Food allergies are challenging. The risk and fear of allergic reactions make life hard for children and parents. Unfortunately, food allergies are becoming more common and taking longer to outgrow. Oral Immunotherapy (OIT) is a new option that may help to keep your child safe while reducing anxiety, allowing your child to eat out or attend school with less worry. OIT involves retraining the immune system to tolerate the allergic food (i.e. peanut or milk). This is done by feeding the food allergic person small amounts of the food. The amount increases slowly over time. As the dose goes up, so does the level of protection. Working as a Nurse Practioner at the food allergy institute of Mount Sinai in NYC, allowed me to gain valuable experience and insights regarding OIT. Historically, food allergy treatment included strict avoidance and carrying emergency medications. That was it, do your best and wait. OIT is a novel option. Studies have shown OIT reduces allergic reactions from cross contamination and increase quality of life. As the treatment is still new, there are uncertainties. It is currently unknown if OIT leads to long term tolerance and a ‘cure’ for food allergy. Or is the benefit only temporary. Optimal dosing protocols are still being worked out. Also, it is not clear which patients would benefit from addition of adjuvants, like Xolair or probiotics. OIT can be a great option for some patients. It should only be done in an office that has the training and staff to safely navigate them through the process. The undertaking can be difficult and time consuming and there can be side effects. Despite the unknowns and risks, OIT can have a huge impact on reducing food allergy reactions and increasing quality of life. It can be a great option for families to be less afraid of cross contaminations and to gain the possibility of eventually outgrowing their allergy. OIT has great potential and I am excited and hopeful to see further success.
The U.S. Food and Drug Administration is alerting consumers to Meridian Medical Technologies’ voluntary recall of 13 lots of Mylan’s EpiPen and EpiPen Jr (epinephrine injection) Auto-Injector products used for emergency treatment of severe allergic reactions. This recall is due to the potential that these devices may contain a defective part that may result in the devices’ failure to activate. The recalled product was manufactured by Meridian Medical Technologies and distributed by Mylan Specialty. While the number of reported failures is small, EpiPen products that potentially contain a defective part are being recalled because of the potential for life-threatening risk if a severe allergic reaction goes untreated. Consumers should keep and use their current EpiPens if needed until they get a replacement. Consumers should contact Mylan at 800-796-9526 or email@example.com with any questions. As stated on the product label, consumers should always seek emergency medical help right away after using their EpiPens, particularly if the device did not activate. At this time, the 13 lots identified – distributed between Dec. 17, 2015, and July 1, 2016 – are the only EpiPen lots impacted by the U.S. recall. Consumers who have EpiPens from lots that are not included in this recall, do not need to replace their EpiPen prior to its expiration date.
The FDA asks health care professionals and consumers to report any adverse reactions or device malfunctions to the FDA’s MedWatch program, by:
|Product/Dosage||NDC Number||Lot Number||Expiration Date|
|EpiPen Jr Auto-Injector, 0.15 mg||49502-501-02||5GN767||April 2017|
|EpiPen Jr Auto-Injector, 0.15 mg||49502-501-02||5GN773||April 2017|
|EpiPen Auto-Injector, 0.3 mg||49502-500-02||5GM631||April 2017|
|EpiPen Auto-Injector, 0.3 mg||49502-500-02||5GM640||April 2017|
|EpiPen Jr Auto-Injector, 0.15 mg||49502-501-02||6GN215||September 2017|
|EpiPen Auto-Injector, 0.3 mg||49502-500-02||6GM082||September 2017|
|EpiPen Auto-Injector, 0.3 mg||49502-500-02||6GM072||September 2017|
|EpiPen Auto-Injector, 0.3 mg||49502-500-02||6GM081||September 2017|
|EpiPen Auto-Injector, 0.3 mg||49502-500-02||6GM088||October 2017|
|EpiPen Auto-Injector, 0.3 mg||49502-500-02||6GM199||October 2017|
|EpiPen Auto-Injector, 0.3 mg||49502-500-02||6GM091||October 2017|
|EpiPen Auto-Injector, 0.3 mg||49502-500-02||6GM198||October 2017|
|EpiPen Auto-Injector, 0.3 mg||49502-500-02||6GM087||October 2017|
- Completing and submitting the report online at www.fda.gov/medwatch/report.htm, or
- Downloading and completing the form, then submitting it via fax at 800-FDA-0178.
There is much interest in wheat sensitivity in people without celiac disease, many of these patients have been labeled with nonceliac wheat sensitivity. Little is known about any risks associated with nonceliac wheat sensitivity. A recent study published in the journal of Gastroenterology evaluated autoimmune diseases in patients with nonceliac wheat sensitivity and investigated whether they carry the autoimmune antibody (ANA). The study looked at patients who were given the diagnosis of nonceliac wheat sensitivity, celiac disease and control subjects. The ANA (autoimmune antibody) was measured in 3 groups. The authors concluded from the study that significantly higher proportions of patients with nonceliac wheat sensitivity or celiac disease have autoimmune disorders with positive ANA’s. This data provides physicians with an awareness that patients with nonceliac wheat sensitivity might have an increased risk of autoimmune diseases. Nonceliac wheat sensitivity remains a not well defined clinical condition. In fact there are some doubts about whether it is a real diagnosis. This study showed a higher frequency of autoimmune diseases, in particular thyroiditis, psoriasis and type 1 diabetes mellitus were reported. Allergists see many patients who are concerned regarding gluten allergy, many patients may in fact have nonceliac wheat sensitivity. This is relatively new diagnosis that there is not much information about. These are patients who do not have celiac disease or wheat allergy, but do have problems with eating gluten and/or wheat. Although allergy testing may be negative for these patients, this study shows that patients with nonceliac wheat sensitivity may have some autoimmune issues. There is still a lot to learn about nonceliac wheat sensitivity and as more studies come out we will learn more about it. Celiac disease has been in the news a lot recently http://allergylosangeles.com/allergy-blog/gluten-free-in-the-news/ As always speak to your doctor about any concerns that you have regarding gluten or wheat.
Consensus Communication on Early Peanut Introduction and the Prevention of Peanut Allergy in High-Risk Infants On behalf of American Academy of Asthma Allergy and Immunology, American Academy of Pediatrics, American College of Allergy, Asthma & Immunology, Australasian Society of Clinical Immunology and Allergy, Canadian Society of Allergy & Clinical Immunology, European Academy of Allergy and Clinical Immunology, the Israel Association of Allergy and Clinical Immunology, the Japanese Society for Allergology, Society for Pediatric Research, and the World Allergy Organization Introduction and Rationale Peanut allergy is an increasingly troubling global health problem, which affects between 1-3% of children in many westernized countries. Although multiple methods of measurement have been used and specific estimates differ, there appears to be a sudden increase in the number of cases in the past 10 – 15 year period, suggesting that the prevalence may have tripled in some countries, such as the USA. Extrapolating the currently estimated prevalence, this translates to nearly 100,000 new cases annually (in the USA and UK), affecting some 1 in 50 primary school-aged children in the USA, Canada, UK, and Australia. A similar rise in incidence is now being noted in developing countries such as Ghana.1-6 The purpose of this brief communication is to highlight emerging evidence to existing guidelines regarding potential benefits of supporting early, rather than delayed, peanut introduction during the period of complementary food introduction in infants. The recent study, entitled “Randomized Trial of Peanut Consumption in Infants at Risk for Peanut Allergy (Learning Early About Peanut – LEAP Trial),” demonstrated a successful 11% – 25% absolute reduction in the risk of developing peanut allergy in high-risk infants (and a relative risk reduction of up to 80%) if peanut was introduced between 4 and 11 months of age. In light of the significance of these findings, this document serves to better inform the decision-making process for healthcare providers regarding such potential benefits of early peanut introduction. More formal guidelines regarding early-life, complementary feeding practices and the risk of allergy development will follow in the next year from NIAID-sponsored Working Group and EAACI, and thus this document should be considered as interim guidance. Summary of New Evidence In the LEAP trial, 640 high-risk UK infants (See Textbox 1) between the ages of 4 to 11 months were randomized to consume peanut products at least three times a week (6 g of peanut protein; equivalent to 24 peanuts or 6 teaspoons of peanut butter per week) or to completely avoid peanut products for the first five years of life. This included 542 infants found to have negative skin prick tests (SPT) to peanut at study entry, and 98 infants with SPT wheal diameters to peanut between 1 to 4 mm (minimally SPT positive) at study entry. An additional 76 children were excluded from study entry prior to randomization based on SPT > 5mm, which was assumed to have a very high likelihood of reacting to a peanut challenge. In an Intention-To-Treat (ITT) analysis, 17.2% in the peanut avoidance group compared to 3.2% in the peanut consumption group developed food challenge-proven peanut allergy by age 5 years, corresponding to a 14% absolute risk reduction, a number needed to treat (NNT, e.g. number of persons needed to be treated for one to receive benefit) of 7.1, and a relative risk reduction of 80%.7 When examined in further detail, the isolated beneficial effects for both the primary and secondary prevention of peanut allergy translated to a NNT = 8.5 within the SPT negative and NNT = 4 within the minimally SPT positive infants. Secondary analyses also showed similar levels of prevention in White, Black and Asian (Indian and Pakistani) children. Overall, the risk of early introduction in this group was low– 7 of the 319 children randomized to the consumption group reacted to peanut at the baseline food challenge suggesting that peanut food challenges and introduction, even in minimally SPT positive infants, is safe and feasible. Six children in the consumption group developed peanut allergy during the study indicating that peanut allergy can still develop despite attempts at primary and secondary prevention. Finally, the LEAP trial only included high-risk infants with a minimal or negative SPT to peanut, and therefore does not address a strategy for those without these risk factors for developing peanut allergy.7 How Does The LEAP Trial Affect Present Guidance for Early Complementary Feeding Practices? Existing guidelines pertaining to the early introduction of complementary foods have indicated that the introduction of highly allergenic foods, such as peanut, need not be delayed past 4 or 6 months of life. However, they do not actively recommend introduction of peanut between 4 – 6 months of age in high-risk infants, and some of these guidelines specify that those infants considered at risk for the development of allergic disease are strongly recommended to first consult an expert.8-14 The LEAP data provide Level 1 evidence that the practice of early peanut introduction is safe and effective in selected high-risk infants. This study is the first prospective, randomized trial of early peanut intervention, and informs provider decision-making regarding high-risk infants, including those already with a positive peanut SPT but not yet clinically reactive, to receive the benefits noted in the LEAP study, which may reduce the risk of developing peanut allergy up to 80%. Of note, since children with lesser risk factors for peanut allergy were excluded from enrollment in LEAP, there are no prospective, randomized data investigating the benefit or risk of early peanut introduction in the general to low-risk populations. However, multiple guidelines have not recommended delaying allergen introduction in these populations. On this basis, this communication is limited to helping integrate the findings learned in the LEAP trial to other similar high-risk children in more diverse settings internationally. Interim Guidance Regarding Early Peanut Introduction Based on data generated in the LEAP trial and existing guidelines, the following interim guidance is suggested to assist the clinical decision-making of healthcare providers: There is now scientific evidence (Level 1 evidence from a randomized controlled trial) that healthcare providers should recommend introducing peanut-containing products into the diet of “high-risk” infants early on in life (between 4 – 11 months of age) in countries where peanut allergy is prevalent, since delaying the introduction of peanut may be associated with an increased risk of developing peanut allergy. Infants with early-onset atopic disease, such as severe eczema, or egg allergy in the first 4-6 months of life (see Text Box 1 for example LEAP criteria), may benefit from evaluation by an allergist or physician trained in management of allergic diseases in this age group to diagnose any food allergy and assist in implementing these suggestions regarding the appropriateness of early peanut introduction. Evaluation of such patients may consist of performing peanut skin testing and/or in- office observed peanut ingestion, as deemed appropriate following discussion with the family. The clinician may perform an observed peanut challenge for those with evidence of a positive peanut skin test to determine if they are clinically reactive before initiating at-home peanut introduction. Both such strategies were used in the LEAP study protocol. Adherence in the LEAP trial was excellent (92%) with infants randomized to consume peanut ingesting a median of 7.7 g peanut protein (interquartile range: 6.7 – 8.8 g)/week during the first 2 years of the trial compared to a median of 0 g in the avoidance group (see Text Box 2 for examples of peanut-containing foods utilized in the LEAP trial). While the outcome of the LEAP regimen was excellent, the study does not address use of alternative doses of peanut protein, minimal length of treatment necessary to induce the tolerogenic effect, or potential risks of premature discontinuation or sporadic feeding of peanut. Rationale for evaluating and applying this policy to a high-risk population The LEAP study demonstrates that early peanut introduction can be successfully carried-out in a high-risk population (such as the population defined in the LEAP trial). However, without intervention by healthcare providers, there is the potential that such high-risk infants will remain at risk for delayed introduction of solids and allergenic foods into their diet because of the widespread belief that such foods may exacerbate eczema. Future more extensive guidelines will be forthcoming from the NIAID Working Group and EAACI Guidelines Group with their multidisciplinary stakeholders. These groups will consider all the available data and determine whether there is sufficient evidence to apply prevention strategies to the general population. However, engagement of the primary care, allergy and dermatology communities to rapidly implement these findings and change the culture of early feeding practices is essential, and the forthcoming NIAID Working Group’s and EAACI Guidelines Group’s documents will better clarify a best-practices approach. Acknowledgements: Primary Contributors: (AAAAI) David Fleischer, MD; (AAP) Scott Sicherer, MD; (ACAAI) Matthew Greenhawt, MD; (ASCIA) Dianne Campbell, MB BS FRACP PhD; (CSACI) Edmond Chan, MD; (EAACI) Antonella Muraro, MD, PhD & Susanne Halken, MD; (ISACI) Yitzhak Katz, MD; (JSA) Motohiro Ebisawa, MD, PhD; (SPD) Lawrence Eichenfield, MD; (WAO) and Hugh Sampson, MD. LEAP Study Team: Gideon Lack, MD, (WAO); George duToit, MD; and Graham Roberts, MD (EAACI); and Tee Bahnson, PhD, (Rho, Inc). Secondary Contributors: (AAAAI) Jonathan Hourihane, MD, Jonathan Spergel & Michael Young, MD; (ACAAI) Amal As’aad, MD; (ASCIA) Katrina Allen, BMedSc MB BS FRACP PhD & Susan Prescott, BMedSc MB BS FRACP PhD; (CSACI) Sandeep Kapur, MD; (JSA) Hirohisa Saito, MD, PhD; (EAACI) Ioana Agache, MD, Cezmi Akdis, MD, PhD, Hasan Arshad, MD, Kirsten Beyer, MD, Anthony Dubois, MD, Philippe Eigenmann, MD, Monserrat Fernandez-Rivas, MD, Kate Grimshaw, Karin Hoffman –Sommergruber, PhD, Arne Host, MD, Susanne Lau MD, Liam Mahoney, MD, Clare Mills, PhD, Nikos Papadopoulos, MD; (ISACI) Nancy Agmon- Levin, MD, and Aharon Kessel , MD; (SPD) Richard Antaya, MD, Beth Drolet, MD; (WAO) Lanny Rosenwasser, MD. References 1. Nwaru BI, Hickstein L, Panesar SS, et al. The epidemiology of food allergy in Europe: a systematic review and meta-analysis. Allergy 2014;69:62-75. 2. Osborne NJ, Koplin JJ, Martin PE, Gurrin LC, Lowe AJ, Matheson MC, et al. Prevalence of challenge- proven IgE-mediated food allergy using population-based sampling and predetermined challenge criteria in infants. J Allergy Clin Immunol. 2011;127:668-76. 3. Venter C, Hasan Arshad S, Grundy J, et al. Time trends in the prevalence of peanut allergy: three cohorts of children from the same geographical location in the UK. Allergy 2010;65:103-8. 4. Sicherer SH, Muñoz-Furlong A, Godbold JH, Sampson HA. US prevalence of self-reported peanut, tree nut, and sesame allergy: 11-year follow-up. J Allergy Clin Immunol 2010;125:1322-6. 5. Soller L, Ben-Shoshan M, Harrington DW, Fragapane J, Joseph L, St Pierre Y, et al. Overall prevalence of self-reported food allergy in Canada. J Allergy Clin Immunol. 2012;130:986-8. 6. Amoah AS, Obeng BB, Larbi IA, Versteeg SA, Aryeetey Y, Akkerdaas JH, et al. Peanut-specific IgE antibodies in asymptomatic Ghanaian children possibly caused by carbohydrate determinant cross- reactivity. J Allergy Clin Immunol 2013;132: 639-47. 7. DuToit G, Roberts G, Sayre PH, Bahnson HT, Radulovic S, Santos AF et al. Randomized trial of peanut consumption in infants at risk for peanut allergy. N Engl J Med 2015; 372:803-813 8. Greer FR, Sicherer SH, Burks AW; Effects of early nutritional interventions on the development of atopic disease in infants and children: the role of maternal dietary restriction, breastfeeding, timing of introduction of complementary foods, and hydrolyzed formulas. Pediatrics 2008: 121: 183-91 9. Muraro A, Halken S, Arshad SH, Beyer K, Dubois AE, Du Toit G, et al. EAACI food allergy and anaphylaxis guidelines. Primary prevention of food allergy. Allergy 2014; 69: 590-601 10. de Silva D, Geromi M, Halken S, Host A, Panesar SS, Muraro A, et al. Primary prevention of food allergy in children and adults: systematic review. Allergy 2014; 69: 581-9 11. Fleischer DM, Spergel JM, Assa’ad AH, Pongracic JA. Primary prevention of allergic diseases through nutritional interventions; J Allergy Clin immunol Pract 2013; 1: 29-36. 12. Chan ES, Cummings C; Canadian Paediatric Society, Community Paediatrics Committee and Allergy Section. Dietary exposures and allergy prevention in high-risk infants: A joint statement with the Canadian Society of Allergy and Clinical Immunology. Paediatr Child Health. 2013;18:545-54 13. Agostoni C, Decsi T, Fewtrell M, Goulet O, Kolacek S, Koletzko B, Et al. Complementary feeding: a commentary by the ESPGHAN committee on nutrition. J Pediatr Gastroenterol Nutr 2008; 46: 99-110 14. Australasian Society of Clinical Immunology and Allergy (ASCIA). [Internet] ASCIA Infant Feeding Advice: Available from URL: http://www.allergy.org.au/images/stories/aer/infobulletins/2010pdf/ASCIA_Infant_Feeding_Advice_2010. pdf. (Accessed April 2, 2015) Text Box 1: Enrollment Criteria Used in the LEAP Study Infants considered at “high risk” as defined by the LEAP study criteria: Egg allergy: Children with either – 1) a SPT wheal diameter ≥6 mm from exposure to raw hen’s egg white and no history of previous egg tolerance, or 2) a SPT wheal diameter ≥3 mm from exposure to pasteurized hen’s egg white and allergic symptoms related to exposure to hen’s egg. Severe eczema: An eczematous rash that – 1) requires the application of topical creams and/or ointments containing corticosteroids or calcineurin inhibitors, and if the participant is <6 months of age, lasted for at least 12 out of 30 days on two occasions, or if >6 months of age, lasted for at least 12 out of 30 days on two occasions in the last 6 months, or 2) is currently or was previously graded ≥ 40 using the modified SCORAD evaluation Example of method of skin prick testing: used in the LEAP study • Skin prick test to peanut extract done in the presence of a negative control and a positive histamine control. • Skin prick testing should be performed in duplicate and the maximum wheal diameter of the two skin prick tests should be calculated and rounded up to the greatest whole millimeter Of note, in the LEAP trial, the use of IgE measurement to peanut resulted in considerably higher rates of sensitization compared to skin testing, which could lead to numerous unnecessary oral peanut challenges. Text Box 2: Examples of Peanut-containing Foods Utilized in the LEAP Trial Smooth peanut butter (2 teaspoons) mixed with milk or with mashed or pureed fruit *Bamba® snack (Osem; ~2/3’s of 1 oz. (25 g) bag; 21 sticks of Bamba®) – for young infants (<7 months), softened with 20 – 30 ml water or milk and mixed with milk or with mashed or pureed fruit or vegetables Peanut soup Finely ground peanuts mixed into other foods such as yoghurt (*Other foods more customary to particular nations/cultures may be substituted) Whole peanut is not recommended for introduction as this is a choking hazard in children under the age of 4.
A recent abstract promoted at the American Thoracic Society meeting on the topic of children with asthma being prone to peanut sensitization. The authors suggest children who do have asthma are more likely to be sensitive to peanuts and therefore kids with asthma should be tested for peanut allergy. This abstract was received with a lot of controversy. If there is no clinical history of peanut allergy in a child that has asthma, no there is no indication to test for peanut allergy, but environmental testing may be helpful. There is no evidence in diagnosing peanut allergy helps treat asthma. Chronic asthma is not a manifestation of peanut allergy or peanut sensitization. The diagnosis of food allergy results in symptoms of cough, wheezing, hives, swelling, vomiting etc. Without a history of this, food testing is not indicated. These reactions usually occur within 2 hours after ingesting a food, and usually it occurs much sooner. Besides peanuts, the most common food allergies are tree nuts, shellfish, fish, wheat, milk, soy and eggs. Chronic and poorly uncontrolled asthma is not a result of a hidden food (peanut) allergy. There is no reason to do food allergy testing in these patients unless the clinical history indicates it as above. But asthmatic children who have asthma could benefit from inhalant (environmental testing). i.e. pollen, animal dander, dust mites. Food allergy testing from a blood test or a skin test is insufficient to diagnose a food allergy. Many patients on food testing show up positive to a food and there is no clinical history after eating the food in question. Positive food testing results should always be interpreted with a clinical history. If a patient has no history of any allergic reactions after eating a certain food, then allergy testing for that food is not necessary. While children who have food allergy have a higher risk of asthma, and children who have asthma have a higher risk of food allergies, food allergy testing every asthmatic child is not indicated. What is more worthwhile is environmental allergy testing. Many children with asthma are triggered by allergens in the environmental such as trees, grass, weeds, dust mite, molds, dogs and cats. Knowing which inhalant allergens a child is allergic to can help manage asthma. So in conclusion if your child has asthma it is not necessary to do allergy tests for foods (especially peanut), but allergy testing for inhalant allergens is actually more beneficial. Your local allergy doctor or allergist can perform allergy testing in the office for you. ORIGINAL TEXT AVAILABLE AT http://allergylosangeles.com
The hygiene hypothesis is the most common theory for increased food allergy. It begins with a lack of early childhood exposure to infections. Without proper stimuli the immune system does not receive necessary education. When presented with food proteins, the normal response (tolerance) is replaced by hypersensitivity. A recent article, in the early edition of Proceedings of the National Academy of Science*, adds further support for a revised hygiene hypothesis, with emphasis on symbiotic microorganisms living in the gastrointestinal tract. The authors identified a common bacteria found in the gut (aka probiotic) that may prevent development of food allergy, specifically peanut. Much research is needed but here is another potential pathway to a cure for peanut allergy.
A new diagnosis of food allergy is life-changing. The questions are endless. I am putting together a new section on the website for parents and patients with food allergy, new and old. I will include links, recipes, diet sheets and school forms. If you have a valuable resource that you would like to share, please let me know. Check it out.
Eosinophilic esophagitis (EoE) is an inflammatory condition affecting the esophagus (the tube that connects the throat with the stomach). The esophagus contains too high a number of eosinophils, an allergic white blood cell. This causes several gastrointestinal symptoms, including difficulty swallowing, nausea,vomiting and reflux. Diagnosis: To confirm the diagnosis requires an upper endoscopy and biopsy. Unfortunately, no less invasive procedures are available to diagnose or monitor EoE. The Role of Allergies: The majority of individuals with EoE have family histories of allergies and symptoms of one or more allergic disorders such as asthma, nasal allergies, atopic dermatitis or food allergy. Food allergy is a major cause of EoE in children, and a less probable factor in adult EoE. Environmental allergies such as dust mites, animals, pollens and molds may also play a role. Treatment of EE: – Diet. Avoidance of common allergens (milk, egg, soy, wheat, nuts and fish) may eliminate the symptoms and underlying inflammation of EoE. Atopy patch testing may help to guide food choices. – Medications. Steroids are effective at shutting down inflammation and eosinophil production. Local delivery helps to lessen side effects. This is achieved by swallowing those steroids indicated for asthma (either a fluticasone inhaler or budesonide for the nebulizer machine). The initial diagnosis of EoE can be overwhelming. Working closely with your healthcare team is the best way to assure you are receiving proper care. Additionally, families often benefit from participation in support groups, such as the American Partnership for Eosinophilic Disorders (APFED) at www.apfed.org.
Probiotics are defined as live microorganisms which when administered in adequate amounts confer a health benefit (FAO/WHO 2002). The potential benefits include inhibition of pathogens, improved integrity of the gastrointestinal (GI) barrier and enhanced immune responses. These effects may be useful for the prevention and treatment of multiple allergic conditions. Rationale: – Allergies occur more in developed nations. The hygiene hypothesis states that a highly sanitized environment provides insufficient bacterial stimulation at a young age. Without proper ‘training’ the immune system is unable to distinguish harmful bacteria from healthy foods (tolerance). – As we get older, the GI associated immune system continues to play an important role. Unfortunately, the composition of gut microbiota can be altered by diet, stress, aging, antibiotics or infection. – The composition and diversity of intestinal microbiota varies in allergic versus non-allergic children. – Children born via vaginal delivery are less likely to have allergies than those children born via c-section. Exposure to beneficial bacteria in the maternal vaginal tract helps to colonize the child. Also, this benefit may occur in those children who are breast fed. Evidence: – The effectiveness of probiotics for the prevention and treatment of allergies is controversial. There are a large number of published studies with a wide range of results. Several studies show a great benefit and several studies show no benefit at all. – The variable results are likely the result of variable protocols. The strain of bacteria, the amount of bacteria and the age of the patient are important factors in determining outcome. It is likely that different strains produce different immunologic effects leading to different outcomes. One probiotic may help asthma and another may help eczema. Examples of beneficial probiotics include, Lactobacillus rhamnosus HN001 and Bifidobacterium longum BB536. – Eczema (atopic dermatitis). Probiotics have shown value for preventing eczema when given to expecting mothers. Probiotics have shown value for treating eczema when given to young children. – Allergic rhinitis (sneezing). Several studies from Japan have shown decreased allergy symptoms for patients with tree pollen allergy. – Food allergy. Infant formulas supplemented with probiotics may improve the symptoms of milk allergic colitis. Unfortunately, supplementation did not accelerate cow’s milk tolerance in those infants with milk allergy. Conclusion: Probiotics may be a useful adjunct in the fight against allergic disease. They provide a natural way to stimulate the immune system. Most importantly, proper timing may prevent future allergies. Further research is needed to determine which strains are useful and when they should be taken.