A Matter of Taste
Yet why would humans have evolved in such a way that most were repelled by a nonnatural substance? The answer, which didn’t emerge until the 1950s, was that disliking PTC—and a related synthetic chemical, PROP—was a kind of accident. The innate aversion of those who could taste those compounds was to bitter chemicals, called glucosinolates, in cruciferous vegetables such as kale and brussels sprouts (PTC happens to mimic natural glucosinolates). One glucosinolate, goitrogen, is toxic to the thyroid in large quantities, so it made sense, in evolutionary terms, for people to have a sensitivity to it. However, in smaller amounts, other glucosinolates may help ward off cancer.
By the 1960s, a few scientists had confirmed what the earlier research seemed to predict—that whether someone could taste PTC/PROP predicted how many foods they disliked. But that observation was largely ignored until the 1990s, when Linda Bartoshuk, then at Yale University and now at the University of Florida, discovered additional layers of complexity.
Bartoshuk found that some people qualified not only as tasters but as “supertasters,” at the opposite end of the spectrum from nontasters. Rather than determining whether people could detect low concentrations of PROP—the acid test dividing tasters from nontasters—Bartoshuk looked at how intensely people perceived higher concentrations. Using sound and light as a frame of reference, she discovered a wide range of intensities. “Most of us live in a world of pastel tastes, but about 25% of us have neon tastes,” she says. To those supertasters, bitter is more bitter, salt is saltier and sugar is sweeter—and food likes and dislikes tend to be more extreme.
Bartoshuk’s work led others to explore how genes influence taste. In subsequent studies, scientists found that each type of tastant—bitter, sweet, salty, sour or umami—triggered a different kind of chemoreceptor, and the observation of differences in how tastes are perceived suggested that those receptors might vary from person to person, because of variations in the genes controlling the receptors.
In the late 1990s, researchers began to identify those receptor genes, first in mice and then in humans. They knew that different strains of mice had distinct preferences for sweet and bitter, judged by how voraciously they would lap up sugar water of a particular concentration and whether they would shun water laced with bitter compounds. By then, human and mouse genome sequencing projects were well under way, and in 2000, Charles Zuker, a neuroscientist at Columbia University, working with National Institutes of Health scientists, identified a family of bitter receptors and showed that the mouse genes for those receptors came in taster and nontaster variants that resulted in different sensitivities to bitter chemicals.
Bitter receptors (and also those for sweet and umami) belong to a class called G protein–coupled receptors (GPCRs), with seven loops that span cell membranes, and have an extracellular extension like a Venus flytrap. This flytrap can bind to a chemical of a particular shape floating by on the tongue in lock-and-key fashion. When a bitter compound fits the lock, that connection causes the taste cell to send a signal to the brain.