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To Calm a Storm

A physician-scientist teams with a journalist to illuminate the science behind food allergy

4 min read

The statistics are clear: food allergies have skyrocketed in the past couple of decades. One of our main sources for that assertion is the federal collection of studies known as the National Health and Nutrition Examination Survey (NHANES). According to the most recent NHANES survey, between 2007 and 2010, 6.5 percent of U.S. children were living with food allergy. That’s nearly 5 million children, or 7 out of every 100. A more recent estimate by researchers at Northwestern University, led by Ruchi Gupta, puts food allergy prevalence at 7.6 percent of U.S. children. As for adults, a 2014 estimate put the prevalence among U.S. adults at about 5 percent, or about 14 million. A 2019 survey that we conducted with researchers at Northwestern of more than 40,000 U.S. adults found that nearly 4,400—11 percent—had food allergy. Applying that figure to the U.S. population as a whole means that more than 26 million U.S. adults harbor an allergy to peanuts, shellfish, dairy, or other food. And out of every 100 patients with food allergies, about 6 will be allergic to just one food but 40 will be allergic to at least two, often more. Regardless of whether you focus on the most or the least conservative figures, it’s clear that food allergy is rampant in the United States. …


Having delved into the harrowing numbers and unraveled the possible explanations for the food allergy epidemic, it’s time to understand how food allergy works. And that requires a trip to the microscopic world of the immune system. …

We are focusing on reactions triggered by antibodies called immunoglobulin E or IgE. Families coping with food allergy will often hear the term IgE-mediated food allergy. These are the most common types of food allergies and the ones responsible for the reactions we typically associate with food allergy. Food sensitivities are not the same as food allergy. … Here we are speaking about a diagnosable, testable, and dangerous immune disease called food allergy. …


IgE antibodies were discovered in the mid-1960s by two different research groups simultaneously, one in Colorado and one in Sweden. … The two groups joined forces in 1968 to persuade the scientific powers that be to officially name their mystery antibody IgE. The discovery of IgE is a defining moment in the history of allergy research. …

covere of the book The End of Food AllergyThe thousands of studies spawned by these early findings have painted an intricate picture of how allergy works. Work by many research teams has brought this once-hidden world to light. When an allergen enters the body, IgE attaches to mast cells, which sit at the boundary between our tissues and the outside environment, as well as other types of cells. The next time the allergen appears (through a person eating the food it comes from), it encounters the mast cells with its specific IgE all over the body. That encounter coaxes the cells to release histamine; along with chemicals called cytokines, which cause inflammation; a variety of enzymes; and other compounds that contract muscles, including those governing our airways and force the body into other uncomfortable and unsafe states; all with the goal of pushing the dangerous food out of the body. The binding of IgE to mast cells and the activity that causes are at the heart of the allergic reaction that we see from the outside.

Researchers still don’t know exactly why certain foods cause the immune system to produce IgE antibodies in the first place. We know that the body creates antibodies specific to each invader … The next time that invader tries to gain entry, the immune system recognizes its antigens, compounds that stand like flagpoles on its surface, and prepares to fight to the death using antibodies. But these fights are typically waged with IgG antibodies … IgE antibodies to allergens are different. They are often involved in the atopic march—eczema (or atopic dermatitis), “hay fever” (or allergic rhinitis), allergic asthma. But science hasn’t gotten to the bottom of why a harmless food would be misread as an enemy in the first place.  

Kari Nadeau, MD ’93 PhD ’95, is the Naddisy Foundation Professor of Pediatric Food Allergy, Immunology and Asthma at Stanford University School of Medicine and director of the Sean N. Parker Center for Allergy and Asthma Research at Stanford.

Excerpt is reprinted with permission from The End of Food Allergy by Kari Nadeau, MD, PhD, and Sloan Barnett. Published by Avery, an imprint of Penguin Group, a division of Penguin Random House, LLC. Copyright © 2020 Kari Nadeau, MD, PhD, and Sloan Barnett

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