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  Of all our flavor senses, taste is the one most tightly identified with the mouth. Yet even that is a little misleading: Now that scientists know what several of our taste receptors look like, they’re finding them all over the body—in our guts, in our brains, even in our lungs. Taste, it seems, plays a wider role than we thought, though many of the details still aren’t clear.

  The best known of these “other” taste receptors are the ones in the gut, where receptors for sweet and umami (and perhaps fatty acids, as well) signal to the brain that a nutritious meal has arrived. This helps us learn what flavors we should seek when we’re looking for our next meal. Our guts have bitter taste receptors, too, which may activate defensive responses to toxins. A few researchers have suggested that these may be responsible for some of the side effects of bitter-tasting medicines.

  We even have bitter receptors in our respiratory passages, of all places. Why do we need to taste the air we breathe? Well, because it has bacteria. As it turns out, one of the chemicals that bacteria use to communicate with one another has a bitter taste. Bitter receptors in our sinuses and the lining of our bronchial passages detect this and alert our immune system to fight back against the invaders. Curiously, the bitter receptor responsible for this, T2R38, is the same receptor that determines our sensitivity to PROP and phenylthiocarbamide (PTC). And, in fact, people who can’t taste PROP—that is, who have a broken T2R38 receptor—turn out to have more sinus infections. Some researchers even think that bitter receptors may have evolved originally as part of the immune-defense systems of our ancient animal ancestors, and only later turned out to be useful in our mouths, too. If so, we have disease to thank for much of the flavor of coffee, beer, and broccoli.

  By now, you might have noticed a glaring gap in our taste repertoire. The sense of taste is all about identifying good stuff to put in our mouths: sweet carbohydrates, salty sodium, protein-rich umami. It also helps us recognize bad stuff we want to avoid eating, such as sour, unripe fruit and bitter, poisonous plants. But there’s another category of good stuff we haven’t talked about yet, one that might be the most treasured of all: fat. Surely, our taste system ought to have evolved to recognize this energy-rich and (in the prehistoric world of our ancestors) scarce resource. And in fact, we probably can. In the past few years, researchers have been piling up a convincing heap of evidence that suggests we ought to include a sixth taste, fat, in addition to the familiar five. But there’s a surprising twist to the story: we hate the taste.

  Rick Mattes, a nutrition scientist at Purdue University in Indiana, probably knows more about our taste for fat than anyone in the world. The fats we find so appealing in foods—the butter we put on our bread, the olive oil in our salad, the cream on our strawberry shortcake—are what chemists call triglycerides. These are big molecules composed of a backbone molecule with three so-called fatty acids stuck to it, like a small box kite with three long tails. There’s no evidence that triglycerides have any taste at all, says Mattes. Instead, we recognize them in our mouths through the sense of touch, which picks up their creamy lubricity.

  On the other hand, there’s more and more evidence—much of it from Mattes and his colleagues—that we do indeed taste fatty acids when they become separated from their backbone. We have receptors on our taste buds that recognize fatty acids and respond by sending electrical signals to the brain’s taste center.

  And the taste seems to be distinct from any of the other five primary tastes. That’s easy to show in rodents, by pairing a nausea-inducing chemical with a fatty acid taste. The rats quickly learn to avoid the sick-linked taste, just like a hangover from too much rum and Coke can put you off of cola for a while. But the fat-avoiding rats don’t avoid sweet, sour, salty, bitter, or umami tastes, which implies that their learned aversion is to a sixth taste instead. Mattes has shown that humans, too, perceive fatty acids as a distinct taste. Since “fatty” calls to mind an oily texture, rather than a taste, Mattes suggests using the term oleogustus (Latin for “fatty taste”) for the taste sensation.

  By this point you might be wondering: If fatty acids have their own taste, what is it? Not good, it turns out. “They are really awful,” says Mattes. Most of the time, free fatty acids—that is, ones that aren’t bound up as triglycerides—signal decay or rancidity. In fact, the food-processing industry spends a lot of time and money trying to keep free fatty acids below detectable levels in their products. If you want to know what free fatty acids taste like, says Mattes, find a batch of old french-fry oil that’s gone rancid. Hold your nose, to eliminate the strong odor, and then taste it. But don’t expect to be able to describe it. “If you ask people to give you a description of it, it’s like they have blinders on,” says Mattes. “We don’t have a language for it. They’ll frequently call it bitter or sour, but what I think they mean is that they don’t like it.”

  So it looks like our ability to taste fatty acids is more like our taste for sour or bitter—that is, a defense against eating the wrong things—than like our taste for sweet, salty, or umami, all of which signal the right things to eat. But the story might be a little more complex than that, Mattes thinks. After all, we know of other cases where a tiny bit of an unpleasant taste actually enhances the overall flavor of a food. “Wine without a little bit of bitterness would not be as good,” he says. “Chocolate without bitterness would not be as good.” In the same way, a hint of the nastiness of fatty acid taste does pop up in a few foods we learn to like, most notably some fermented foods and stinky cheeses.

  As the evidence for fat taste piles up, more and more experts are now willing to add it to the list, expanding our repertoire of basic tastes from five to six. And there might be other basic tastes out there, too. There’s some evidence that we have a taste for calcium, and for carbon dioxide. Rodents look like they have a taste for starch, though it’s not clear that humans do as well. Some researchers even suggest that we might have a basic taste for water. And there’s a mysterious one called kokumi, which many Asian researchers think might qualify as yet another basic taste—though many Western scientists remain skeptical. Weirdly, kokumi seems to have no taste of its own, but when you add it to something that already has a salty or umami taste, it enhances those flavors.

  In a lab at Monell, I tasted some popcorn sprinkled with kokumi powder. It had a haunting, elusive flavor that was hard to put my finger on—sort of cheesy, sort of meaty, like the flavor powder on the surface of Doritos. Clearly, kokumi does something to taste perception, but it’s hard to say exactly what. (You can taste it yourself—look for kokumi powder at Korean groceries.) Scientists don’t know exactly how we perceive kokumi, though a calcium-sensing receptor called (surprise!) the calcium-sensing receptor seems to be involved. Things are changing fast in this field. Who would have thought there could be such complexity to something as seemingly simple and obvious as the four basic tastes we learned in school?

  To complicate things still further, the basic tastes interact with one another. Salt suppresses our perception of bitterness, as we’ve seen. Similarly, sweet and bitter suppress each other. Tonic water is a great example of this: The bitterness means we don’t notice how sweet the drink actually is, while the sugar helps bring the bitterness down to a level that most of us find palatable. Except for people like Linda Bartoshuk, of course.

  Which brings us back to supertasters. The ability to taste PROP turns out to be mostly a function of one particular bitter receptor, T2R38. There are two common variants of this gene: one version that responds strongly to PROP and one that doesn’t. This suggests that people with two copies of the nonresponding gene (one from each parent) are nontasters, those with two copies of the high-responding gene are supertasters, and those with one of each are normal tasters. And, indeed, researchers sometimes genotype people for T2R38 as a quick, objective way to determine their taster status.

  But it’s not that simple. The T2R38 receptor recognizes just one group of chemicals: those that contain a particular set of atom
s called a thiourea group. Your ability to taste those should have nothing to do with your ability to taste sweet, salty, or other kinds of bitter—including quinine—let alone your perception of the burn of chili peppers, which involves an entirely different set of receptors and nerves. And it certainly shouldn’t affect the number of fungiform papillae on your tongue.

  T2R38 probably has nothing to do with supertasting, at least not directly. Your T2R38 genes determine whether you have the genetic ability to taste PROP at all—but if you do, the amount of bitterness you experience probably depends on how well the rest of the taste machinery in your mouth and brain responds. The genes that control that machinery are what really make the difference between a taster and a supertaster—and if you can taste PROP at all, the amount of bitterness you experience is a decent measure of how sensitive the rest of your machinery is. That’s probably why people who rate PROP as intensely bitter also tend to rate salt as saltier, sugar as sweeter, and chili peppers as hotter than people who find PROP less bitter. If so, people with broken T2R38 genes might still be supertasters for anything that doesn’t require that bitter receptor. They just need to find a different way to prove it.

  One way might be to measure the density of fungiform papillae, which is why Bartoshuk painted my tongue blue. Each papilla contains several smaller clusters of cells bearing taste receptors. These clusters are the real taste buds, technically speaking, and the cells within them send nerve impulses up the taste nerves to the brain, signaling which of their receptors has encountered its particular taste quality. It makes sense that tongues with more papillae would generate stronger nerve signals and hence experience more intense tastes. Sure enough, most studies do support that hunch—although there are a few annoying studies that fail to find a link between number of papillae and taste perceptions.

  So what determines how many papillae you have on your tongue? Nobody knows for sure, but there are intriguing hints that a protein called gustin might be involved in stimulating the formation of fungiform papillae. People with one particular variant of the gustin gene have abundant, normal papillae, while those with a different variant have large, misshapen, sparsely scattered papillae. No doubt, too, there are plenty of other genes that affect overall taste sensitivity and thus help to define whether you’re a supertaster, an ordinary taster, or a (relative) nontaster. But the science doesn’t seem to have caught up with our curiosity on this matter.

  Fortunately, scientists do know a fair bit about the genetics that underlie some of the differences in people’s taste perceptions—enough, in fact, to make it clear that each of us lives in a unique world of flavor. Genetic differences likely explain some (though not all) of why former president George H. W. Bush hated broccoli, why a gin and tonic is ambrosia to one person and anathema to another, or why some of us put sugar in our coffee. I wanted to learn more—and, especially, I wanted to know where my own taste perceptions fit into the picture. Once again, that brought me to Monell.

  In particular, I wanted to see Danielle Reed, who has done a lot of the best work on genetic differences in taste perception. A few months before my visit, I had drooled into a vial and shipped it off to Reed for genetic analysis. (Saliva contains enough cells that geneticists no longer need blood samples or even cheek swabs to run their DNA tests.) Now it’s time to see how my sense of taste compares with everyone else’s.

  Reed’s taste-test procedure couldn’t be more low-tech. Her assistants hand me a box containing several numbered vials of liquid, plus a large plastic cup to spit into. Starting with vial 1, I sip the liquid, swish it around in my mouth, and spit into the cup, indicating on a questionnaire how sweet, salty, sour, and bitter I found the sample; how intense the sensation is; and how much I like it. And then I go on to vial 2. It’s a bit like a wine tasting, but without the pretentiousness. And without the wine.

  A few hours later, test scores in hand, it’s time to sit down with Reed to see how they match up with my genes. In person, Reed is a short, plump, cheerful woman with frizzy dark hair who clearly thinks unpacking someone’s genes is a bit like unwrapping a present. She must have done this hundreds of times by now, if not thousands, but the excitement is still there.

  The first test turned out to be a bit of a trick: Vial 1 held plain old distilled water. I’m relieved to see that I scored its taste intensity to be “like water”; rated it dead neutral on the liking spectrum; and detected no sweet, salty, sour, or bitter tastes. At least I’m not tasting stuff that isn’t there. Now on to the real tastes, and the genes.

  First up, T1R3, the gene that contributes to the receptors for sweet and umami. Reed had tested my genome for a variant that, other researchers had found, affects sweet perception. These genetic variants are like spelling changes in the genome. Just as changing a single letter—”dog” to “dig,” say—can alter a word’s meaning, changing a single letter in the DNA sequence of a gene can alter the resulting receptor protein. For the T1R3 variant, people with a T at one particular spot are less sensitive to sweet taste, and like it more, than those with a C. “It’s like they can’t taste sweet as much, so they are choosing the higher concentrations,” says Reed.

  I turn out to be a TT—one T from each parent—which should make me a classic sweet craver. But that really didn’t make sense, I told her. Just that morning, I’d been given a sweetened iced coffee at Starbucks by mistake, and I had ended up pouring most of it out, because it was much too sweet to drink. As far as I’m concerned, it’s also no big deal to skip dessert after dinner—it’s not important to me. Had something gone wrong with the genotyping?

  Reed turned to my taste-test result and burst out laughing. “Oh, look at you! You’re not so far off here.” I’d rated the 12 percent sugar solution—roughly equivalent to a (flat) soda—as only moderately sweet, and highly pleasant. Reed herself—a CC—finds it disgustingly syrupy. Clearly, the link among genes, taste perceptions, and actual food choices is not a simple one.

  That complexity is also evident in some of my bitter receptor genes that Reed tested. One of these was the bitter receptor T2R19, which detects quinine, the bitter chemical found in tonic water. I had the low-responding gene variant, according to the genetic test. Sure enough, when I sipped Reed’s quinine solution, I scored it only mildly bitter and not very intense. That squares nicely with my liking for tonic water, which you may recall is about the only soft drink I ever drink. But it doesn’t explain Reed’s fondness for gin and tonic, because she carries the high-intensity gene variants. “I taste gin and tonic as very bitter,” she says, “but I love it!”

  Then there’s our old friend T2R38, the bitter receptor that determines sensitivity to PROP, PTC, and the bitter thiourea compounds in broccoli and brussels sprouts. The genetic test backs up what I already knew from talking with Bartoshuk: I’m one of the “lucky” ones who reacts strongly to these bitter chemicals. And when I tasted the PTC solution, I scored it as intensely bitter.

  So why does Dani Reed like gin and tonic, which she finds intensely bitter? Why am I drawn to the foods and drinks I taste as bitter, instead of avoiding them?

  “What you taste isn’t always what you like,” says Reed. “I always say, ‘It’s the brain, stupid!’ You can learn! Within the correct context, it’s very much beloved.” Indeed, we quickly learn to find pleasure in flavors—even ones we initially find repulsive—that are paired with attractive rewards. The bitter coffee that delivers a wake-up jolt soon becomes pleasant in its own right. Same for the bitter beer or gin and tonic that accompanies an evening with good friends.

  There may be another dimension to taste preferences, too, says Beverly Tepper, a sensory scientist at Rutgers University in New Jersey. Some of us are what Tepper likes to call “food adventurous.” That means there are really two kinds of supertasters, according to Tepper. Those who are not food adventurous are the classic, picky eaters: they don’t like things too sweet, too hot, too fatty, too spicy. “They know what they like, and their food choices are guided by
their previous experiences. They’re a little bit finicky,” says Tepper. Mr. Lima-beans-and-milk presumably falls into that category.

  On the other hand, supertasters who are food adventurous are willing to be surprised, even by intense tastes, and will try something again even after a disconcerting first experience. Because they’re not put off by intense experiences, this category of supertasters resembles nontasters in their food preferences. “I’m a supertaster, and I actually like a lot of the foods that theoretically I shouldn’t like. But I’m also food-adventurous,” says Tepper. That describes me to a T, too. I get the intense sensory jolt from a highly flavored food—but I like the stimulation.

  These few genes that I had tested are probably just the tip of the iceberg when it comes to genetic differences in taste perception. Reed thinks there could be dozens—perhaps even hundreds—of genes that affect our taste acuity and our perceptions of particular tastes. In addition to the taste receptor genes themselves, many other genes probably affect how our cells respond once a taste receptor has been stimulated, how readily signals are sent to the brain, and every other step of the taste-sensing pathway. My flavor world, it seems clear, is different from yours. We can serve ourselves from the same bowl of soup and have different taste experiences. And taste is only one part of the flavor equation.

  Chapter 2

  BEER FROM THE BOTTLE

  The Association for Chemoreception Sciences, North America’s main conference for smell and taste researchers, meets every April in southern Florida. The location isn’t accidental—the whole point is to give researchers the opportunity to leaven their scientific geekery with at least a few hours of sun and sand. This lends the meeting a remarkably relaxed, nonacademic feel, with sun-deprived, middle-aged folks clad in shorts and Hawaiian shirts thronging the bar or basking poolside in the sun. But that stereotypical Florida hotel ambiance quickly turns surreal, as the conversations on the sundeck turn not to shopping or the kids, but to G-protein-coupled receptors, the psychophysics of odor perception, or the olfactory abilities of mosquitoes. For four days in April, the Hyatt Regency Coconut Point in Bonita Springs is not your average Florida resort.