Nutrient Support for Allergies
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).
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, have potentially deadly side effects over the long-term.
Apart from allergy testing to significantly reduce your allergic symptoms by identifying and avoiding the dietary or environmental culprits driving them, you can also support your body using 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. An imbalance within the Th1-Th2 paradigm favoring Th2 underlies the increased susceptibility to allergies, called atopy, that some individuals experience (Berger, 2000).
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 (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 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 - 30 % 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 hyper-responsiveness 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). 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 is a global health burden; it is estimated to affect up to 10% of the population (Sicherer 2011).
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 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.
NUTRIENT SUPPORT FOR ALLERGIES
In recent years, there has been an increased interest in the role that vitamin D plays in the immune system and, in particular, allergic diseases. It is known that vitamin D receptors are found in multiple tissues and cells in the human body, including mononuclear cells, T lymphocytes and dendritic cells, which are important in the recognition of antigens. Vitamin D also has multiple cytokine-modulating effects and can decrease proliferation of both Th1 and Th2 cells, and lower the production of interleukins and interferons (Searing 2010). This vitamin has also been shown to have a role in airway remodeling, which may be important in understanding and treating asthma (Clifford 2009). Molecular studies also provide evidence that vitamin D can modulate inflammatory responses, enhance antimicrobial peptide activity and promote the integrity of the permeability barrier of the skin (Searing 2010).
Epidemiological studies revealed that Vitamin D deficiency is associated with an increased incidence of asthma and allergy symptoms (Weiss 2008; Litonjua, 2009; Freishtat, 2010), higher IgE responses to food and environmental allergens in children and adults (Sharief 2011) and severity of atopic dermatitis (Peroni, 2011). Similarly, children with well-controlled asthma were found to have higher levels of vitamin D (Chinellato 2011) and adults with chronic urticaria (hives) have lower vitamin D levels than controls (Thorp 2010). A randomized controlled trial involving 45 atopic dermatitis patients provided evidence for the beneficial effect of vitamin D and E supplementation on clinical manifestations. Symptom scores significantly improved in the treatment groups for vitamin D and vitamin E was associated with more favorable symptom scores (Javanbakht 2011).
On the role of vitamin D in preventing asthma and atopic diseases, studies demonstrated that a woman’s high intake of vitamin D during pregnancy lowers the risk of her child developing wheezing (Camargo 2007) or rhinitis at age 5 (Erkkola 2009). This correlation was found in different populations, regardless of the amount of vitamin D intake. A prospective follow-up study showed conflicting results.
A recent longitudinal study demonstrated vitamin D as a predictor of asthma or atopy in later years. The study, involving 689 children from a cohort unselected for asthma or atopy who were examined at age 6 and again at age 14, showed that among male children, inadequate levels of vitamin D is a risk factor for developing atopy, bronchial hyperresponsiveness and asthma. More importantly, vitamin D levels at age 6 were predictive of atopy/asthma-associated phenotypes at age 14 years (Hollams 2011).
Vitamin E is a fat-soluble vitamin that acts as a free-radical scavenger. It protects cell membranes and prevents damage to membrane-associated enzymes. Research suggests that vitamin E inhibits the activation of neutrophils – cells that contribute to respiratory inflammation in asthmatics (Centanni 2001). Studies also indicate that vitamin E can influence and halt the proliferation of mast cells in culture (Zingg 2007; Kempna. 2004 ), suggesting a role for vitamin E in modulating allergies, atherosclerosis, cancer and other diseases in which mast cells play a role.
Several studies provide evidence on the relationship between vitamin E intake and asthma or allergic diseases. A Japanese prospective study reported that low maternal vitamin E intake during pregnancy was associated with increased likelihood of wheezing in children younger than 2 years of age (Miyake 2010). A Scottish birth cohort study reported that low alpha-tocopherol intake during the first trimester of pregnancy was associated with an increased risk of wheezing and asthma in 5-year old children (Devereux 2006). A case-control study reported that childhood asthma is associated with low dietary vitamin E intake (Hijazi et al, 2000), and a 10-year prospective study of adult-onset asthma also reported similar findings (Troisi 1995). In a clinical study of atopic dermatitis, patients randomly selected to orally receive 400 IU of vitamin E daily for 8 months reported remarkable improvement in facial erythema (redness) and lichenification (scaling and thickening of the skin). Eczematous lesions were also reportedly healed as a result of decreased itch sensation (Tsoureli-Nikita 2002).
Animal models have shown that supplementation with high dose vitamin E reduced proliferation of splenic lymphocytes, the production of IL-4, IL-5 and total serum IgE levels. Sneezing and nasal allergic response were also suppressed in the treatment group (Zheng 1999). In a randomized controlled trial, patients with seasonal allergic rhinitis who received vitamin E supplementation during hay fever season experienced improvement in their symptoms (Shahar, 2004).
Vitamin C (ascorbic acid) increases the function of many immune cells, including T cells, phagocytes (which destroy pathogenic organisms), and others. As an antioxidant, ascorbic acid can protect cells from reactive oxygen species known to cause tissue damage and disease. Vitamin C has anti-histamine properties (Johnston CS, 1996) that can help relieve allergy symptoms, but the evidence is still controversial.
Early studies demonstrated that 2 grams of vitamin C improve pulmonary function one hour after ingestion, compared with a placebo (Bucca 1990) and another study found a fivefold increase in bronchial hyperreactivity among those with the lowest intake of vitamin C (Soutar 1997).
An animal model showed that high dose vitamin C supplementation significantly decreased inflammation in the lungs (Chang 2009).
Magnesium is utilized by every cell in the body and participates in energy metabolism and protein synthesis. Magnesium participates in at least 350 enzymatic processes within the body. Evidence from animal models indicates that magnesium plays a role in immune response, and that deficiency leads to increased inflammation (Laires 2008).
Results from randomized clinical trials showed that children and adults who were hospitalized for severe, acute asthma benefited from using intravenous (IV) magnesium sulfate (Ciarallo 1996; Devi 1997; Gürkan 1999; Ciarallo 2000). One of these studies used a higher dose of magnesium sulfate (40 mg/kg) and observed a faster and more prolonged improvement in pulmonary function (Ciarallo 2000). But, one randomized study found no evidence that IV magnesium sulfate can treat moderate to severe asthma (Scarfone 2000).
A randomized study found that taking 200 - 290 mg of magnesium for 16 weeks significantly reduced the use of bronchodilators in children with mild to moderate asthma (Bede 2003). Similar beneficial effects of 12-week magnesium supplementation were found in a small study involving children with moderate persistent asthma treated with inhaled fluticasone (Gontijo-Amaral 2007). More recently, long term treatment with oral magnesium (170 mg twice a day for 6.5 months) in adults with mild to moderate asthma showed improvement in objective measures of bronchial reactivity and in subjective measures of asthma control and quality of life (Kazaks 2010).
Fish oil and Fatty Acids
Fish oils contain the omega-3 fatty acids docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA). EPA and DHA exert anti-inflammatory and antithrombotic (anti-clotting) effects (Calder 2005) because omega-3 fatty acids compete with arachidonic acid, which serves is converted into pro-inflammatory eicosanoids (Leaf 2002; Connor 2001; Calder 2001). Studies suggest that fish oils reduce the production of inflammatory cytokines such as interleukin-1, IL-2, and tumor necrosis factor, which are all involved in the allergic response. Additionally, lower levels of omega-3 fatty acids in the blood are associated with delayed-type hypersensitivity skin reactions in elderly malnourished subjects (Cederholm 1994).
In one study, an ointment containing DHA and EPA produced satisfactory results in 64 patients with refractory dermatitis (Watanabe 1999). A systematic review of maternal supplementation with omega-3 polyunsaturated fatty acids (n-3 PUFA) found evidence that they reduced the prevalence of childhood asthma, but supplementation during lactation did not prevent asthma or food allergy (Klemens 2011). Intake of n-6 PUFA among 1,002 pregnant Japanese females showed a tendency towards lesser allergic rhinitis in the children (Miyake 2007).
The perennial shrub Butterbur (Petasites hybridus) is known to inhibit plasma histamine, leukotrienes, and the priming of mast cells in response to allergens (Thomet 2002; Shimoda 2006). Traditional Chinese Medicine has used Butterbur to treat asthma, migraine stress and gastric ulcer (Lee 2011). Petasin, a pharmacological compound extracted from the plant, has been commercialized as Ze 339 and approved in Switzerland as an anti-allergic drug to treat seasonal allergic rhinitis.
A randomized controlled study found Ze 339 effective in improving asthma scores compared to placebo (Schapowal 2004). Other studies found the effect of Ze 339 comparable to cetirizine (Schapowal 2002) and fexofenadine (antihistamine drugs) (Schapowal 2005; Lee 2004). A systematic review of 6 randomized controlled trials found that butterbur extract is effective as a non-sedative antihistamine for intermittent allergic rhinitis as well (Guo 2007). Ze 339 reduced allergic airway inflammation in the lungs of asthmatic animals and inhibited the production of Th2 cytokines, interleukins and RANTES (Regulated upon Activation, Normal T-cell Expressed, and Secreted), which facilitates infiltration of white blood cells during the inflammatory response (Brattström 2010).
Extracts from the Japanese butterbur (Petasites japonicus), which contains a profile of active compounds similar to Petasites hybridus, inhibited eosinophil infiltration and reduced mucus secretion in an animal model of asthma. In cell culture studies, the extract inhibited the release of interleukins triggered by house dust mites (Lee et al., 2011), suggesting that butterbur can suppress the pathogenesis of airway inflammation.
Quercetin, one of the most common flavonoids found in a variety of foods such as red wine, green tea, and apples, has been studied for its ability to reduce the symptoms of allergies. It has been shown to inhibit leukotrienes, mast cells, and the release of histamine (Chirumbolo 2010), which makes it a good candidate for anti-allergy therapy. Evidence also demonstrated that quercetin blunts the inflammatory response of immune cells upon antigen recognition (Huang et al, 2010).
In an animal model of peanut allergy, quercetin completely stopped peanut-induced anaphylactic reactions after challenge. Histamine levels in quercetin-treated rats were significantly lower than the positive control group (Shishehbor 2010). In guinea pigs sensitized with ovalbumin, a relatively low dose of quercetin reduced the hyperactivity of airways and caused significant bronchodilation (Joskova 2011). Quercetin microemulsion treatment exhibited anti-inflammatory properties in a similarly designed murine model (Rogerio et al, 2010).
Patients with nasal allergies treated with nasal spray containing quercetin and Artemisia abrotanum L experienced rapid and significant relief of nasal symptoms that was comparable to antihistamine preparations (Remberg 2004). In two independent randomized controlled studies among patients with pollen allergies, taking 100 mg of a quercetin-related compound for 8 weeks, significantly reduced nasal symptoms compared to placebo group (Kawai 2009; Hirano 2009).
Urtica dioica acquired the common name ‘stinging nettle’ because the leaves, flowers, seeds and root contain different chemicals such as histamine, formic acid, acetic acid and other irritants that cause mildly painful stings, itchiness or numbness on contact (Anderson 2003).
Historically, stinging nettle has been used to treat allergic rhinitis, but very few clinical studies have been conducted. In an open trial of 69 patients with allergic rhinitis, 58% of subjects who took 600 mg freeze-dried nettle leaf reported a relief in symptoms of rhinoconjunctivitis, and 48% found it more effective than over-the-counter medications (Mittman 1990). Long-term use of the stinging nettle extract, IDS 30, was shown to have anti-inflammatory effects and to be effective in preventing chronic colitis in animal models (Konrad 2005).
Recently, data from bioassay experiments revealed that bioactive constituents in nettle extract inhibit histamine receptors, inhibits enzymes involved releasing cytokines and chemokines that cause allergy symptoms, and reduces the production of allergy-specific prostaglandins. For the first time, these results provided a mechanistic understanding of the role of nettle extracts in reducing allergy and other inflammatory responses (Roschek 2009).
The term “spirulina” refers to the dried biomass of a species of cyanobacterium called Arthrospira platensis. It is widely consumed by humans as a dietary supplement and even used as a food source for some aquatic species and poultry.
Spirulina is a source of a variety micronutrients and phytonutrients; it is also, by weight, a good source of non-animal protein (Deng 2010). Studies have shown that spirulina exerts a number of favorable biologic effects in both humans and animals when it is consumed as a food or a supplement (Deng 2010). Additionally, the United States Pharmacopeial Convention (USP) recently assigned a safety rating of “Class A” to spirulina, meaning that data support a high level of confidence regarding the safety of spirulina when used as a dietary supplement (Marles 2011).
Several trials have examined the role of spirulina in modulating the biology of allergic response. Administered at 2,000 mg per day, spirulina was shown by Mao et al (2005) to shift the T-cell profile away from Th2 in allergic rhinitis patients by inhibiting IL-4 signaling. Upon analyzing their results, the scientists stated “this… human feeding study …demonstrates the protective effects of Spirulina towards allergic rhinitis.”
In a similarly designed clinical trial, Cingi and colleagues (2008) corroborated Mao’s findings by showing that “spirulina consumption significantly improved the symptoms and physical findings [in allergic rhinitis patients] compared with placebo including nasal discharge, sneezing, nasal congestion and itching”.
To better explore the mechanisms by which spirulina blunts allergic reactions, Chen et al (2005) studied its biological effects in a murine model of allergic rhinitis. They found that spirulina lowered IgE levels and, correspondingly, attenuated degranulation of nasal mast cells, resulting in suppressed histamine levels in serum. Very similar findings were reported by Remirez (2002) as well.
In order to prevent the development of childhood allergic diseases, an infant’s immune system must mature from a Th2- to a Th1-dominated response through microbial contact soon after birth. In comparison with the time before antibiotics and common presence of infectious diseases, along with the widespread use of antimicrobial agents in consumer products like soap, individuals in modern times have reduced contact with microbes. In the theory known as the “hygiene hypothesis”, scientists speculate that an antiseptic environment results in a lack of microbial stimulation to the gut immune system and causes an increase in allergic disease (Penders 2007; Pan 2010). In fact, studies have shown that non-allergic children have higher levels of Bidifobacteria and Lactobacilli compared to allergic children (Kalliomaki 2001). The presence of these ‘harmless’ probiotic bacteria in the intestinal biota seem to correspond with protection against allergy.
Many randomized trials, clinical and experimental studies and meta-analyses have been conducted on the efficacy of probiotics on the treatment or prevention of allergic diseases.
Randomized controlled trials (RCTs) showed that using probiotics provided significant clinical benefits to children with allergic rhinitis. Lactobabillus casei decreased the frequency and severity of nose and eye symptoms and improved the quality of life for children who were sensitized to house dust mites (Wang 2004; Peng 2005). Among preschool children with seasonal allergic rhinitis, L. casei was also found to reduce symptoms and the number of episodes, and lessen the use of relief medications. The effect, however, was not statistically significant for asthma (Giovannini 2007). Similar positive effects were observed among children with pollen-sensitized allergic rhinitis who were treated with oral Bacillus clausii spores (Ciprandi et al, 2005).
Studies that examined the effects of probiotics at the level of the immune system also showed some positive effects. Supplementation with L. gasseri significantly reduced serum IgE specific to Japanese cedar pollen in children with seasonal allergies (Morita 2006).
Positive effects were also observed among patients who received Bifidobacterium longum BB536 supplement (Xiao 2006). Moreover, BB536 seems to suppress Th-2 cell attraction and activation, suggesting it may be effective in blunting the IgE-mediated allergic response (Iwabuchi 2009). In a 28-week clinical trial, BB536 favorably modulated intestinal microbiotia, lessening the burden of allergens, in subjects with cedar pollen allergies (Odamaki 2007). In an experimental model, a BB536 DNA oligodeoxynucleotide, shunted the cytokine profile in favor of Th1 and suppressed IgE levels, both markers of and contributors to a lessened allergic response (Takahashi 2006).
In two randomized controlled trials studying the clinical effects of L. plantarum No. 14 (LP14), eosinophil counts decreased immediately after intake in the group that took LP14, and the percentage of Th1 helper T cells increased after 6 weeks. LP14 also strongly induced the gene expression of Th1-type cytokines, indicating that probiotics are clinically effective in the management of seasonal allergic disease.(Nagata 2010).
A review of 13 randomized, controlled trials on the effectiveness of probiotics in the treatment or prevention of atopic dermatitis found that, regardless of IgE sensitization, Lactobacillus rhamnosus GG (LGG) and other probiotics were effective in preventing AD. Probiotics also reduced the severity of AD in half of the trials evaluated, although there was no significant change observed in the inflammatory markers (Betsi 2008).
In terms of preventing allergies, a meta-analysis of six studies reported significant benefits in infants at high risk of allergy who used probiotic supplements containing L. rhamnosus. A recent study (Berni 2011) demonstrated that infants with suspected cow’s milk allergy who were given partially hydrolyzed infant food supplemented with LGG had a higher probability of acquiring tolerance to cow’s milk protein at 6 and 12 months compared with infants who were not given LGG supplementation. In addition, skin patch test responses were negative in all infants who acquired tolerance.
Clinical improvements have been reported among patients with allergic rhinitis and IgE-sensitized atopic eczema, but studies on the efficacy of probiotics in the management of asthma remain inconsistent. Possible reasons include differences in study designs, types of probiotics used and duration of probiotic supplementation, which limits the comparability of results (Ozdemir 2010).
Initial strategies to reduce allergy symptoms should include:
- Avoid known allergens as much as possible’
- Ensure that your environment is kept clean; regular vacuuming and use of an air purifier may help;
- Work with a qualified healthcare practitioner to identify allergens that you react to (using IgE antibody testing).
- Quantitative IgG antibody testing can be clinically effective for food allergies – alternative practitioners could advise you on elimination diets
In addition, the following natural compounds may help ease allergy symptoms:
- Vitamin D: 5000 – 8000 IU daily; depending upon blood levels of 25-OH-vitamin D
- Natural Vitamin E: 100 – 400 IU alpha-tocopherol and 200 mg gamma-tocopherol daily
- Vitamin C: 1000 – 2000 mg daily
- Magnesium: 140 – 500 elemental milligrams of highly-absorbable magnesium
- Fish oil (with olive polyphenols): providing 1400 mg EPA and 1000 mg DHA daily
- Butterbur: standardized extract: 75 – 150 mg daily
- Quercetin (providing quercetin glycoside derivatives and free quercetin): 250 – 500 mg daily
- Stinging nettle (leaf); standardized extract: 500 – 1500 mg daily
- Spirulina: 1000 – 2000 mg daily
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