The Origins of Peanut Allergy

The piece asks why peanut allergy, once considered extraordinarily rare, became a significant concern in the United States, where about 1% of children are affected and roughly a dozen people reportedly die each year. It argues that genetics and peanut consumption alone do not explain the American pattern, and notes that guidance to delay introducing peanuts arose after allergies were already increasing. Peanut butter, unusually central to US diets, offers a possible clue: unlike whole peanuts, it can conceal mold or other signs that a batch is spoiled. The author briefly considers emulsifiers used in peanut butter, but says the cell-culture results presented by a researcher did not support the idea that they damage the intestinal barrier.

The proposed alternative centers on the Great Peanut Crisis of 1980. A severe drought devastated the US crop, while Aspergillus flavus contaminated some surviving peanuts and could produce aflatoxin, a potent toxin that damages DNA and can cause severe illness. The author speculates that aflatoxin exposure alongside peanut proteins might have provoked immune systems to treat those proteins as dangerous, creating later allergic reactions. This could also fit the concentration of peanut allergy in the US and the apparent timing of its rise. The argument remains a hypothesis, not a demonstrated cause: the author recounts that an immunology institute director dismissed the connection, and the piece offers no direct evidence linking aflatoxin exposure to the onset of peanut allergy.