Flavor: The Science of Our Most Neglected Sense - Bob Holmes 2017

Broccoli and Tonic

As a journalist, and a classically polite Canadian, I don’t often stick my tongue out at the people I’m interviewing. It seems bad form, somehow. But I’m doing it now to Linda Bartoshuk, the grande dame of taste research. Fortunately, she doesn’t seem to mind.

“Oh, your tongue is gorgeous,” she gushes. She leans close and paints the tip of my tongue with a Q-Tip dipped in blue food coloring, which highlights the taste buds on my tongue. (To be accurate, they’re not actually taste buds, which are microscopic. Those mushroom-shaped bumps on the surface of the tongue that most people call taste buds are, technically speaking, really fungiform papillae, an impressive-sounding Latin term that means “mushroom-shaped bumps.”)

I hold up a mirror to see what Bartoshuk sees on my tongue. Tiny pink islands stand out in a sea of blue dye. “You see those red dots on the front? Those are fungiform papillae,” she says. “You have a lot. Oh, and you have them all the way back! You’re very close to a supertaster.”

Understanding this notion of the supertaster—that some people have a much more acute sense of taste than others—is what has brought me to Bartoshuk’s lab here at the University of Florida in Gainesville. It was Bartoshuk who first suggested, back in 1991, that people tend to fall into three groups, based on their ability to taste a bitter compound known as propylthiouracil, or PROP.

You may have encountered PROP in a high school biology lab or at a science museum somewhere. You’re handed a little piece of filter paper infused with a modest amount of PROP, which you put on your tongue. Some people—the nontasters—just shrug, tasting basically nothing apart from filter paper. Others—the tasters—notice an unpleasant bitter taste, while the third group experiences extreme bitterness. This third group, the supertasters, are easy to recognize: They’re the ones who make an anguished face and rush off to find something—anything—to wash that horrible taste out of their mouth. Bartoshuk often asks people to rate the intensity of PROP’s bitterness on a scale from 0 to 100, where 100 is the most intense sensation they’ve ever experienced—the pain of childbirth, say, or a broken bone, or the visual sensation of looking directly at the sun. Supertasters often rate the bitterness of PROP in the 60—80 range, nearly in broken-bone territory. Sure enough, I’d score it a 60: nasty, but not debilitating. “That’s into supertaster territory,” says Bartoshuk. “That’s in the area where you’re not screaming, but you’re definitely much higher than normal, and your tongue looks it.”

And it’s not just bitterness. Supertasters tend to rate sweets as sweeter, salt as saltier, and chili peppers as hotter. They even report that food aromas are more intense, says Bartoshuk—probably because taste and smell reinforce each other in the brain.

Before I get too smug about my taste acuity, though, Bartoshuk points out that supertasters tend to be pretty boring eaters. Most of them prefer to avoid the intense taste experiences that come with highly flavored foods, so their diets are often bland and narrow. (I knew a man once who lived on a habitual diet of lima beans and milk. I would bet good money he was a supertaster.) In particular, bitter greens and other vegetables don’t show up very often on the plates of most supertasters.

That’s where I start to get confused, because that doesn’t sound like me. I love collard greens, rapini, and other bitter vegetables; I always pick the hoppiest beer I can find; I drink my coffee black and without sugar; tonic water is my soft drink of choice—indeed, the only one I ever drink. In contrast, Bartoshuk—a nontaster—has very pronounced food aversions. She detests tonic water, for example. “When I first tasted it, I couldn’t believe it was a beverage,” she says. “I cannot stand greens. The bitter taste is just beyond belief to me.”

So what’s going on? It’s time to look more closely at this whole supertaster notion, which turns out to be more complex than it appears at first glance.

A little background: Even though we talk loosely about “tasting” complex foods like wine and cheese, most of their flavor actually comes from our sense of smell. In fact, even though we usually treat smell and taste as one and the same, they actually have different jobs to do. Smell is all about identification—it answers the question, “What is it?” It tells you the difference between rosemary and oregano, Brie and Stilton, or Cabernet Sauvignon and Pinot Noir. It tells you when something is burning on the stove, and it tells you that the dog needs a bath. We can even recognize the odor of our own bodies and those of our sweethearts.

Taste, in contrast, answers a different question: “Do I want to eat this?” Taste is all about broad categories of good and bad, the yes/no, red-light/green-light decisions that would have been so crucial for our hunter-gatherer ancestors. As omnivores without access to grocery stores, they had to make these calls every day, and our taste repertoire bears witness. Everyone knows the “four basic tastes”: sweet, salty, sour, and bitter. If you’ve been paying attention the past few years, you’ve probably heard of a fifth: umami, a Japanese term that means “delicious flavor” and is usually translated as “savory,” “brothy,” or “meaty.” (There might be additional basic tastes, too, as we’ll see.) A closer look at each of those five tastes reveals a lot about what was important to our ancestors.

Sweet tastes, most obviously, mark the presence of sugars, an important source of calories. Even starchy foods such as potatoes and grains yield a hint of sweetness as we chew, because enzymes in our saliva break down the starches into sweet-tasting sugars. Umami comes from amino acids—in particular, one called glutamate, though others contribute as well—that indicate the presence of proteins, another major class of nutrients. And our taste for salt would have helped our ancestors identify the electrolytes that were so precious and hard to find before salt shakers sat on every table. Hardly surprising, then, that we’re hardwired, even as infants, to be drawn to sweet, umami, and salty tastes.

But taste also warns us when we’re about to eat something that might be harmful. Many toxins taste bitter, so we’re hardwired to reject bitter foods. Just watch the face of a toddler who unknowingly sips from a glass of tonic water—or, for that matter, an adult who gets surprised by a bitter-tasting berry or a first taste of aquavit or Fernet-Branca. The bitterness triggers our poison-avoidance reflex, and we make a “yucky face,” sticking out the tongue in a reflex that pushes the threatening food out of the mouth. Similarly, we tend to reject sourness, which could signal spoilage or unripe, indigestible fruit. With experience, and practice, we often learn to override that hardwiring for certain foods—coffee, hoppy beers, brussels sprouts, sour candy—but few, if any, people like them right away. Remember your first sip of coffee?

Other species, with narrower diets, have fewer decisions to make and can often get by with fewer tastes. In the use-it-or-lose-it world of evolution, that often means they lose those extraneous tastes. Cats, for example, are entirely carnivorous, so they would never need to recognize high-sugar foods—and, in fact, they seem indifferent to sweetness. Sure enough, when researchers looked more closely, they found that cats have lost a crucial gene that would allow them to taste sweetness. Other carnivores, such as otters, sea lions, and hyenas, have also lost the ability to taste sweet. In each case, a different genetic defect was responsible, suggesting that the taste for sweet has been lost several different times on the evolutionary tree—presumably, each time an omnivorous ancestor switched to an exclusively carnivorous diet. In contrast, pandas, which eat nothing but bamboo, have no need to detect protein in their diet and have lost the taste for umami. Other scientists recently discovered an even more extreme example of taste loss: vampire bats, with their blood-only diet, live in a taste world focused so tightly on recognizing the saltiness of blood that they lack the ability to taste sweet, umami, or bitter.

And by the way, while we’re talking tastes: You’ve no doubt seen one of those “taste maps” of the tongue that purports to show that we taste sweet at the tip, salty and sour along the sides, and bitter at the back. If you’re up to date on your reading, you may also have heard that it’s completely wrong. As it turns out, though, both sides of the debate are guilty of a little exaggeration. There do seem to be minor differences in sensitivity to the various tastes across the tongue, with some regions a little more sensitive to sweet and others a little more sensitive to bitter, but the differences probably don’t matter much. And you can easily verify that the tastes aren’t tightly segregated into distinct zones, simply by dipping a Q-Tip in salt water and painting the tip of your tongue. You’ll taste the saltiness, even though you’re in what’s supposed to be the “sweet” zone. Best to just forget the whole notion of the taste map.

Those five basic tastes seem like a pretty unimpressive set compared with the vast array of aromas we encounter in our food. Is taste really all that important to us, or is it only a minor part of our flavor experience? To answer that question, I headed from Bartoshuk’s lab in Florida to the Monell Chemical Senses Center in Philadelphia.

You could think of Monell as the Vatican City of flavor research, but without the fancy architecture. The nondescript brick office building, on the fringes of the University of Pennsylvania campus just west of downtown, could house anything: doctors’ offices, accountants, engineers. Only a giant bronze sculpture of a nose and mouth, on a concrete plinth next to the front door, hints that something more unusual is inside: one of the planet’s greatest concentrations of researchers on the basic biology of the flavor senses.

Inside, Monell’s boardroom looks much as you’d expect for such an august institution: long, dark wood table polished to a high gloss, high-backed leather chairs, off-white walls hung with framed memorabilia and interesting-but-not-too-interesting art. It all adds up to a clear message: significant discussions of important ideas take place here.

Over the years, many of those ideas have come from Gary Beauchamp, the center’s longtime director. (He stepped down in 2014.) Beauchamp is a small, dapper man with silver hair, a neatly trimmed goatee, and a dignified manner. It’s easy to imagine him charming a sizable check out of a deep-pocketed donor. Right now, though, he’s leaning back in his chair at the head of the table, gazing thoughtfully at the ceiling. “Glaarglglglgl,” he says gently.

“Glaarglglglgl,” we all gargle in response. We each lean forward to spit into a plastic cup, then wipe stray droplets from lips and face.

This peculiar boardroom meeting had its genesis at a conference three months earlier, where I met Beauchamp for the first time. We’d been talking about the relative importance of taste versus smell in determining flavor. Most experts come down rather heavily on the side of smell as carrying the lion’s share of flavor, since it carries so much more information than just sweet, sour, salty, bitter, and umami. Some say smell accounts for 70 percent of flavor; others put it at 90 percent or more.

But Beauchamp wasn’t buying it. In fact, he disagreed vehemently when I suggested this at the conference. “Clearly, olfaction is very, very important,” he said. “But the idea that it’s 70 percent of flavor is complete bullshit, in my view.” Olfaction gets all the attention, he went on, because we all know what it’s like to lose the sense of smell. Anyone who’s ever had a head cold knows that a plugged nose makes food bland and tasteless (though in fact, “tasteless” is actually the exact opposite of the truth—what you’re experiencing is taste alone, in isolation, with smell taken out of the equation). And the jelly bean test gives an even more dramatic demonstration, because it’s so quickly reversible.

On the other hand, most of us have never had the inverse experience, since nothing in our everyday life can take away the sense of taste while leaving smell intact. There is no reverse jelly bean test where you can hold your tongue to keep yourself from tasting. Doctors, too, often see patients who have lost their sense of smell as a result of head injury, viral infection, or just as a consequence of aging. By contrast, relatively few people lose their sense of taste. The big exception is cancer patients who undergo radiation to their head and neck, which often damages taste receptors and nerves. And their experience tells a terrible story, said Beauchamp, whose wife’s uncle was one of the unlucky ones: as bad as it is to lose your sense of smell, losing taste is far, far worse. “When people lose their sense of taste, they don’t eat. They starve themselves to death,” he said. “My view is that taste is absolutely the bedrock of flavor.”

Moreover, Beauchamp thought he had a way to test that claim—an experiment that would be, in effect, something fairly close to a reverse jelly bean test. Certain drugs, it turns out, can block the perception of salt and sweetness, two of the most important tastes in many meals. “When those things are gone, my guess would be that your dinner would be absolutely awful,” Beauchamp said. He’d taken the salt-blocking drug before, out of curiosity, but had never tried knocking out both tastes at once. We agreed that it would be an interesting test to try sometime.

Which brings us back to the Monell boardroom, several months later. Beauchamp, two of his colleagues, and I are gargling with chlorhexidine, an over-the-counter mouthwash sometimes used to treat gum disease, which has the odd side effect of blocking the taste of salt. Each of us tosses back four little cough-syrup cups of the bitter-tasting stuff, one after another, swishing each around in our mouth for thirty seconds and gargling occasionally to make sure the solution reaches well back in the throat, before spitting it out. We follow that with four more cough-syrup cups of a swampy-flavored tea made from a South American plant called Gymnema, which knocks out sweet taste.

Sure enough, all that gargling and swishing seems to have obliterated those two tastes. A sip of Pepsi yields a brief prickling on my tongue—the mouthfeel, or touch, sensation from the carbonation—then its flavor vanishes completely. I dip my finger in salt crystals and lick it off: nothing, except a tiny residual saltiness at the very back of my throat where the chlorhexidine didn’t quite reach. Now we turn to our experimental “lunch,” a burger and fries from the food truck parked in front of the building, now quartered into individual servings. Without the most important parts of our sense of taste, would we be able to stomach the meal, or would we, like Beauchamp’s wife’s uncle, just give up?

Sure enough, downing the burger is like eating a mouthful of textured clay or soft plastic pellets. Have you ever accidentally left the salt out of homemade bread and been bored by the blahness of the resulting loaf? This burger is like that, but much more so—and we’ve only knocked out two of the five basic tastes. When I eliminate smell, too, by pinching my nose shut, it’s even worse: a totally nondescript experience. But even the loss of taste alone is really crippling—much worse than doing without smell, as I have when eating a burger while nursing a cold. So it looks like the burger, at least, bears out Beauchamp’s theory that taste trumps smell.

The fries, though, aren’t so bad—partly because I get a little residual saltiness at the back of my tongue, where the gargle didn’t reach, but partly because there’s still something interesting going on when I put them in my mouth. Could this be the “fat taste” that many researchers now think belongs in the canon, or the fat’s pleasant mouthfeel? Then, too, the ketchup still gives a pleasantly tart/umami kick, though it’s oddly altered by the lack of sweetness.

All in all, I think Beauchamp might be right. If I had to pick one flavor sense to lose, I’d probably rather give up smell and keep taste. Food that lacks the basic tastes is not actively bad or repugnant, just utterly unfoodlike. If every meal was like this, I’d certainly have a hard time sitting down to eat three times a day.

You’d think that such a vital sensory system—especially one that’s relatively simple, with only a handful of basic tastes—would be completely understood by now. Not so: Huge gaps remain in our understanding of how taste works. Scientists can’t even agree on how many basic tastes there are.

At the simplest level, we know a fair bit about some parts of the story. Tasting happens when the thing we taste—the tastant—binds to receptors on taste cells on the tongue or palate. The tastants for salty and sour—sodium and acids, respectively—go right into the taste cells and activate them, in a process that’s still not fully understood. The process is pretty well worked out for sweet, umami, and bitter, though, so let’s look at them in a little more detail.

Leo Tolstoy famously wrote that happy families are all alike, while each unhappy family is unhappy in its own way. Taste is kind of like that, too. The good tastes, umami and sweet, are each recognized by a single receptor, a two-part protein that’s woven into the outer membrane of taste cells. (There may be other, unrelated receptor molecules that are also sensitive to sweet and umami tastes, but the evidence there isn’t conclusive yet.) For umami, the two parts are called T1R1 and T1R3, while for sweet it’s T1R2 and T1R3. The amino acid glutamate, or one of several sugars, slip into fitted pockets on these combo receptors. The traditional metaphor here is a key fitting into a lock, but you could also think of the way an expensive camera slots into a foam carrying case. If you have the wrong case for the camera, it doesn’t fit. If they match, the camera slips in perfectly.

The bad, bitter taste, on the other hand, makes use of a huge committee of receptors called T2R receptors. Each member of the committee—there are at least twenty-five in humans—handles a different range of bitter compounds. Some, like T2R10, T2R14, and T2R46, are what the scientists like to call “promiscuous,” mating with a wide range of bitter compounds. In fact, if you just had those three T2Rs and no others, you’d be able to detect more than half of a test sample of 104 diverse bitter-tasting chemicals. Some other bitter receptors, like T2R3, seem to be monogamous, with only a single chemical known to activate them. It works the other way, too: Some chemicals activate many different T2Rs, while other chemicals trigger just a single bitter receptor. What’s more, bitter receptors seem to come and go over the course of evolution: The human genome is littered with the rusting hulks of bitter receptor genes that no longer function. These must have been important in our evolutionary past, but—like the sweet receptors of cats—they have become irrelevant enough that we no longer need them, and we haven’t noticed their absence.

Scientists still don’t know whether all those bitter receptors send identical signals to the brain—in which case there’s just a single taste we call “bitter”—or whether we can actually taste the difference among different classes of bitter. Part of the problem is that when you compare, say, the bitter of a hoppy ale to that of coffee, you’re not just comparing the output of particular bitter receptors, particularly T2R1 for hops and T2R7 for caffeine. Instead, you’re really comparing the whole flavor profile of the two drinks. Even if you hold your nose while drinking—which few of us do in a social setting—the two differ in other tastes such as sweet and sour. We don’t generally experience, let alone compare, pure bitter tastes in our everyday lives. But research scientists do, and at least one expert is convinced that there’s more than one bitter taste. “When you do a lot of bitter research, and taste these things side by side, you realize they taste different,” says John Hayes, a flavor researcher at Penn State University. And that plays out in our food preferences, he thinks. “I like my beers very hoppy,” he continues. “I love a good IPA. And yet I can’t stand grapefruit, because I find it bitter. If there was only one kind of bitterness, then the learning process that I went through to learn to like my IPAs presumably would have generalized over to grapefruit juice. And the fact that it hasn’t generalized, to me, starts to provide some of the argument for why there’s more than one kind of bitterness.” He’s now hard at work in his lab trying to prove this hunch.

There’s a lot left to learn about umami, too. Now that scientists have found the receptor responsible for umami, there’s little doubt that it deserves to be considered the fifth basic taste. But for most people, it’s still a little hard to accept. After all, everyone knows exactly what you mean when you talk about sweet, salty, sour, or bitter. If umami is just as fundamental a taste, then why does it so often need to be explained? What makes umami so obscure?

Two reasons, says taste researcher Paul Breslin of Monell. First, we routinely experience the other tastes in nearly pure form: the sweetness of honey, the sourness of lemon juice, the bitterness of radicchio, a pinch of salt. “You get, like, a pure shot of those,” he says. “But you’re never going to experience pure glutamate in the world. You’re not going to find a pile of it that you can lick. We really only experience it in combination with a lot of other things.”

That inability to isolate the taste of umami is reinforced by Breslin’s second reason: Our umami receptors max out at low intensity, so we’re physically unable to experience very umami in the same way we can taste very salty or very bitter simply by piling on the salt or brewing a cup of extra-strong espresso. Thanks to our perceptual apparatus, umami can never be anything more than a subtle sensation. It’s as though you could understand the color red from referring to a crimson rose, yellow from a lemon, and green from a midsummer forest, but then had to try to figure out blue from skim milk.

There’s also a cultural component to our umami blindness, however. Most people from Western countries struggle to put a name to umami taste sensations, but that’s not the case for people from Asian countries. “If you look at Japanese kids, you put MSG in their mouth and they say ’umami’ like that,” says Danielle Reed, Breslin’s colleague at Monell, with a snap of her fingers, “like American kids put sugar in their mouth and say ’sweet.’” As umami becomes a more prominent part of our food culture—with food writers tossing the term around freely now, and restaurants like Umami Burger part of the general conversation—it’s likely that our umami blindness will gradually recede into the past.

When that happens, it will be interesting to see whether our appreciation of umami rescues the reputation of MSG. MSG—monosodium glutamate—is, after all, merely sodium, which is pure salty taste, and glutamate, which is pure umami taste. When chefs work hard to enhance umami by adding dashi or soy sauce to stocks, incorporating mushrooms in stews, aging their meat, or incorporating fermented ingredients, they are simply boosting the glutamate content of the finished dish—and we love the result. Why, then, do so many of us shudder at the thought of boosting glutamate directly, by adding it in pure form? We routinely see signs in restaurant windows or labels on packaged foods proclaiming “No MSG!” But what self-respecting cook would ever boast of doing without salt, sugar, or lemon juice?

The reason for MSG’s bad reputation, of course, is that many people feel that it causes an unpleasant reaction when they eat food that has had MSG added. This notion, which is now commonplace, is actually a relatively new idea. It first appeared in 1968 when a Chinese American doctor, Robert Ho Man Kwok, published a letter in a leading medical journal describing “numbness at the back of the neck, gradually radiating to both arms and the back, general weakness and palpitation” beginning a few minutes after starting a meal at a Chinese restaurant. Kwok wasn’t sure what caused this “Chinese restaurant syndrome,” but he suggested MSG as one possibility.

The news media quickly picked up the story, and similar anecdotes began popping up all over. Soon researchers began giving MSG to volunteers, who reported symptoms similar to Kwok’s syndrome and added others, such as headache, to the list. The idea that MSG could be bad for you became widespread. Soon Ralph Nader and others were urging governments to regulate its use.

But even then, skeptics wondered: If MSG really produces such unpleasant symptoms, why didn’t anyone notice this sooner? After all, the food industry had been using MSG for decades, and not just in Chinese food. By the time Kwok published his letter, the United States alone produced fifty-eight million pounds of MSG every year, and it showed up in everything from baby food to canned soup to TV dinners. Yet no one had remarked on a “TV dinner syndrome” or “canned soup syndrome.”

All this made MSG research a hot topic during the 1970s. As scientists dug deeper into the compound’s effects, though, Chinese restaurant syndrome began to look more and more iffy. The most damning evidence came from several studies of people who claimed to be sensitive to MSG. Researchers gave all the volunteers a capsule to swallow, without telling them whether it was MSG or a dummy capsule containing inert ingredients. (Using a swallowable capsule prevented the volunteers from tasting the difference.) If there was any truth to their self-professed sensitivity, participants should have developed symptoms of Chinese restaurant syndrome when they consumed MSG, but not when they took the placebo. In fact, though, the volunteers reported just as many symptoms with the placebo as with MSG—strong evidence that their symptoms stemmed from what they expected to happen, rather than from what they actually ate.

That’s not as surprising as it sounds. Most of us have felt a little funny after eating now and then. Maybe you ate a bit too much, or too fast, or were feeling tense for other reasons. And many of us are especially cautious after eating something new, as Chinese food would have been for many people in the 1960s. Once one unsettling experience has planted a seed of doubt, our expectations can start to turn our future responses into a self-fulfilling prophecy.

In fact, when researchers looked back at the early studies that first suggested a link between MSG and Chinese restaurant syndrome, most of them suffered from this expectation problem. Usually, the researchers had not bothered to hide the taste of MSG, so that participants in the study could probably guess whether they’d consumed MSG or a placebo. Some studies didn’t even attempt a placebo but simply gave MSG to people and asked them if they felt any symptoms—an ideal situation for expectations to take the driver’s seat.

Even so, there are no doubt a few people out there with a genuine sensitivity to MSG. But if pure MSG causes problems, those people should also have trouble with dishes containing mushrooms, soy sauce, Parmesan cheese, and other foods naturally rich in umami flavor. And of course, overuse of MSG could bring its own problems, just like overuse of salt or lemon juice or any other seasoning. With those cautions in mind, though, there’s no reason why most cooks shouldn’t incorporate MSG into their repertoire of seasonings. After all, most kitchens have recourse to pure chemical seasonings to boost the tastes of salt (sodium chloride), sweet (sucrose), and sour (acetic acid, aka vinegar). Why not keep a little MSG on hand for those times when a dish needs a boost of pure umami?

When it comes to industrial taste research, though, umami is small potatoes. The big money is in sweet. Like umami, sweetness is all about a single taste receptor, as far as we know (although, as we’ll see in a moment, there may be some reason to suspect other receptors, too). And that simplicity has sparked a huge effort from scientists—mostly working for Big Food—to find alternative ways to tickle that receptor that aren’t accompanied by the caloric charge of real sugar.

Most of the artificial sweeteners already on the market are the result of pure dumb luck. The oldest was discovered by accident in 1878 when Constantin Fahlberg, a chemist working on coal tar products in Baltimore, forgot to wash his hands before supper and noticed that his bread tasted “unspeakably sweet.” He thought nothing of it until he noticed the same sweetness on his napkin, his water glass, and, eventually, his thumb. Fascinated, Fahlberg dashed back to the lab and started tasting everything he could find. Fortunately, he found the sweet compound, which we now know as saccharin, before he got to anything too toxic.

Cyclamate has much the same story: in 1937, a chemist at the University of Illinois set his cigarette down on the corner of his lab bench and noticed when he picked it up again that it tasted sweet. Aspartame: a chemist working on antiulcer drugs in 1965 licked his finger to help pick up a piece of paper and noticed a sweet taste. Sucralose: a chemist in London was asked by his boss in 1976 to “test” a new chemical, but misheard it as “taste”—a potentially lethal error for a chemist, but one that worked out well for the company.

Artificial sweeteners reduce calories for two reasons. Some, such as saccharin and sucralose, are not broken down by the body and thus provide no calories. Others, such as aspartame, taste sweet at lower concentrations than regular sugar, so even though they are digestible, they deliver their sweetness with fewer calories. There’s a catch—even though some of these chemicals start tasting sweet at low concentrations, their sweetness often maxes out early, too. No matter how much saccharin you dump in your coffee, for example, it never tastes sweeter than a 10.1 percent sugar solution. That’s a problem for soft drink manufacturers, because regular Coke is 10.4 percent sugar, and Pepsi is about 11 percent.

That’s not the only reason artificially sweetened drinks taste a little weird to many people. Another is that most of the artificial sweeteners trigger not just the sweet receptor but also one of our many bitter receptors, producing a bitter aftertaste that many people find highly objectionable. Since people have different sets of bitter receptors, some of us are bothered by certain sweeteners and not others. I get a bitter taste from saccharin, for example, which suggests that my T2R31 bitter receptor works well. On the other hand, I get no bitter taste from the low-calorie natural sweetener stevia, so I probably have a broken version of whichever bitter receptor (still unknown) responds to that sweetener.

But bitterness isn’t the only problem with the taste of artificial sweeteners. Linda Bartoshuk, for example, can’t taste the bitterness of aspartame or saccharin, yet she knows them when she tastes them. “The sweet of saccharin is nothing like the sweet of sucrose. I don’t know how anybody could ever confuse them,” she says. “And if I accidentally get a beverage with aspartame in it, I’m not confused for a moment. I don’t like it. So it’s pretty clear that not all sweets are the same.”

Part of the reason for that is that each sweetener has its own distinctive timing for triggering the sweet receptor. Real sugar reaches its peak sweetness in about four seconds, then the taste trails off about ten seconds later. Most artificial sweeteners hang on too long, producing a cloying aftertaste. Aspartame, for example, starts a second later and lasts four seconds longer. But Bartoshuk thinks the taste differences might also point to the existence of a second kind of sweet receptor, as yet unknown. It’s hard to believe that we don’t know everything yet about something as obvious—and as lucrative for Big Food companies—as sweetness, but there you are.

If artificial sweeteners are the king of taste research, dollar-wise, then salt substitutes would have to be the queen. The average American consumes about 9 grams of salt daily, almost half again as much as the recommended maximum of 5.8 grams per day, and the majority of that comes from processed foods. That high salt intake is a big reason why sixty-five million American adults have high blood pressure. As a result, food-processing companies are under a lot of pressure to find ways of reducing the sodium in their products.

The problem is, that’s not easy to do. As anyone who’s spent time in a kitchen knows, salt contributes much more than just a salty taste to the flavor of a dish. Used judiciously, salt can enhance all the other flavors, making meat meatier, beans beanier, and potatoes potatoier. That’s largely because the sodium ions help draw other flavor compounds—mostly components that enhance smell, not taste—out of the ingredients and into solution, where we can detect them. Omit the salt, and your food literally has less flavor. This explains why a skilled cook can often tell by smell whether a dish needs more salt.

To find out how food scientists are working around the problem, I asked Peter de Kok, who works for the food science company NIZO in the Netherlands. De Kok—who, like most Dutch scientists, speaks flawless English—comes across as a cheerful fellow with a boundless enthusiasm for salt reduction. There are three ways to deliver all the flavor bang of regular salt with less sodium, he says. You already know about the first one if you’ve ever bought “low-sodium salt” in the grocery store: simply replace some or all of the sodium with another salt ion. The more chemically similar your replacement is to sodium, the better job it does of substituting. In practice, that pretty much restricts the choice to potassium, which is about 60 percent as salty as sodium. (Lithium would actually be a better substitute, flavor-wise, but it has powerful psychological effects—just ask anyone with bipolar disorder.) Unfortunately, many people—though I’m not one of them—also get a bitter taste from potassium, so companies can only swap out part of the sodium in their low-sodium salt.

If you don’t want to replace sodium with a different ion, a second approach is to find a way to get more flavor from the same amount of salt. Smaller salt crystals dissolve more quickly, so they taste saltier when sprinkled atop food. (The converse is also true, of course—when you eat a pretzel topped with the traditional big salt grains, you’re actually getting more sodium than necessary for the amount of salty flavor it delivers.) De Kok and his colleagues also try to find ways of getting more of a food’s sodium out of the food and into your mouth, where you can taste it. For example, they’ve been working on changing the texture of sausages to make them juicier. In essence, he says, when you chew these juicier sausages you squeeze more of the salty moisture out into your mouth, so the sausages taste just as salty with 15 percent less salt. Yet another strategy exploits the value of contrast: They’ve patented a method of making bread with alternating layers of salted and unsalted dough. As you bite through the layers, the contrast makes the salty parts stand out, so that the whole bread tastes about 30 percent saltier than it otherwise would.

The third way to cut back on salt without reducing flavor is a bit more devious: Trick the brain into thinking the food is saltier than it is. As we’ll see, your brain blends aromas and tastes together into a unified perception of flavor. Knowing this, de Kok and his team have been experimenting with adding aromas that we’re used to smelling in high-salt contexts. Because anchovies are typically salty, for example, you mentally “add salt” whenever you get a whiff of anchovies, whether the salt is really there or not. You can’t flavor everything with anchovies, though, so de Kok found an alternative that’s more universally beloved but still salty: bacon. The researchers isolated about two dozen different aroma compounds from bacon, then tested each one to see if it enhanced people’s perception of saltiness. Sure enough, they found three that did. By selecting meat that’s naturally high in those three compounds, de Kok’s team was able to make sausages that still tasted right but used 25 percent less salt.

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 atoms 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.