In the early 1990s, Joel Weinstock, a gastroenterologist, encountered a puzzle. The prevalence of inflammatory bowel disease (I.B.D.) across North America increased markedly during the 20th century. Many thought that “bad” genes would eventually explain the spike, but Weinstock didn’t buy it. In areas where fewer than two generations ago the I.B.D. incidence might have been as low as 1 in 10,000, it was now 1 in 250. A defective gene couldn’t spread that quickly, he reasoned. It had to be something in the environment. But what? Stumped, Weinstock tried turning the question around. Instead of asking what triggered I.B.D., he asked what, before the 20th century, protected against it?