified as perennial or seasonal, although patients can respond to both types of triggers. Symptoms can also last up to 4 to 9 months of the year (Meltzer 2009). Risk factors of allergic rhinitis in childhood include a family history of atopy, birth by cesarean section, exposure to cigarette smoke in infancy, endotoxin levels in house dust of inner city homes and pollutants (Sabin 2011).

Conventional treatment of allergic rhinitis usually begins with controlling exposure to the allergen(s), followed by use of intranasal corticosteroid sprays and non-sedating antihistamines. A survey of pediatric allergies in the U.S. (Meltzer 2009) reported that parents and physicians consider nasal allergy medications as insufficient for relieving immediate and long-term symptoms and often have bothersome side effects. Some of the adverse side effects reported include nasal dryness, nose bleeds and drowsiness from antihistamines.


Asthma is a life-long inflammatory disease characterized by airway hyperresponsiveness and airflow obstruction. In people with asthma, the inner lining of the airways become inflamed and the muscles surrounding the airways tighten up. Mucus glands in the airways secrete thick mucus. Together, these changes cause the airway to narrow and leads to difficulty breathing, shortness of breath, cough and wheezing.

Between 60% and 70% of asthma cases in children are allergic or atopic. Children with allergies have a 30% increased risk of developing asthma (Pawankar 2011). Genes play an important role in the susceptibility to develop asthma and several candidate genes have been identified in this regard (Zhang 2008). Genes can impact a child’s response to medications, and in particular, to beta-adrenergic agonists, glucocorticoids and leukotriene modulators (Chang 2011). Other factors that affect the development and severity of asthma include indoor allergen exposures, outdoor pollens, viral upper respiratory infections, exercise, foods, occupational history of the child and parents, environmental smoke, pollution and exposure to day care.

Inhaled corticosteroids are anti-inflammatory medications for the treatment of persistent asthma. However, clinical control deteriorates within weeks to months once corticosteroid treatment is discontinued. The most effective long-term medications are long-acting inhaled beta-agonists (Pawankar 2011), but they come with potentially serious adverse effects (Chang, 2011).

Food Allergy

Food allergy is a global health burden; it is estimated to affect up to 10% of the population (Sicherer 2011). In the U.S. alone, food allergy is responsible for 200 anaphylaxis-related deaths and 2,000 hospitalizations every year (Branum 2008).

The most common food allergens include cow’s milk, eggs, peanuts, tree nuts, seafood, soy and wheat. Symptoms of food allergy, which may occur following ingestion, inhalation or contact, are mediated by IgE and non-IgE reactions. Upon sensitization of an allergen, IgE synthesis increases and elevated numbers of cytokines are produced in the serum and intestinal fluids (Yu, 2012). IgE-mediated reactions occur within minutes to hours of exposure and include symptoms like angioedema (swelling of the inner layers of the skin), nausea and vomiting, swelling of the throat, hives, swelling and itchiness of the mouth area, diarrhea and wheezing. Symptoms of non IgE mediated reactions can occur hours to days later and may include constipation, atopic eczema, protein-induced enterocolitis syndrome, allergic proctitis or rectal inflammation and Heiner syndrome (a pulmonary disease) (Bahna 2003).

The health of the gastrointestinal system plays a pivotal role in food allergies and food sensitivities. The gastrointestinal system acts as a semipermeable barrier, allowing only usable molecules into the bloodstream after food has been broken down. Studies have shown that allergen challenge in sensitized individuals can cause the intestinal walls to become more permeable (Troncone 1994; Pizzuti 2011). When the intestinal wall has been weakened by infection or inflammation, the barrier function is compromised, allowing large molecules to pass through the intestinal wall and into the bloodstream (Moneret-Vautrin 2005; Yu 2012). Allergic sensitization can occur as the immune system responds to these abnormally large molecules, causing digestive complaints such as upset stomach or diarrhea, or symptoms such as joint pain and headaches (Moneret-Vautrin 2005).

Healthy individuals host 100 trillion symbiotic bacteria that include Lactobacillus, Clostridium, Bacteroidetes, Proteobacteria and Bifidobacteria (Frank 2007). Enteric bacteria modulate intestinal morphology; they also produce short chain fatty acids, vitamins, ferment dietary fiber, and shape mucosal immunity (Kelly 2005; Kelly 2007). Animal models have shown that enhancing or restoring intestinal commensal bacteria through supplementation (i.e. supplemental probiotics) (Sudo 2002) can induce tolerance and prevent allergy. Evidence also suggests that a healthy population of intestinal bacteria can help reduce intestinal permeability (Vinderola 2004; Gun 2005).

Probiotic bacteria include Lactobacilli, Bifidobacteria, and Bacillius coagulans Saccharomyces boulardii is a probiotic yeast (Casas 2000; Pelto 1998; Goldin 1998; Cross 2001). Also, prebiotics, such as fructooligosaccharides, may be included to encourage the growth of beneficial bacteria (Bouhnik 1999). Consuming plenty of dietary fiber each day supports intestinal microbiota as well (O’Keefe 2011).

IgG-Mediated “Food Sensitivities”

A number of innovative doctors advocate an elimination diet based on quantitative IgG antibody testing for the relief of a wide array of patient complaints (Russel 2010). This involves assessing levels of IgG antibodies in a patient’s blood using an ELISA method (described below) and then instructing the patient to eliminate any foods to which high levels of IgG4 antibodies are detected.

Innovative doctors suggest that this method can be effective for relieving ambiguous symptoms, such as headaches, fatigue, and mood imbalances when other causes cannot be identified. The postulated link is that IgG’s, particularly IgG4, facilitate a delayed reaction to foods, which is often referred to as a “food sensitivity”. These hypothesized IgG4-mediated “food sensitivities” are not the same as true IgE-mediated food allergies, and although some prominent alternative medical practitioners believe these to be separate & distinct phenomena, others disagree. IgG4-mediated food sensitivities are not a generally recognized phenomenon among mainstream medical professionals.

Clinical trials have noted improvements in patient symptoms with an elimination diet based on IgG4 testing. Mitchell and colleagues (2011) found that when subjects who experienced frequent migraine-like headaches eliminated foods to which they produced high levels of IgG antibodies, headaches occurred less often 4-weeks after initiating the diet; although by 12-weeks there was no difference.

In another trial, an IgG-based elimination diet slightly improved stool frequency in Crohn’s disease patients (Bentz 2010). Similarly, Anthoni et al (2009) found that levels of IgG against milk proteins correlated with self-reported gastrointestinal symptoms after consuming milk in subjects with abdominal symptoms. Atkinson’s team (2004) showed that a 12-week IgG-based elimination diet improved symptoms in patients with irritable bowel syndrome, and that better compliance with the elimination diet was associated with greater symptom improvement.