anaphylaxis

Eczema and Food Allergies: To Eat or Not to Eat–Is that the Question?

November 17, 2017 By Admin

Peter A. Lio, MD

**Do I dare to eat something that might make my skin flare?**

It is written that Hippocrates, father of modern medicine, once said: “Let food be thy medicine and medicine be thy food.” There is deep wisdom in this sentiment and many have suggested that diet is the key to atopic dermatitis. The truth, unfortunately, seems a little bit more complicated.

Despite heroic leaps in scientific understanding of the disease, the fundamental cause of atopic dermatitis (AD) remains obscure. That said, we certainly have some new ideas about what causes it, and have probably learned more in the past 10 years than in the past 10,000. Beyond a better understanding of the type of inflammation and immune system issues, we have discovered a great deal about the role of the skin barrier. In particular, a protein called “filaggrin” explains a lot about why patients might develop AD in the first place, but also—possibly—why they develop other types of allergies, including food allergies. [Dennin M] This protein, or more precisely the lack of it, leads to a condition that I like to refer to as “leaky skin”. Similar to the “leaky gut” phenomenon that is increasingly discussed in some alternative medicine circles, the idea here is that lacking normal filaggrin due to a gene mutation can lead to a weakened skin barrier that allows for water to leak out and allergens, irritants, and even infections to sneak in. This is not just speculation: there is good evidence that having leaky skin really does lead to AD. [Dennin M] And abnormal filaggrin is probably just one of many factors that can lead to leaky skin. And, in a way, this is compelling in its own right: if you trace your skin as it rounds the lips, it becomes the lining of the digestive tract! It does not seem so strange that leaky gut inside correlates with leaky skin outside. While there are still many details to work out, this basic understanding has led to something of a revolution in thinking about AD and has important implications for the connection between foods and AD as well.

Root Cause?

Many families in my practice have felt strongly that food is the “root cause” of the disease. And this does not appear to be an anomaly: in one study, parents had manipulated the diet in children with AD in some 75% of cases in an attempt to control it. [Johnston GA] This thinking is not new. In fact, a paper from the British Medical Journal from way back in 1830 said this about the relationship between food and atopic dermatitis: “There is probably no subject in which more deeply rooted convictions have been held…as regards the causation and treatment of the latter…”[Mackenzie, 1830]

And there are some good reasons for this. Most importantly, there is a clear association between AD and food allergies. Real, verifiable, and often dangerous food allergies are much more common in AD, and probably occur in up to a third of patients with eczema. [Schneider L] Undoubtedly, if someone with AD eats a food that he or she is allergic to, the resulting hives and itching could cause a flare up of the eczema—that makes perfect sense. And many providers still stress this idea: in order to avoid triggers for an eczema flare, we also must consider foods.

Now, here comes the hard part: the kind of food allergies we’re talking about here are fairly easy to test for and usually cause a clear clinical pattern: almost immediate hives, swelling, and itching, vomiting, diarrhea, and sometimes progressing to more severe angioedema and even anaphylaxis. So, if someone has a true food allergy, it may well cause an eczema flare, but that’s usually the least of their worries! They would have much more powerful and urgent issues almost universally. Because of this clear relationship, what we’re focusing on here are the situations where people suspect that this is some hidden food in the diet that are causing the eczema.

This situation might be called an “eczematous food reaction.” They certainly exist and there is no doubt that some patients over the years have found a food or foods driving all or almost all of their skin disease. So, while it is certainly possible, it is also important to note that there are some people that have fallen from an airplane without a parachute and survived just fine [Wikipedia]. But… I would not recommend trying that out! In other words: just because something can happen does not make it likely.

Such an extreme example is not very helpful. How common (or uncommon) is it? That is a useful question to answer as it could be worth investigating foods even if it is only a small percentage of patients: the risks and costs are fairly low but the potential benefits are very compelling: to be cured or even better just by avoiding certain foods is an almost irresistible concept!

Testing the Connection in a Controlled Environment

To get better insight, it is worth closely examining a study by Dr. Jon Hanifin’s group to address this issue. In this study, children with severe, refractory atopic dermatitis were admitted to the hospital where they could have strict dietary control. [Rowlands 2006] The patients were in air-conditioned, low-allergen environments and placed on a “rare foods” diet—foods rarely consumed and rarely allergenic—consisting of lamb or turkey, rice, rare fruits and vegetables. After 2 days of topical therapy to decrease inflamed skin, food challenges were conducted and patients were observed carefully for 5-7 days. Notably, this is very different than a prick test which looks for immediate reactions (within minutes) or a blood test that generally is looking for the same type of reactions. By observing the patients for days, this study could capture both types of reactions. The challenges consisted of foods like milk, wheat, egg, and soy (very common allergens and difficult to avoid completely), as well as other common foods such as chicken, pork, beef, fish, and various other common vegetables. Seafood and nuts which are common causes of anaphylaxis and generally not considered essential for a balanced diet were not tested.

In the 17 children hospitalized and food challenged in the study, a total of 91 food challenges were performed. One patient developed an eczematous reaction to milk that occurred within 30 minutes. A repeat challenge was also positive, but prior skin prick testing was negative to milk, suggesting that this was the real deal: a true eczematous food reaction! But that was about it. Essentially all of the other tests to eggs, wheat, soy, various meats, fish, vegetables, potatoes, and citrus were negative (with the exception that the same patient with the milk reaction also had a reaction to chicken). And this was in a very select group of patients, most prone to food allergy, and most likely to have something driving their severe disease. [Rowlands 2006]

It is important to stress that some of these patients had a known food allergy to things like peanuts or seafood—these were not tested for the reasons we discussed above: they cause a very different type of allergy and were strictly avoided by the families so were clearly not playing a role in the eczema.

So if the foods are usually not the cause of the eczema, what is the relationship between them? That remains an extremely compelling question that is still being worked out. But, perhaps the biggest breakthrough came in 2015 with the publication of the “Learning Early about Peanut Allergy (LEAP) study. [Du Toit, 2015] In this landmark study, the notion that peanut allergy is rare in countries where peanuts are introduced early, and that telling families to hold off on introducing peanuts until later might actually be causing the allergy was tested. Importantly, it worked really well: giving infants peanut-containing foods seemed to decrease the risk of peanut allergy significantly! What was perhaps even more interesting was the connection between eczema and peanut allergy. The idea put forth was somewhat revolutionary: “…early environmental exposure (through the skin) to peanut may account for early sensitization, whereas early oral exposure may lead to immune tolerance.” [Du Toit, 2015] This concept—that leaky skin could actually lead to developing food allergies—turns the whole thing upside down. Instead of looking for foods that are causing the eczema, it sounds like we need to stop the eczema (and its associated leaky skin) in order to prevent the food allergies!

Sealing the Skin

This is still somewhat speculative, but has been borne out in one other very tantalizing way: there are now studies that suggest simply moisturizing the skin from birth can actually prevent eczema and possibly even food allergy! [Horimukai 2014 and Simpson 2010] This supports the concept that leaky skin may be the doorway for all of these conditions to develop and that by “sealing up” the leaky skin moisturizers and perhaps supplements to help strengthen the skin, we can actually prevent the cascade of events that leads to atopic dermatitis and food allergies. This is incredibly exciting as the possibility of prevention has tremendous ramifications in both quality of life and cost to both patients and the healthcare system. [Xu 2017]

But why not try it? What harm can there be to at least see if it is a food, however rare that may be? There are two main issues that I worry about. The first is more practical: while we are working to find a potential food driving the disease, sometimes people are not doing any other treatments so as not to complicate things. For an adult this is fine, I suppose, but especially in a child I hate to see someone suffering with itch, poor sleep, and sometimes even infections and pain while we’re searching for a proverbial needle in a haystack… especially one that might not even be there. The second is more insidious: I have had the unfortunate experience over the years of working with colleagues who feel strongly that diet is the cause. They feel so strongly that this is the case that they keep pushing the patients to try harder, wait longer, and avoid more foods. It can be a dangerous game. To hear something like: “You’re so close, if we just go another month or two without gluten and dairy, I think you will be cured!” is almost irresistible. But for so many it seems to be false hope, and even a source of guilt for some families. I’ve heard things like: “We really tried our best to keep the diet, but there was a birthday party about 4 months in, and our provider said that the cupcake ruined everything and we would need at least 6 more months…” And there are stories about severe malnutrition and even death from extreme diets, some that seem more like nightmares than reality. [Benny-Morrison 2016]

Which brings us back to that paper from the British Medical Journal in 1830. The paper concluded that in most instances, diet plays an “exceedingly unimportant part in the production and cure of diseases of the skin.” And, nearly 200 years later, the verdict is not too different: looking broadly at all the published studies strongly suggests that elimination diets do not seem to help most patients with AD. [Lim NR] What to do in the meantime? I think we have to do what we have done thus far until we know more, and fortunately we know that getting the skin under better control not only leads to direct improvements in quality of life, but also seems to allay some of the food allergy concerns, suggesting that it is a helpful approach while we learn more about this terrible skin disease. [Thompson 2005]

Peter A. Lio, MD is an Assistant Professor of Clinical Dermatology & Pediatrics at the Northwestern University Feinberg School of Medicine, and a Diplomate of the American Board of Dermatology. Dr. Lio received his medical degree from Harvard Medical School, completed his internship at Boston Children’s Hospital and his dermatology training at Harvard. He served as a full-time faculty at Harvard (Beth Israel & Children’s Hospital Boston) from 2005-2008 before returning home to his native Chicago to join Northwestern and Children’s Memorial Hospital. He is also a trained acupuncturist and a leader in the Chicago integrative health care community.

What Doctors Still Don’t Know About Anaphylaxis

July 27, 2017 By Admin

By Dr. Paul Ehrlich

The British Medical Journal recently published a survey about Russian physicians and anaphylaxis. What they knew and didn’t know should surprise no one.

Surveys containing a clinical scenario pointing to food anaphylaxis went out to 707 physicians and 315 (45%) responded. Sixteen who reported training in allergy-immunology excluded from the analysis, leaving the final sample size of 299. Two-thirds (68%) were pediatricians 32% were other specialties and adult physicians. All told 33% diagnosed anaphylaxis correctly, but only 10% recommended intramuscular injection of adrenalin (English English for epinephrine).

This lack of knowledge is not confined to Russia. While I couldn’t find another survey with the same methodology for the United States, I did come across two that are in the ballpark.

In the United States, a 2012 study of internal medicine residents by a group at North Shore Jewish Health System (by coincidence this is the modern version of the hospital where my father was on staff for pediatrics for decades) surveyed 146 eligible participants, with 55 (38%) participating. 81% had not previously diagnosed anaphylaxis, 75% had not managed, 96% had not used an epinephrine autoinjector, 79% had not demonstrated autoinjector use, and 81% had not referred a patient to an allergist after an anaphylaxis. Only 52% felt confident in their ability to diagnose anaphylaxis, while 40% felt confident in their ability to manage it.

In 2013 the same group surveyed 140 pediatric residents with 61 (44%) responding. They found that 41% had diagnosed anaphylaxis, 67% had managed anaphylaxis, 7% had used an epinephrine autoinjector, 56% had demonstrated how to use an autoinjector, and 56% had referred a patient for further allergy evaluation after an anaphylaxis episode. Just 46% felt confident in their ability to diagnose anaphylaxis, while 49% were confident in their ability to manage it.

Other countries show similar levels of knowledge. In Korea, a single-hospital survey of 1,615 health provides included 128 doctors, along with nurses, students, and “health personnel.” While most of the physicians cited epinephrine as the “drug of choice,” only 48% included epinephrine within the first 3 steps of treatment.

I am intimately familiar with the shortcomings of anaphylaxis knowledge among primary care physicians. That’s why for many years I have hosted a monthly rotation for residents at NYU in my practice. One of these, Dr. Maureen Egan*, reflected on the paucity of training the average resident receives when we interviewed her following a presentation to her fellow residents.

She told us, “I would say that I knew only approximately 10% of the information presented before the allergy elective and 75% of the information I acquired through the rotation. The remaining 15% (which was mostly on the rare disorders) I learned through my reading in preparation for the presentation. You are correct that unless my fellow residents pursue an allergy elective (and many do not) they may not learn these key points. We have very little training in food allergies as part of our core curriculum.”

A few years ago I wrote about the fact that there was no common diagnosis of anaphylaxis for both emergency physicians and allergists, and no agreement on the use of epinephrine. That chasm still has not been bridged.

Too many patients. Not enough allergists. We still have lots of work to do.

*For patients in the Denver area, Maureen is now at Denver Children’s following a fellowship at Mount Sinai.

Food Allergy Urban Myths: Two Experts Separate Fiction from Fact

January 17, 2017 By Admin

By Carina Venter, PhD, RD and David Fleischer, MD

Year after year, despite dramatic gains in research, some misconceptions are remarkably stubborn, both among patients and their doctors. We canvassed our friends in practice and research around the world to compile a list, and there was broad consensus that these are the most prevalent. (See list below of those who helped.)

1. You can’t be allergic to a food that you have not eaten
False:
Sensitization to foods can happen via the skin, particularly in children with eczema(1) During pregnancy, the fetus can be exposed to allergens their mother is eating; during breastfeeding, allergens can be passed to the infant via breast milk(2).

However, allergen avoidance during infancy when children suffer from eczema, or during pregnancy or lactation, does not seem to prevent food allergies. Allergen avoidance during pregnancy and breastfeeding is not advised until we understand the role of dietary intake better. Eating of allergens early in an infant’s life, however, seems to protect against the development of food allergies.

2. You can’t be allergic to rice, and most definitely not to banana or sweet potato!
False: Imagine the difficulties of trying to convince food allergy sceptics that your child is really peanut-allergic. Now try to imagine telling them that your child is allergic to rice! Parents who make this claim are generally met with amused condescension–“No one is allergic to rice!” Unfortunately, many of the allergens involved in food protein-induced enterocolitis syndrome (FPIES) are “atypical” allergens such as rice, sweet potato, and banana(3). (But try to explain FPIES to the average skeptic.) So yes – severe allergic reactions to foods not considered to be part of the top eight allergens are possible.

3. The size of your skin prick test (SPT) or the level of food-specific IgE tests predicts the severity of reactions
False: The size of a SPT or the level of specific IgE to a food indicates the likelihood of being allergic but not the severity of the reaction, i.e., the larger the size of the SPT or the higher the level of serum specific IgE the more likely you may be allergic to that food(4). The reaction history remains the most important indicator.

4. Each allergic reaction to a food becomes subsequently worse
False: There is no evidence to indicate that each allergic reaction becomes worse. Many people who had only mild symptoms in the past, end up with anaphylaxis on subsequent exposure(5). There is however some evidence that a history of anaphylaxis and suffering from eczema or asthma, may increase the risk of anaphylaxis(6).

5. Everyone with food allergy develops anaphylaxis
False: Many people with IgE-mediated food allergies never develop anaphylaxis. There are a number of factors that indicate if a person may develop anaphylaxis, including(5):
– Presentation of the food allergen (e.g. baked or not, fat content*)
– Infections
– Immunological and hormonal factors
– Behavior (e.g. risk taking, alcohol)

6. If you are allergic to one peanut or a tree nut, you need to avoid all nuts
False: Individualized avoidance of nuts should be advised to those with nut allergies – taking into account the family’s preferences/needs. About one-third of patients with peanut allergy may have tree nut allergies. People with certain tree nut allergies often tolerate other tree nuts. The tree nut allergies that most often co-exist are: cashew and pistachio; walnut and pecan, although you can be allergic to one of these but not another(7).

7. My child reacts to corn starch or corn syrup in foods (most often corn syrup in infant formula)
False: Although we can find no studies to reference, personal discussions with food scientists confirm that there are only trace amounts of protein left in corn starch and undetectable amounts in corn syrup, glucose syrup, dextrose (granular) or high fructose corn syrup. Many years of clinical practice, using these products in corn-allergic individuals, have reassured us that they are perfectly safe to use from an allergy point of view, although added sugar presents other problems.

8. I tolerate soy/peanut/sesame/tree nut oils
Perhaps true: The processing of oils across the world differs a lot, and even we find it confusing. Check to find out how the oil was produced: refined/expeller/heat-pressed oils, including the big brand names, are safer to eat, but crude/cold-pressed oils are best avoided due to a higher chance of having more residual protein.

9. My/his/her food allergy is not severe as I can eat(or /my child) can eat “trace amounts” of the foods
False: Many people belief that if they have safely eaten a product that states “may contain traces”/”produced in a factory” that they are tolerant of “trace amounts” of the allergen. This is, however, not true. “May contain” is a legalism, not a guarantee that any allergen is present. Most products with some kind of “may contain” warning do not have any detectable contamination, and those that do, contain a range of different amounts. It is also important to remember that some products without a “may contain” warning may contain trace amounts of the allergen(8).

10. Everyone with an allergy needs to avoid even trace amounts of the food
False: We change “strict” avoidance to “individualized” avoidance in every paper we review. We have long passed the times era when all food-allergic individuals have to strictly avoid allergen exposure. We understand that some people can tolerate baked milk and egg(9). Oral and epicutaneous immunotherapies have also made it possible to tolerate allergens, either fully or to some degree(10).

11. A baby/child that who is gaining weight cannot have a food allergy
False: Many infants with food allergies have a normal, perhaps even increased weight, and just referring to the weight to make a diagnosis will lead to a lot of misdiagnosis(11). Picky eating may be a sign that the child is uncomfortable eating certain foods, and parents compensate by relying on fattening foods.

12. Breastfed babies do not develop food allergies
False: Particularly in the case of cow’s milk allergies, where over 40% of babies with milk-induced proctocolitis, a non-IgE-mediated food allergy, are exclusively breastfed.(12)

13. If you do not have IgE-mediated food allergies, it is just an intolerance
False: Although the exact mechanisms of non-IgE/gut-related food allergies are not fully understood, it is clear that the immune system is involved in non-IgE-mediated food allergy; strictly speaking, intolerances are not immune-mediated(13), most prominently lactose intolerance, which results from an enzyme deficiency.

14. Young infants will have false negative SPTs
False: SPT can be performed from any age. SPT of very young infants may be smaller than older children, but there is no lower age limit to perform SPT or food-specific IgE tests(14).

15. IgG tests are reliable to test for food intolerances
False: Our present knowledge regarding IgG indicates that IgG4 is marker of food intake or development of tolerance (it is sometimes difficult to separate the two), but there is no association with IgG to a food and food intolerance to it(15).

* High fat content allows you “tolerate” the allergen to a much higher dose BUT then have very severe reactions once you react – i.e. you miss those initial warning symptoms. Hence using low-fat peanut flour for challenges.(16)

1. du Toit G, Tsakok T, Lack S, Lack G. Prevention of food allergy. J Allergy Clin Immunol. 2016;137(4):998-1010.
2. Pastor-Vargas C, Maroto AS, Diaz-Perales A, Villalba M, Esteban V, Ruiz-Ramos M, et al. Detection of major food allergens in amniotic fluid: initial allergenic encounter during pregnancy. Pediatr Allergy Immunol. 2016.
3. Venter C, Groetch M. Nutritional management of food protein-induced enterocolitis syndrome. Curr Opin Allergy Clin Immunol. 2014;14(3):255-62.
4. Peters RL, Allen KJ, Dharmage SC, Tang ML, Koplin JJ, Ponsonby AL, et al. Skin prick test responses and allergen-specific IgE levels as predictors of peanut, egg, and sesame allergy in infants. J Allergy Clin Immunol. 2013;132(4):874-80.
5. Turner PJ, Baumert JL, Beyer K, Boyle R, Chan CH, Clark A, et al. Can we identify patients at risk of life-threatening allergic reactions to food? Allergy. 2016.
6. Flinn A, Hourihane JO. Allergic reaction to peanuts: can we predict reaction severity in the wild? Curr Allergy Asthma Rep. 2013;13(6):645-50.
7. Brough HA, Turner PJ, Wright T, Fox AT, Taylor SL, Warner JO, et al. Dietary management of peanut and tree nut allergy: what exactly should patients avoid? Clin Exp Allergy. 2015;45(5):859-71.
8. Allen KJ, Remington BC, Baumert JL, Crevel RW, Houben GF, Brooke-Taylor S, et al. Allergen reference doses for precautionary labeling (VITAL 2.0): clinical implications. J Allergy Clin Immunol. 2014;133(1):156-64.
9. Nowak-Wegrzyn A, Groetch M. Nutritional aspects and diets in food allergy. Chem Immunol Allergy. 2015;101:209-20.
10. Nowak-Wegrzyn A, Fiocchi A. Is oral immunotherapy the cure for food allergies? Curr Opin Allergy Clin Immunol. 2010;10(3):214-9.
11. Meyer R, De Koker C, Dziubak R, Venter C, Dominguez-Ortega G, Cutts R, et al. Malnutrition in children with food allergies in the UK. J Hum Nutr Diet. 2014;27(3):227-35.
12. Yilmaz EA, Soyer O, Cavkaytar O, Karaatmaca B, Buyuktiryaki B, Sahiner UM, et al. Characteristics of children with food protein-induced enterocolitis and allergic proctocolitis. Allergy Asthma Proc. 2017;38(1):54-62.
13. Boyce JA, Assa’a A, Burks AW, Jones SM, Sampson HA, Wood RA, et al. Guidelines for the diagnosis and management of food allergy in the United States: summary of the NIAID-Sponsored Expert Panel Report. Nutrition. 2011;27(2):253-67.
14. Bock SA. Diagnostic evaluation. Pediatrics. 2003;111(6 Pt 3):1638-44.
15. Du Toit 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(9):803-13.
16. Grimshaw KE, King RM, Nordlee JA, Hefle SL, Warner JO, Hourihane JO. Presentation of allergen in different food preparations affects the nature of the allergic reaction–a case series. Clin Exp Allergy. 2003 Nov;33(11):1581-5.

Carina Venter, PhD RD, is a Research Associate/Dietitian at Cincinnati Children’s Hospital Medical Center and currently the Chair of the International Network of Dietitians and Nutritionists in Allergy, a member of the AAAAI, BSACI and EAACI. She is a registered dietitian in the United Kingdom, United States and South Africa. She has had numerous publications in international journals, and has authored book chapters and edited a book on Food Hypersensitivity. She was, until recently, working as a Senior Lecturer at the University of Portsmouth, where she was doing research into food allergies and allergy prevention, based at the David Hide Centre on the Isle of Wight.

Carina was a member of the Expert Panel of the National Institutes for Allergy and Infectious Diseases Peanut Allergy Prevention Guidelines, making her the only dietitian to contribute to both US and European food allergy guidelines.

David Fleischer, MD, studied medicine at Emory University School of Medicine. He was a pediatric resident at Johns Hopkins where he also training in Pediatric Allergy/Immunology. He joined the staff of National Jewish Health in Denver in August 2005, where he worked until December 2013. In January 2014, Dr. Fleischer joined the new Allergy Section at Children’s Hospital Colorado (CHCO), where he is currently an Associate Professor of Pediatrics and the University of Colorado Denver School of Medicine.

Dr. Fleischer’s clinical interests include food allergy, eosinophilic gastrointestinal disease, and atopic dermatitis. His research has focused on the natural history of food allergy and novel treatments for food allergy, including oral, sublingual, and epicutaneous immunotherapies. He has been involved in several projects examining the primary prevention of allergy, including as a member of the 2015-16 National Institutes for Allergy and Infectious Diseases (NIAID) Expert Panel that is updating the 2010 NIAID Food Allergy Guidelines on the topic of the Prevention of Peanut Allergy.

Dr. Fleischer has published many peer-reviewed articles, review articles, and book chapters on food allergy and eosinophilic gastrointestinal disease.

{Note, the authors would like to thank those who helped to put their list together: Marion Groetch (USA), Berber Vlieg-Boerstra (The Netherlands), Rosan Meyer (France), Hannah Hunter (UK), Lianne Reeves (UK), Marianne Williams (UK), Paul Turner (UK), Isabel Skypala (UK), Fallon Schultz (USA), Raquel Durban (USA)}

The False Alarm Hypothesis

August 7, 2016 By Admin

Interview with Dr. Peter K. Smith

By Henry Ehrlich

Hypothesis
noun
A supposition or proposed explanation made on the basis of limited evidence as a starting point for further investigation.

For many years, the allergy epidemic has been blamed on the “hygiene hypothesis”–also known as the “pound of dirt theory,” the “farm effect,” and probably many others that add up to the idea that we have removed so many accustomed bacteria and microbes from our environment that our immune systems, lacking their natural prey, go looking for new targets. My own criticism is that it mostly seemed to revolve around how people respond to the word hygiene—from hand sanitizer to overuse of antibiotics. A true hypothesis is testable. The farm effect seems to work with asthma–see our new piece on the Amish study here. But we need a new one for food allergies.

Now we have one. “The False Alarm Hypothesis” comes to us from Dr. Peter K. Smith, Professor of Medicine at Griffith University in Australia, and three co-authors who work at Mount Sinai in New York, Madhan Masilamani, PhD, as well as Dr. Hugh Sampson, and Dr. Xiu-Min Li (both contributors to this website). A few years ago, Dr. Li told me that food allergies and other immune disorders arise from confusion of innate immunity and acquired immunity. A healthy immune system will attack things like cold viruses automatically. They don’t have to learn new skills. Acquired immunity allows the system to respond earlier instead of having to go through a full cycle of inflammation, fever, and other unpleasantness.

Another thing we do without coaching is eliminate cells dying a non-programmed death. After damage from a bruise or a cut, our bodies recognize that cells are dying and get rid of them before they fester and poison us. The cells release molecules called alarmins, which mobilize a response from various protective cells.

Other things chemically mimic that triggering effect and they are found in many common foods. They are called “advanced glycation end products” (AGEs), which bind to their own high-affinity receptors (RAGE) on cells, the way IgE binds to high-affinity receptors on mast cells. They create a chemical SWAT team that isolates and expels the cells before they can infect the surrounding tissue. But when food is the culprit instead of dying tissue, chaos can ensue. When the cat trips your home alarm, you don’t want SWAT to answer the call.

Unfortunately, the things we do to make foods taste better aggravate the problem. It’s that sear on a good steak or the crisp brown skin on a roast chicken, the result of the “Maillard reaction” that caramelizes the natural sugars into something more tasty. It’s roasting peanuts (boiling them makes them less allergenic). Microwaving raw milk for a minute increases AGEs 5-fold and three minutes 86-fold. Fructose, which has become the industrial sweetener of choice over the past generation, is a massive source of AGEs.

We reached out to Dr. Smith to find out more:

AAC: Thanks, Dr. Smith, for taking time with our readers. To start I’d like to ask some questions on how science gets done. First, where did the idea come from? Australia has some of the highest rates of allergies and asthma in the world, and Australians are noted for being avid barbequers. Was there a connection?

PKS: Thanks Henry – actually double thanks: first for the opportunity to discuss this with your readers and secondly, for what you are doing to reach out and explain many aspects of allergy to the wider community. Like you, I am not totally happy with the hygiene, vitamin D and microbiota stories. I think they hold part of the key, but do not explain a several hundred-fold increase in food allergy in the last 2-3 decades in young children. Yes we barbeque and consume sugars to excess in Australia and we have the highest rates of food allergy in the world. We live in a land of milk, honey, steak and “glycotoxins”. The connection actually came to me 4 years ago when looking at plant compounds that modify skin inflammation and I found publications that linked glycation and ageing (and this was accelerated in diabetics). High AGE diets accelerated ageing and diabetic damage (and also several other inflammatory conditions). Dietary AGEs could also mimic cell damage signals (they have a promiscuous receptor). I plotted epidemiological data with dietary patterns and then sought reviews on how AGEs and tissue alarmins work to stimulate the immune system. The more we looked, the more the story was strengthened. It integrates in very well with current theories.

AAC: I am also intrigued by the combination of authors. How did you end up working with a team almost 10,000 miles away?

PKS: Professor Sampson has always been generous with his time, knowledge and friendship. I am intrigued by innate immune responses and how threat signals are propagated. Many of the components of Professor Li’s Chinese herb mixtures have actions on cellular ion channels and we have discussed these for the last 3-4 years. Two years ago when developing the False Alarm Hypothesis – we identified that some plant compounds including isoflavones could block peanut allergy occurring in an animal model. These actually reduce the formation of AGEs. This work was already being done by Dr. Masilamani, and Professors Sampson and Li. They were just not aware of the AGE-RAGE axis yet. It makes great sense to work with people who have established models and are the best in the world and we are continuing to do lab work in this area – I have been over there a few times and we try to have Skype meetings every fortnight. The world is a very small place with IT (and planes) these days.

AAC: Could you describe as simply as possible the basics of how AGEs transform the various cells, both in utero and in newborns. I am particularly interested in the permeability of the digestive system.

PKS: AGEs bind to the same receptor as a couple of key cell damage products (S100 proteins and another called HMGB1) – called the RAGE receptor. This is a key activation switch for the early immune response. It activates the mast cells (a key cell in allergic response and tissue defense) within 20 seconds and this activity is maintained for up to 60 minutes. If there is further stimulation – these cells go on and make products with amplify the response. Dendritic cells (problem spotting cells) require RAGE stimulation to mature and present the problem’s chemical signal to T cells. They start secreting HMGB1 to enhance T cell responses. Others have shown allergic T cells responses are blunted in the absence of RAGE signaling. We hypothesize that alarmins are being copied by our western diet.

The newborn is somewhat of a “blank canvas” immunologically. There are genetic and antenatal environmental stimuli and evidence that maternal IgG passes in utero and via breast milk to influence early immune responses. It is up to the baby to develop tolerance. AGEs can cause tissue inflammation as part of an innate danger response. We need to do work looking specifically at skin and GI permeability and AGEs. Diabetes is a naturally occurring high endogenous AGE producing state – and in late pregnancy, diabetes is associated with increased eczema and food sensitization in infancy. AGEs also pass through in utero and in breast milk. Methygloxal from cigarette smoke is a great example of an AGE that widely disperses through all tissues.

AAC: Since all living tissue is subject to unprogrammed cell death, I am guessing that all parts of the body would be susceptible to respond to false alarms, given the right receptors (RAGE) and exposure to AGEs. Is this correct and does it account for systemic reactions to allergen exposure—aka anaphylaxis?

PKS: Yes – diabetes affects multiple organs– kidney, blood vessels–and disease is also distributed around the body: atherosclerosis, cataracts, skin ageing, Parkinson’s disease and Alzheimer’s. We do have an enzyme called glyoxolase 1 that reduces as we get older – making us more susceptible to damage. This raises the question – why do we not get more allergies with age? I think the acquisition of tolerance helps explain that. We hypothesize that with higher RAGE stimulation – the body looks for the reason why and may falsely react to foods that are present. Genetic and environmental risk factors are likely to feed in. Higher AGE pattern diets have been linked to asthma, rhinitis, and eczema and these are known amplifiers of systemic anaphylaxis responses.

AAC: Do you think mothers with allergies themselves have to be more careful about AGEs? Do you think families with no history of allergies can be pushed in that direction through excessive consumption of AGEs?

PKS: I think we have to stress that this is still a hypothesis. We published this hypothesis and the most relevant data to discuss it. We expect people question it, challenge it, include it in consideration of their analyses of food allergy risk factors, allergies in general, and then look at modifying it. I think we are a good 5 years away from making dietary recommendations. Fortunately, the worse case scenario of this advice is to suggest eating fresh fruit and vegetables, do not fry or microwave meat, use fresh herbs and spices with cooking, reduce excess free sugars you eat, do not over-eat, exercise, don’t smoke, sleep well and try to reduce stress. Make sure you are not vitamin D deficient. All of these appear to influence AGEs or the RAGE receptor. These are pretty common public health messages anyway.

AAC: You mention the rise of food allergies in conjunction with the fast food industry. I am particularly struck by your observation that candy and soft drinks used to be occasional treats and are now everyday items for kids (and adults). Why does fructose, also found in fruit juice, which is supposed to be good for us, make such a difference? What does McDonalds have to do with the food allergy epidemic?

PKS: McDonalds is not the cause; it just is an indicator of the foods consumed and patterns of eating (too much in calories, less fiber, more fried foods and more sugar). Fructose consumption – as pointed out in the paper – has risen several hundred fold in the last 30 years. This sugar is a fast track substrate to a nasty AGE called methygloxal. Having more fructose than we can deal with results in more AGEs being made. When did eating candy and having soda every day become normal? Cheaper fructose as a sweetener may have something to do with certain crops being subsidized commodities, particularly corn. Fiber in foods helps us excrete some dietary and bacterial AGEs. Orange juice (fresh) actually seemed to be protective for asthma in US children. However, juice as a food actually does not make much sense – it gives a rush of fruit sugars without all the chewing to stimulate salivary and digestive enzymes or the time it takes to consume intact fiber and provide satiety. Try eating 1 raw carrot – this will fill you more than 3 that are juiced and your fructose rise will be far less and drop again with a single chewed carrot. It is the spikes that cause more AGEs to be formed. Our bodies just have not evolved to process the levels of sugar and ultra-heated meats we see in contemporary diets. Our dietary and lifestyle trends have diverged from evolution and we think our bodies are responding to them as if we are in crisis. Alarms (and alarmins) go off and the troops arrive.

AAC: One characteristic of a useful hypothesis is that it should be testable. It’s the difference between a circumstantial case and an evidentiary case. It appears to me that evidence can be gathered to support the False Alarm, such as the experiment on mice without the receptor. What are the next steps?

PKS: Yes – there are knock out mice – they do not develop as strong allergic inhalant allergy responses. As mentioned, some plant compounds that reduce AGEs being formed have been shown to reduce peanut allergy. We are developing in-vivo and in-vitro models. We do need a solid funding injection to cover research.

AAC: Everyone who spends time with food allergy mothers hears the question, “what did I do wrong?” Does your hypothesis give them one more thing to regret? What would the basics be of a low AGE diet?

PKS: The Mediterranean diet and Asian traditional diets are really quite low AGE diets. The have lots of herbs and spices – fresh is better. If you want meat – marinate it in lemon, garlic and herbs – and slow cook. Use fresh vegetables. Bacon is really high in AGE as are grilled cheese and French fries. If you want the browning as flavoring, do this with the occasional vegetable rather than meat (hold back on the fries though). Use your microwave for vegetables rather than high-protein foods. Reheating in the microwave amplifies AGE formation. Avoid soft drinks and snacking on candy. Rice is a great food to feed children. It is low glycaemic and has some anti-inflammatory compounds. I would love to see more of this instead of apple juice in infants’ diets. Bad bacteria produce more AGEs – and there is also convergence of signaling with RAGE and Toll receptors to signal threat. The RAGE receptor tends to increase if vitamin D is low, and it also coincides with being overweight, if you are stressed, do not sleep well, or are not exercising.

Life balance is also about context and the journey. Enjoy it all, including food, but now armed with knowledge (and a hypothesis) – eat sensibly. When I share a meal with an AGE expert I notice that many do eat meats, but not in large amounts, not char-grilled and they mix it with herbs, spices and fiber (not French fries). They tend not to finish off meals with a large dessert. We all should enjoy treats but not every day – (or several times a day).

AAC: Thank you very much for your time.

PKS: Pleasure. I hope this invokes discussion and more research. If this provokes any funding interest, please direct it towards Professor Li at Mt Sinai in New York and I hope this can progress answers sooner in their world-leading, established food allergy models.

Pete Smith is a Professor in Clinical Medicine at Griffith University in Queensland Australia. He trained in Pediatrics and did his PhD in molecular immunology at Flinders University South Australia and has worked as a Senior Lecturer at the Institute of Child Health London and an Honorary Consultant in Allergy at Great Ormond St Hospital London. He consults in Clinical Medicine in Southport Queensland and is Medical Director of Allergy Medical Group in Brisbane and Sydney. Current research includes AGEs and allergy, molecular ion channels in hypersensitivity and allergy, molecular activation pathways in allergic rhinitis and clinical studies in food allergy and rhinitis.

Biphasic Reactions Not a Big Factor for Food Challenges

February 5, 2016 By Admin

In the December 2015 issue of Annals of Allergy Asthma and immunology, I saw a letter written in response to an earlier article called “Epidemiological and Clinical Predictors of Biphasic Reactions in Children With Anaphylaxis”, which had somehow escaped my eagle eye. The original article said that about 15% of children experiencing anaphylaxis who went to the emergency department had biphasic reactions, that is delayed reactions that may occur up to 72 hours after the initial event, urging EDs to prolong observation to a minimum of six hours after even mild reactions. The letter writers said, “The authors [of the original piece] did not discuss the reactions after observed exposure to allergenic foods, such as those exposures during oral food challenges (OFCs) or oral immunotherapy (OIT) dosing.”

The authors continue, “We are concerned that adopting a recommendation for an extended period of observation may deter allergists from performing an OFC, an important and underused procedure.”

We have been following this issue on and off around here, recently with a piece by Dr. Scott Sicherer called “Who’s afraid of the food challenge?” and further back with Paul’s response to a survey showing fewer than half of allergists had learned to do OFCs during their training. In that survey, the reasons respondents gave time (3-4 hours), low reimbursement, and risk of adverse events as the top three reasons for not doing them.

With that threshold in mind, no wonder the authors of this new letter were concerned. If 3-4 hours are a burden, what will happen when 6 hours is on the table? When I looked at the names of the letter writers, I was delighted to see that one of them was our contributor and my friend, Anna Nowak-Wegrzyn of the Jaffe Food Allergy Institute at Mount Sinai along with doctors from Israel and Philadelphia, so I reached out to her. (The other authors are Yitzhak Katz, MD, of Assaf Harofeh Medical Center in Tel Aviv, Israel, and Jonathan M Spergel, MD, PhD, of Children’s Hospital of Philadelphia.) – Henry Ehrlich

AAC: Thanks, Anna, for taking your time to answer questions for our readers. First, why do biphasic reactions happen?

Dr. Nowak-Wegrzyn: During an acute, IgE-mediated allergic reaction, caused by food or other allergen, basophils and mast cells release previously formed chemicals, so called mediators, such as histamine and tryptase that are responsible for the early symptoms of anaphylaxis. In some patients, a second phase of anaphylactic reaction may occur and it is caused by the release of newly synthesized mediators such as leukotrienes or cytokines that are produced by the activated mast cells or basophils and usually are released within few (2-4) hours from the onset of the reaction.

AAC: How did this letter come to be written? Your co-authors are not people whom you meet around the water cooler. One is in another U.S. city and one in a distant country.

Dr. Nowak-Wegrzyn: Yitzhak Katz and Jonathan Spergel and I are colleagues and share special interest in food allergy. We have spoken before about the importance of oral food challenges for the diagnosis and management of food allergy and share the concern that food challenges are underutilized by the physicians caring for patients with food allergy.

AAC: You have administered food challenges—double-blind placebo-controlled and unblinded—and also done OIT in a research setting. What do these procedures involve that makes them less likely to result in a late-phase reaction than an emergency case?

Dr. Nowak-Wegrzyn: Food challenges are done in a very controlled and careful manner, the patient is usually fasting before the challenge and the food is eaten in gradually increasing amounts. Fasting means empty stomach and no interference from the other foods in the GI tract that may delay the absorption of the allergic food, causing delayed onset of symptoms caused by a larger dose of the allergic food. The patient is examined carefully to identify any signs of an allergic reaction before each dose of the challenge. These precautions allow the physicians to capture allergic reaction at an early stage at the lowest possible amount of the allergic food and treatment is initiated immediately without any delay. In contrast, none of these factors are controlled during a food allergic reaction at large and as such, these “spontaneous” reactions are usually associated with a higher amount of the ingested food allergen, delayed recognition of the symptoms and delayed administration of epinephrine, compared to a physician-supervised oral food challenge. More severe initial reactions seem to be associated with a higher likelihood of second-phase of anaphylaxis.

AAC: Could you talk about the severity and sequence of treatment? You say in the letter that they are typically brief and easy to treat.

Dr. Nowak-Wegrzyn: In my experience, true biphasic reactions are very uncommon in the setting of an oral food challenge, less than 2%. When we reviewed our data, we found that among 568 positive food challenges performed in the inpatient hospital and in the ambulatory unit, 62 reactions were treated with epinephrine, and there was 1 biphasic reaction (1.6%) This patient had a delay in onset of his initial anaphylactic symptoms, which did not occur until an hour after the OFC had already been discontinued because of milder symptoms. His anaphylactic symptoms responded to the initial dose of epinephrine but reoccurred after an hour and required administration of a second dose of epinephrine.

AAC: Because the study is retrospective, it’s possible some of the reported biphasic reactions were actually “prolonged” reactions. Could you describe the difference and tell us whether it’s important for patients to be able to distinguish?

Dr. Nowak-Wegrzyn: Biphasic means that initial symptoms go away, with or without treatment and then re-occur after few hours. Prolonged anaphylaxis describes a reaction in which initial symptoms do not resolve completely and then re-escalate within few hours.

AAC: Finally, you mention late phase or biphasic asthma reactions, which may last for several days, as opposed to the usually brief episode with food allergies. Why do the asthma attacks last so long by comparison?

Dr. Nowak-Wegrzyn: Asthma has a different immunologic mechanism, in which T lymphocytes play an important role, e.g. by producing inflammatory mediators and cytokines that affect other allergic cells. In a food-induced anaphylaxis, there is probably less involvement of T cells and less accumulation of the allergic cells, which in turn don’t contribute to the ongoing symptoms.

AAC: Thanks for your time and expertise.

Dr. Anna Nowak-Wegrzyn is one of the leading authorities on food allergies in the world. She is a clinician and clinical researcher in the Jaffe Food Allergy Institute at Mount Sinai Medical Center in New York City. Her research interests, funded by in part by the National Institutes of Health and Food Allergy Initiative, include: egg and milk allergy, food-induced anaphylaxis treatment and risk factors, diagnostic issues in food allergy, food protein-induced enterocolitis syndrome and pollen-food allergy syndrome (oral allergy). She formerly chaired the Adverse Reactions to Food Committee of the American Academy of Allergy, Asthma & Immunology and was President of the New York Asthma & Asthma Society.

Nut-Free Schools: The Good, The Bad, and The Ugly

December 5, 2015 By Admin

By Dr. David Stukus

I couldn’t believe it had come to this. I was the first allergist this family had seen for their 10-year-old son, who had a peanut allergy. They came to see me as a last resort before pulling their son out of school. He had attended public schools since Kindergarten, all of which were “nut free.” However, he was about to start fifth grade at a new school, which was not. Both parents were extremely anxious about his peanut allergy and potential for life-threatening reaction at school, where he was outside of their watchful eye. They requested that I “force” the school to ban all nuts to allow their child to safely attend. After much discussion, it turned out that they had never received counseling about food allergy management, risks, and expectations. I’ll spare the details, but after a productive discussion (and several subsequent visits), they decided to allow their son to attend his new school, without changing its policy. You’ll be happy to learn that he has done great ever since.

What's the mystery ingredient? — What’s the mystery ingredient?

Nowhere is the epidemic of food allergies more contentious than in our nation’s schools. This is where the health problems of an average of two children per classroom run headlong into the “right” of children to eat “America’s favorite food” or other staples of the typical diet, where education professionals must learn emergency medical skills and school nurses are becoming a luxury, and so on.

Current estimates are that 5-8% of children have at least one food allergy, with roughly 2% having allergies to peanut or tree nuts. But while these are the battleground allergens, milk, egg, wheat, soy, fish, and shellfish collectively account for > 90% of all food allergy reactions. Many people do not realize that any food allergy can cause a severe allergic reaction. Although milk, egg, wheat, and soy allergies tend to improve or go away with age, 80% of children with nut or seafood allergies will never outgrow their allergy. The severity of reactions can progress over time and cannot be predicted based upon any test result, or even prior history.

Compounding the school dilemma is the fact that food allergens can represent a threat even when they are not ingested. Because even trace amounts of peanut protein introduced through cross contamination from a shared baking sheet or utensil can provoke a life-threatening allergic reaction in some children, management of food allergies requires constant vigilance at every snack and meal to ensure the food doesn’t contain or didn’t contact any food allergens. Casual contact through touching the food or a surface where the food previously touched can also cause reactions, although these are rarely life threatening, and mostly cause localized hives or swelling. However, transfer of the food from hands to the eyes or mouth can trigger a more severe reaction. Food allergy reactions can occur to some foods through inhalation as well, but the majority of these are when the food is being cooked on the stove top and releases vapors into the air, such as frying fish. It is exceptionally rare for a food such as peanut to cause a life-threatening allergic reaction by merely being in the same room or vicinity without ingestion occurring, but minute amounts may travel on hands and clothing. The exact route these proteins travel may never be known in each case.

Given the prevalence of peanut and tree nut allergies, risk for reaction with every exposure, and multiple routes of exposure, some schools have adopted nut-free policies to try to minimize the risk with their students. This can be a highly charged political and emotional discussion from both sides, and may provoke strong sentiments from families who don’t have children with food allergies. The decision to make a school nut-free affects everyone. Below are some of the things to consider for both sides of this argument.

The Good
Given the large number of students spread throughout multiple different classrooms and moving through various locations throughout the school day, it can be extremely challenging for school personnel to provide constant supervision for students with food allergy. Younger children in particular naturally explore their environments more with their hands and even mouths. Having peanut/nut containing products in the classroom increases the risk that they will accidentally touch or ingest these foods. Having a policy in place that is communicated to all students and school personnel about being a nut-free facility can reduce the number of potential exposures and risk for reaction. This can also bring about a sense of community and promote well-being for all students, acknowledging the challenges that children with nut allergies face every day.

Each school differs in regards to their physical layout and meal preparation/lunchrooms. It may make a lot of sense for a school that serves lunch in the classroom to restrict all nuts to minimize risk of exposure. However, schools that have separate cafeterias and do not allow snacks/meals in the classroom may prefer to implement nut-free cafeterias instead. Each circumstance is different and the age of the students, specifics to the school, and understanding/preparation from the school personnel all must be taken into consideration when deciding whether to go nut-free.

The Bad
There is no evidence that demonstrates nut-free schools protect against allergic reactions. In fact, the opposite may be true. At least one study has shown ongoing reactions to peanut/tree nuts in nut-free schools! How can this be? If you discuss with school nurses and administrators, many of them will tell you that nut-free policies are not enforceable. Despite repeated notifications to families and provision of policy statements, children without allergies may still unintentionally bring nut containing foods to school for lunch. Unless you search every single bag every single day, there is no way to enforce this rule with 100% certainty. Peanut butter is a great source of relatively inexpensive protein and many families rely on peanut butter and jelly sandwiches to feed their children at lunch.

In addition, having a policy about being nut-free may inadvertently cause students with food allergies and school personnel to have a false sense of security and let their guards down. One study shows that accidental exposures happen at higher rates than in schools that allow nuts (and both are far below the rates at home). Labels may not be read every time. Perhaps the students forget to ask about ingredients in the lunch line. Perhaps parents neglect to send injectable epinephrine with their child, feeling secure that they will not be exposed to nuts. One must always consider unintended consequences, which in this instance includes potential for being unprepared to recognize or treat an allergic emergency.

Many who advocate against nut-free schools discuss the need to prepare children with food allergies for living in the ‘real world’. They will always need to follow all standard precautions when visiting public places, other people’s homes, or when traveling. Implementation of nut-free policies within schools may hamper their ability to practice and learn critical self-management strategies that will help them navigate their way through the rest of the world. Counseling the family in the anecdote with which I began this post taught me as much as I taught them about the responsibilities that fall on every food allergy family. Fortunately, they learned and their son has benefited.

The Ugly
Parents of children without food allergies may not understand the real risks involved or the serious nature of living with a food allergy. They may not understand that there is no safe amount and every snack or meal needs to be scrutinized. Poor awareness and recognition of these facts can lead to intentional or unintentional emotionally charged exchanges with families living with food allergies. Animosity may grow towards the select few who force a policy that affects all. Occasionally, conflict erupts that brings out the very worst in parents, who view new restrictions in a political context of ever-more intrusion on personal liberties.

In addition, making a school nut-free does not protect children with other potentially life-threatening food allergies such as milk, egg, wheat, soy, or seafood. Parents of these children may feel as though their child’s needs are not being met and excluded from the communal feeling of the school banding together to protect some children, but not others. This can turn into a slippery slope very quickly.

Lastly, several studies have shown that 25-30% of children with food allergies are subjected to bullying at school. While having nut-free policies won’t change the fact that a student may already have food allergies, it may bring their allergies to the forefront for those with bad intentions to exploit.

Conclusion
Regardless of a school’s decision to adopt nut-free policies or not, everyone within the school should receive annual training and education regarding the recognition and management of food allergies. The Centers for Disease Control published excellent free guidelines in 2014 that provide in-depth discussion of many of the issues raised in this article, in addition to recommendations for ways schools can best accommodate and protect students with food allergies.

You may note that this article does not make any recommendation one way or the other whether schools should adopt nut-free policies. You may also note that no professional medical organizations, including the allergy specialties, have made formal recommendations regarding this topic either. It is simply too complex to apply blanket statements that should be adopted by everyone. While debate can carry on regarding the merits of nut-free policies, no one can argue that there is a lack of evidence for both sides of the argument. Individual 504 plans for children with food allergies can help provide thorough, written communication regarding provisions the school can make to ensure the safest environment possible.

The approaches by schools and families with food allergic children may vary. However, at the end of the day, what matters most is that children with food allergies be able to attend school with their peers, not be secluded from any activities, and learn in a safe environment while minimizing risk of accidental ingestion of their food allergens.

David Stukus, MD, is board certified in Allergy/Immunology and is an Assistant Professor of Pediatrics at Nationwide Children’s Hospital and The Ohio State University in Columbus, Ohio. His clinical and research interests focus on asthma and food allergies, especially improving education and adherence for patients and families. As part of his research, Dr. Stukus has created novel technology and educational tools using mobile health apps to improve the care of patients, for which he was recognized with the Nationwide Children’s Hospital Department of Pediatrics Junior Faculty Award in November 2013. Dr. Stukus has been an active member of the medical advisory team for Kids with Food Allergies since 2009 and was elected to the Board of Directors for the Asthma and Allergy Foundation of America in 2014. Lastly, Dr. Stukus actively engages with food allergy support groups and participates in social media on twitter through @AllergyKidsDoc.

Food Allergies & Prescribed Injectable Epinephrine: Know. Practice. Carry. Use.

December 9, 2012 By Admin

By: Anne F. Russell BSN, RN, AE-C

santa-500x500 — What Unpleasant Surprises is He Bringing This Year?

A Mother’s Story
“It happened so fast!” Melanie told me. “My daughter and I were invited to a neighbor’s Christmas party for their 4 year old twins and their pre-school friends. They are conscientious about food allergy safety. They never serve food with peanuts or tree nuts when Sarah visits. She had a severe allergic reaction to peanut butter when she was a year old. She has not had one since. We avoid peanuts, peanut products and were later told to avoid all tree nuts. I was helping in the kitchen when the hired magician threw chocolate candy Santas toward the children. They were wrapped in shiny red, green and silver foil. Sarah ate some, too. Suddenly, the magician called out. As I entered the family room, I saw hives over Sarah’s face and neck. She was uncharacteristically quiet. I snatched her up and took her to a bathroom. Hives covered her legs and arms. She began vomiting and coughing. Then I heard wheezing. I froze. I had two EpiPens® in my purse but I’ve never given anyone a shot, let alone a loved one. I convinced myself it wasn’t anaphylaxis but knew I should get Sarah to an emergency room. Fast. Just in case. We called 911. When paramedics arrived, Sarah was still wheezing, covered in hives and her lips were swollen. They gave her a shot of epinephrine, started an I.V., placed an oxygen mask over her nose and mouth and gave other medications. Sarah was hospitalized for almost 2 days. Peanuts were listed in the ingredients of the Santa candy. Everyone told me I should have used the EpiPen® immediately, but I had been too scared to do so.”

Emotional versus Intellectual Response
Melanie was weepy as she related the story in clinic. It was a common tale. She intellectually understood how to identify signs/symptoms of anaphylaxis. She could recite the protocol for prompt injection of epinephrine followed by immediate transfer via ambulance to an Emergency Room for further evaluation, treatment and observation. But when the time came, Melanie panicked. The hostess told the magician not to bring any food to the party, but he forgot. Accidental food allergen ingestions happen – especially with young children away from their own homes. Melanie froze. Fear of sticking a needle in her daughter and worry over epinephrine side effects took over. “I was afraid of making a mistake and making the situation even worse.”

It’s not surprising. And I certainly empathize. There’s a reason first responders, nurses and physicians drill and drill again. They have to be able to act automatically under stressful conditions. Unfortunately, Melanie had not practiced with an EpiPen® trainer in over two years. She described herself as “somewhat good” about remembering to never leave home without EpiPens®. But carrying them and being prepared to act are different. Sarah has typically only eaten food from home when attending holiday gatherings. She does not have asthma, atopic dermatitis or other allergies. It’s easy to drop your guard during long periods without reactions. Easy to become complacent about this constant underlying danger. Easy to stop routinely reviewing anaphylaxis protocols and practicing with an EpiPen® trainer.

Sarah does her part. At 3-1/2, she is age-appropriately involved in daily food allergy care. For example, she listens as her parents read food label ingredients to her, wears her medical identification bracelet and helps bake homemade peanut/tree nut-free cookies. The family provided Sarah’s preschool with two EpiPens®, food allergy action plan and training videos. The preschool takes strict steps to minimize peanuts/tree nuts and Sarah has never had an allergic reaction there.

Neither parent has food allergies and did not grow up with anyone that did. “I am so frustrated,” said Melanie. “We live in a world where two people can’t seem to get together without food! I have to constantly strategize food allergy safety which can get bizarre – even to me!”

“What do you think would best help you right now?” I asked. “I’m not sure,” Melanie sighed. “I guess I should re-learn EpiPen® technique.”

Taming the Fear Factor

adrenaline_autoinjector — When in Doubt....

Well, that was certainly part of it. After further discussion and needs assessment I designed an individualized patient/family educational plan to be covered over several successive follow-up visits and then yearly, at minimum. The overall objective was that by providing more in-depth educational services, with time for monitored practice, Melanie would become more comfortable and confident in her ability to appropriately manage anaphylaxis. Examples of topics we reviewed over time:
• Emphasis of avoidance as mainstay of daily food allergy management.
• Listed foods/non-foods that may contain peanuts and tree nuts.
• Poster photos which visually depict ingredient label examples.
• Potential risks of cross-contamination between peanut/tree nuts and safe foods.
• Discussion regarding ‘may contain’ peanut/tree nut labeling and avoidance of such products.
• Calling manufacturers regarding product ingredients (e.g. why, how, what to ask).
• Signs/symptoms of anaphylaxis, including biphasic reaction, with discussion/role-playing of potential scenarios and subsequent actions.
• Injectable epinephrine (e.g. purpose, indications, side effects, care/storage) with risk versus benefit discussion.
• Evaluating need for suggested number of EpiPens® based on family lifestyle. Suggestions for tracking EpiPen® prescription renewal.
• Technical review of using injectable epinephrine with ample opportunity for demonstration, observation, practice and ‘teach back’ for evaluation with a placebo (e.g. trainer) version.
• Sarah’s written food allergy action plan (FAAP) with multiple copies for home, pre-school etc.
• Rationale for carrying a copy of the FAAP and two EpiPens® whenever leaving home.
• Emphasis on immediate call to 911 with prompt transfer of Sarah via ambulance to an Emergency Room after administration of epinephrine.
• Role-playing with entire family on managing potential scenarios which Sarah may encounter involving possible exposures to peanuts and tree nuts.
• Transitioning pre-school FAAPs and management guidelines to elementary school with my provision of on-site food allergy/anaphylaxis training to school staff.
• Suggested coping strategies for anxiety management.
• Planning home anaphylaxis drills to further practice the FAAP, using EpiPen® trainer. Thus increasing probability that such skill practice will more naturally ‘kick-in’ if anaphylaxis occurs.

To Give or Not to Give
It can be heart wrenching to witness your beloved child in the throes of anaphylaxis. But it is one medical emergency that a trained parent/caregiver can act upon. Establish routines for never leaving home without a FAAP, EpiPens® and working cell phone. Over time, it really does become second nature! If your little one develops anaphylaxis after a known or suspected accidental exposure to a food allergen but you are not sure whether to administer the EpiPen® – give it (always into an outer thigh muscle) and call 911.

Err on the side of safety! Epinephrine is safe and the alternative is unthinkable. The side effects (e.g. higher heart rate, jitteriness, headache) usually last only minutes and subside with rest.[1] Timing is essential as delayed administration has been associated with fatalities or near-fatalities.[2] Anaphylaxis episodes are unpredictable in how they may progress – even in the same individual. So, be prepared and have your tools (e.g. FAAP, EpiPens®) available at all times. Practice via anaphylaxis drills as often as necessary to develop greater ease. At clinic visits, review use of the epinephrine auto-injector with health care team members that can provide feedback on your technique.[3]

Anaphylaxis is a medical emergency because it’s life threatening. Seconds really do count. The sooner the epinephrine shot is given with transfer via ambulance to an ER, the better for the child. Yes, anaphylaxis creates a stressful family crisis. It leaves indelible memories. Emotions run high. One way to tame the fear is through ongoing preparation and FAAP practice. For many families it’s a monthly routine with added refresher training before major events, like holidays.

Be mentally and technically prepared. Stay as calm as possible. Act accordingly. You can do this! Then, have a good cry afterward!

From Newly Diagnosed to Knowledgeable Parent
Anaphylaxis is frightening to endure, observe and/or be at risk for. Lack of accurate and/or incomplete information may also fuel fears. This article does not provide an exhaustive listing of all related aspects of this topic. Further information is available in the resource list. Ongoing, comprehensive, individualized patient education from qualified health care professionals with concurrent guidance and evaluation can empower families. Clinical nurse educators with undergraduate and/or graduate degrees in Nursing are trained to provide patient educational services, case management and coordination of care. Essential services for families coping with chronic medical conditions like food allergy/anaphylaxis. Prevention strategies may still feel like a daily grind. And treating anaphylaxis may still be anxiety provoking. But when given multiple tools and personalized, research-based patient education and support, families coping with food allergy and risk for anaphylaxis can conquer fears and thrive!

Selected Resources for Parents
Allergy Free Table
Allergy Home
Anaphylaxis Canada
Anaphylaxis Resources by John Weiner MD
Food Allergy & Anaphylaxis Network: Anaphylaxis Do’s and Don’ts
Food Allergy Education Program by Consortium of Food Allergy Research
Food Allergy Initiative: Anaphylaxis
Get Schooled in Anaphylaxis
My EpiPen® App and Resources
NIAID Guidelines for Diagnosis & Management of Food Allergy in USA – Summary for Patients & Families
The Food Allergy Experience: Real voices. Real disease. Real insights. By R. Gupta MD, MPH & D. Bunning

Carriers for Injectable Epinephrine
Allergy Pack
Epi-Essentials
Epi-Ready
One Spot Allergy

Food Allergies & Children’s Books
Allergic Child – Children’s Books by Nicole Smith
The Bugabees: Friends With Food Allergies by Amy Recob
The No Biggie Bunch Everyday Cool with Food Allergies by Michael Pistiner MD
The Princess and the Peanut: A Royally Allergic Tale by Sue Ganz-Schmitt

Food Allergies & Cookbooks
Allergen-Free Baker’s Handbook by Cybele Pascal
Divvies Bakery Cookbook: No Nuts. No Eggs. No Dairy. Just Delicious! by Lori Sandler
Food Allergy Mama’s Baking Book by Kelly Rudnicki
Go Dairy Free by Alisa Marie Fleming
Learning to Bake Allergen-Free by Collette Martin
Neocate Food Allergy Cookbook
What’s to Eat? The Milk-Free, Egg-Free, Nut-Free Food Allergy Cookbook by Linda Coss

Food Allergies & Holidays
ACAAI Holiday Tips for Those with Food Allergies
Allergies, Asthma and Winter Holidays by AAAAI
Hidden Holiday Food Allergens – Infographic by National Jewish Health
Holiday Allergies/ Food Allergies: How to Plan by AAFA
Home for the Holidays via AANMA

Medical Identification
Medic Alert Foundation

Videos
Anaphylaxis Signs and Treatment – WebMD
Be Safe from Anaphylaxis – Mayo Clinic
How to Use an Epinephrine Autoinjector with Elisabeth Stieb RN, BSN, AE-C
When to Use an Epinephrine Autoinjector-for Parents with Wayne Shreffler MD, PhD

Article References
1. Kemp S, Lockey R, Simons FE. Epinephrine: the drug of choice for anaphylaxis-a statement of the World Allergy Organization. Allergy. 2008;63:1061-1070.
2. Boyce JA, Assa’ad A, Burks AW, et al. Guidelines for the diagnosis and management of food allergy in the United States: report of the NIAID-sponsored expert panel. J Allergy Clin Immunol. 2010;126(6suppl):S1-S58.
3. Russell AF, Gosbee LL, Huber MM. Part 2: Pertinent Food Allergy Education in a Pediatric Ambulatory Care Setting with a Focus on Anaphylaxis. J Asthma Allergy Educators. 2012;3(4)162-171.

Anne F. Russell BSN, RN, AE-C has had a clinical and educational focus on food allergy & anaphylaxis for over 15 years. She served as Food Allergy Program Coordinator in a university allergy department. She was President of Food Anaphylaxis Education, Inc – a state-wide nonprofit. As a food allergy/anaphylaxis community educator, Anne has presented at conferences, numerous schools, daycares and churches. She has also initiated/collaborated on related state legislative efforts. As School Health Director in a preschool-12th grade academy, she coordinated individualized health plans; trained school staff on anaphylaxis prevention, identification and rescue; and provided oversight. Anne has served on the FAAN Member Advisory Council, has collaborated with FAI and is a recipient of a FAAN Make a Difference award. She is a nationally board certified asthma educator by NAECB examination and has done graduate studies toward a Masters in Nursing. As a food allergy/anaphylaxis educator, Anne has also provided clinical nurse educator services within primary pediatrics and allergy clinics. She is also a Nursing faculty member at Spring Arbor University and mother of a beloved son with food allergies, asthma and atopic dermatitis.

(The case description provided in this article is fictional. Information provided in this article does not replace medical advice from a patient’s own health care provider. Any external hyperlinks, websites, and resources cited do not necessarily reflect endorsement by the reviewers, the author, their employers or owners of this website. The author, reviewers and the owners of this website cannot take responsibility for the accuracy or quality of content given in websites, products and resources mentioned in this article.)

Santa by german-sausages-philippines.com
Injection by medicinesforchildren.org.uk

Oral Immunotherapy for Food Allergy: Not Ready for Prime Time

May 11, 2012 By Admin

Hugh A Sampson, MD
Mount Sinai School of Medicine; Jaffe Food Allergy Institute

Food allergy has become a major health problem in westernized countries, now affecting approximately 3.5% of the U.S. population, or about 12 million Americans, and is the leading single cause of anaphylaxis treated in U.S. emergency departments. The standard of care for dealing with food allergies has been to educate patients and their families how to avoid allergenic foods and to recognize and treat allergic reactions if they have an accidental ingestion. In the past 5 years, there has been a growing interest in oral immunotherapy (OIT) for treating food allergy, a practice that was first reported in The Lancet over 100 years ago in an article called “A case of egg poisoning” [Lancet 1908; 1:716]. Considerably more recently, several small clinical trials of OIT for milk, egg and peanut allergies have yielded some promising results, and some practicing allergists have even begun using OIT to treat food-allergic patients.

I certainly can’t fault the desire of patients and patients’ parents to seek relief from the difficulty of managing a severe food allergy (and who pay for these treatments out of pocket). However, I wish to caution that widespread adoption of any OIT methods is premature, and may lead to crushing the hopes of patients, and worse.

Three carefully conducted scientific reviews* of trials have raised serious questions about OIT’s effectiveness, safety and long-term benefits, with the most recent concluding that “the overall low quality of evidence leaves important uncertainty about anticipated effects of immunotherapy due to very serious imprecision of the estimates of effects and the likelihood of publication bias for some of the critical outcomes.” In other words, we can’t judge on the basis of these trials whether it’s really working or not, or whether some researchers are getting the results they want instead of what the data really shows.

Our understanding of the underlying immunologic changes brought about by OIT is very limited and published reports provide inconsistent results. OIT appears to induce “desensitization,” or a clinical state in which the quantity of food required to trigger an allergic reaction is raised while on therapy, in most patients. “Tolerance,” or the long-term loss of allergic reactivity following the discontinuation of therapy, i.e. “a cure,” has been reported in some OIT trials, but most of these trials lack the appropriate controls. Different treatments follow different protocols, creating apples-and-oranges comparisons. In some cases, we can’t distinguish whether improvements with milk are the result of the therapy or whether a child is merely outgrowing the problem, as happens with milk allergies about 80% of the time. In fact, the only OIT trial to date stringently controlling for the natural development of tolerance in food-allergic children failed to find a difference in outcome between treated and control subjects.

In spite of the reservations my colleagues and I have, there are many instances of what we might call “retail OIT” being offered by some practicing allergists. The history of medicine is replete with examples of how premature adoption of new techniques can go wrong. Drugs and technologies that showed “no harm” in trials have often proven to be problematic as they made their way into wider use. We are nowhere near that regulatory threshold with OIT.

Furthermore, administering an experimental therapy creates management problems. Even in a research setting, patients must endure much of the discomfort and reactions that make food allergies a problem to begin with, necessitating a good deal of after-hours support and encouragement; do OIT doctors provide that? And while I trust my fellow allergists to treat emergencies, proliferation of unproven therapies creates more and more probability of mishaps. How long before a patient who believes himself “cured” suffers because he has ignored elementary precautions?

At this time, oral immunotherapy should be considered a promising experimental treatment for food allergy, but proper well-controlled trials are needed to demonstrate that it is safe and effective before the FDA will approve it for general use by practicing allergists.

* [(1)Brozek JL, Terracciano L, Hsu J, Kreis J, Compalati E, Santesso N et al. Oral immunotherapy for IgE-mediated cow’s milk allergy: a systematic review and meta-analysis. Clin Exp Allergy 2012; 42(3):363-74;

(2) Sheikh A, Nurmatov U, Venderbosch I, Bischoff E. Oral immunotherapy for the treatment of peanut allergy: systematic review of six case series studies. Prim Care Respir J 2012; 21(1):41-9; and

(3) Fisher HR, Du TG, Lack G. Specific oral tolerance induction in food allergic children: is oral desensitisation more effective than allergen avoidance?: a meta-analysis of published RCTs. Arch Dis Child 2011; 96(3):259-64]

Dr. Sampson is the Kurt Hirschhorn Professor of Pediatrics and the Dean for Translational Biomedical Research at the Mount Sinai School of Medicine in New York, and the Director of the Jaffe Food Allergy Institute at the Mount Sinai Medical Center. Dr. Sampson’s research interests and publications have focused on food-allergic disorders including the immunopathogenic role of food hypersensitivity in atopic dermatitis and anaphylaxis, characterization of food allergens, and immunotherapeutic strategies for treating food allergies. His research has been funded continuously by a number of grants from the National Institutes of Health and private foundations. Dr. Sampson is the principal investigator of the NIH-sponsored Consortium on Food Allergy Research and an AADCRC program project conducting a number of clinical trials investigating novel therapies for the treatment of food allergy and investigating basic immunologic mechanisms. He has published over 350 articles and 60 book chapters on food-allergic disorders and co-edited four books, and was elected to membership in the Institute of Medicine of the National Academies in 2003 for his research on food allergies. Dr. Sampson is past chairman of the Section on Allergy & Immunology of the American Academy of Pediatrics and past president of the American Academy of Allergy, Asthma and Immunology.

Defining Anaphylaxis–Different Specialties, Different Treatments

March 27, 2012 By Admin

By Dr. Paul Ehrlich

George Bernard Shaw said that England and the United States were two countries separated by a common language. The same can sometimes be said of doctors in different medical specialties. In the March issue of the Journal of Allergy and Clinical Immunology, Dr. Carlos Camargo considers the gap between allergists and emergency department doctors in an editorial entitled “Potter Stewart and the definition of anaphylaxis”. The title refers to Supreme Court Justice Potter Stewart’s criterion for hard-core porn: “I know it when I see it.” He says:
I heard that quote many times when I began clinical research on food allergy and asked my allergist/immunologist colleagues about their definitions of anaphylaxis. I complained that allergy textbooks offered definitions based on IgE levels, mast cells, and other mechanistic details that I had never seen at the bedside. Unfortunately, the experts provided very different clinical definitions, ranging from ‘‘mild anaphylaxis’’ (simple urticaria) to a requirement for hypotensive shock. On that broad severity spectrum, most emergency physicians were in the latter camp, with a reluctance to consider the diagnosis until there was shock.

His research shows that allergists are able to diagnose anaphylaxis pretty accurately based on multiple symptoms, not all of which present themselves in every patient every time, and unsurprisingly resort to the use of injectable epinephrine more readily than emergency department docs.

This is not a theoretical exercise. We read this account a few months ago by one of our friends at the Arizona Food Allergy Alliance [AFAA]:
On December 7th, I was in anaphylactic shock at lunch time at Hospital A. They did a fantastic job treating me and were very knowledgeable. Six hours later, at home I had a secondary (biphasic) anaphylactic reaction. Since I was already on hospital-prescribed meds, I didn’t know if I could use my EpiPen so I went to the hospital near my home and was accused of being a drug addict. I mean OBVIOUSLY I was on street drugs since I was convulsing, gasping for air, couldn’t speak (VCP), and drooling on myself since my throat was closed shut and I couldn’t swallow…and I kept passing out. They ran toxic screens to “see what it was I took” and did X-rays to see “why I couldn’t breath.” My family and I kept insisting I was anaphylactic and kept pointing to my medic alert bracelet and stating I was already treated for this once earlier. The doctor refused to treat me for allergies because MY FACE WASN’T SWOLLEN – which is the ONLY symptom I NEVER get. He said, “You don’t even have a rash!!!” The nurse said, “Oh yes she does, its all over her neck, shoulders and back and spreading down her stomach like hives.” When I checked out the nurse said I should take Ativan so I don’t have these ridiculous panic attacks. Oh, yes, I filed big complaints.

It shouldn’t be this difficult. Hundreds of thousands of parents and food-allergy patients have mastered these criteria:
Any SEVERE SYMPTOMS after suspected or known ingestion: One or more of the following:
LUNG: Short of breath, wheeze, repetitive cough
HEART: Pale, blue, faint, weak pulse, dizzy, confused
THROAT: Tight, hoarse, trouble breathing/swallowing
MOUTH: Obstructive swelling (tongue and/or lips)
SKIN: Many hives over body Or combination of symptoms from different body areas:
SKIN: Hives, itchy rashes, swelling (e.g., eyes, lips)
GUT: Vomiting, diarrhea, crampy pain

Emergency departments can do it, too. All they have to do is click on Action Plans at the top of this page and then go to Food Allergy Action Plan, where these plans are available in a choice of languages, including (a la Mr. Shaw) English and….English.

Traditional Chinese Medicine and Allergy

August 16, 2010 By Admin

by Dr. Xiu-Min Li

Allergic diseases are a significant health problem in “Westernized” countries. They represent a tremendous burden on quality of life for both patients and their families, and health care expenditures for the society as a whole. Food allergy in particular has no definitive treatment. The rise of allergic disease is prominently attributed to the “hygiene hypothesis” which contends that modern hygiene and other byproducts of modern behavior have deprived our immune systems of their natural enemies—mostly parasites–and our immune mechanisms have turned on normally harmless proteins in food, pollen, and so forth, instead. The accustomed medical approach is to control the response through medication and curtailing exposure. Certainly these are valid and important. But in the long run, my colleagues and I believe that the answer to this “Western” problem may be found in the “East.” That is the point of our “integrative” approach.

To be sure, allergic diseases are not only found in modern societies. They have been observed in some form throughout recorded history, including China, where I come from. And that is why I am working to bring what Chinese doctors have learned over the centuries into American medical practice. By combining these components of Traditional Chinese Medicine (TCM) into what we call integrative medicine, we hope to take advantage of the fact that the most powerful medical tool we have is the body itself. TCM is a unique system of theory, diagnosis and treatments including herbal medicines, acupuncture, mind-body therapy and dietary therapy. These are part of mainstream medicine not only in China and other Asian countries such as Korea and Japan, and are beginning to play a role in health care in the US and Europe.

At the Mount Sinai School of Medicine, we have taken a classical herbal formula called Wu-Mei-Wan that has been used in TCM for treating parasite infection and symptoms of food allergy-like conditions, and turned it into an herbal formula named food allergy herbal formula-2 (FAHF-2). We have shown that FAHF-2 can prevent and reverse established peanut allergy in animal-model peanut anaphylaxis, and that the effect is long lasting. There is nothing mysterious about this work, which is often the case with other so-called alternative treatments; our work is conducted according to NIH protocols and has been published in premier peer-reviewed journals. We measure and control and analyze, like any other Western researchers; everything must be repeatable. These data suggest that FAHF-2, and perhaps other Chinese herbal medicines may have a potential for treating food allergy. FAHF-2 is the first botanical drug that has entered clinical trials as an FDA Investigational New Drug (IND). Our phase I studies showed that FAHF-2 is safe and well tolerated. Phase II studies are in preparation at two centers–Mount Sinai, and Arkansas Children’s Hospital Research Institute in Little Rock.

We also developed anti-asthma herbal medicine international (ASHMI), which was shown in preclinical study to affect asthma mechanisms including inhibition of airway hyper-reactivity, inflammation and mucus hyperplasia, and overactive T-cell activity that can result in an allergic response. ASHMI is also effective in aged mice with asthma. Most exciting is that in addition to being safe and effective, ASHMI remained effective long after therapy. Unlike steroids, ASHMI does not induce overall suppression of immune system or adrenal function. This benefit is more than anything representative of the goal I mentioned earlier—to use the body’s own capabilities to fight disease. (I might add that this approach also has implications for the treatment of cancer and autoimmune diseases.)

Our studies provide scientific evidence supporting the use of TCM as a potential treatment for allergy and asthma. The goal of our clinical study is to develop botanical drugs that doctors can prescribe to complement or replace other therapies.

Food allergic children also suffer from other allergic conditions such as eczema, and environmental allergies. Families and physicians are interested in alternative approaches for these multiple allergic conditions. In addition to our research, and because acupuncture and herbal medicines are lawfully used by licensed practitioners in the US, we initiated an off-site TCM clinical program to help children with stubborn eczema associated with food allergies. The clinical outcomes have been well received. Given the growing interest in alternative and complementary medicine (CAM) therapies, and to make the clinical program accessible to more children, Mount Sinai Medical Center has established a new TCM clinical program named “Center for Integrative Medicine for Allergy and Immunology”. This center is supported by Winston-Wolkoff Children’s Holistic Medicine for Allergy Foundation and FARE.

This program will provide an additional health care option for children with multiple allergic conditions. This program will also provide allergists and pediatricians and dermatologists within or outside the Mt. Sinai with a reliable resource of CAM therapy. The combined effort will enhance the patient compliance and clinical outcomes.

Furthermore, we recently organized the first East-West Scientific Conference on Allergy and Traditional Medicine (EWAT) in China. This landmark conference—the first ever to focus on integrative medicine and allergy gathered some of the world leaders in allergy and traditional medicine research to share the most up-to date and comprehensive views on allergic diseases and traditional medicine as well as other new interventions for allergy. It not only provided an opportunity for experts to share knowledge of conventional allergy treatments, but also resulted in new insight into the growing use of traditional medicine and resulted in new collaborative research programs into traditional medicine as a potential solution to the allergy epidemic. Using this conference as a starting point, we continue to build up national and international collaborations to accelerate efforts to develop safe, effective natural products and novel therapies.

Dr. Xiu Min Li is Professor of Pediatrics in the Division of Pediatric Allergy and Immunology at Mount Sinai Hospital in New York. She has published her research in Journal of Allergy and Clinical Immunology and other top journals. She did her medical training at Stanford and Johns Hopkins, as well as Henen Medical University in China.

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The False Alarm Hypothesis

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Nut-Free Schools: The Good, The Bad, and The Ugly

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Food Allergies & Prescribed Injectable Epinephrine: Know. Practice. Carry. Use.

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Oral Immunotherapy for Food Allergy: Not Ready for Prime Time

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Defining Anaphylaxis–Different Specialties, Different Treatments

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Traditional Chinese Medicine and Allergy

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