Tasty (13 page)

Eating and drinking proved the easiest behaviors to manipulate. “The ‘rewarding' parts of the brain,” Olds wrote, “were all related to olfactory mechanisms and to chemical sensors.” Flavor and pleasure were, on some level, one.

Olds's discovery was dubbed the “pleasure center.” It was a stunning advance, and scientists wondered if the same brain structures that drew pleasure from a spoonful of sugar might also be the source of sexual gratification, or the satisfactions of a lively conversation or finishing a good book. The media debated the potential advantages of this insight. Perhaps the terrible personal and social scourges of unhappiness and depression, not to mention the suffering that defined the human condition, could be cured with the flick of a switch.

• • •

But it wasn't quite that simple. In 1987, Kent Berridge, then a thirty-year-old junior faculty member at the University of Michigan, was working on an experiment with rats when he noticed something that bothered him. When rodents taste something sweet, their faces and mouths react in a characteristic manner, gaping a bit and flicking their tongues from side to side, as if licking their lips. This is their version of a smile, a clear outward sign of the inner experience of yumminess. The rats had been given a drug to shut down their pleasure centers, and became logy and indifferent as expected. But they also still licked their lips at the taste of sugar—­apparently, they were enjoying themselves, though that was
supposed to be impossible. At first, Berridge shrugged this off as probably trivial.

Berridge's grinning rats had been given a drug to block a powerful brain hormone called dopamine. In the years since Olds's experiments, it had been identified as the chemical that powered the pleasure center. Dopamine is a neurotransmitter, a hormone that the brain employs to send messages in concert with firing neurons. Neurotransmitters facilitate everything from movement to emotions. In Olds's day, dopamine was an obscure brain chemical, thought to be a building block of more important hormones, adrenaline and noradrenaline, with no apparent function of its own. Scientists first grasped its importance in the 1960s when they discovered that it was essential to voluntary movement—in fact, it's the dying off of dopamine-generating neurons that leads to the tremors and paralysis of Parkinson's disease. Biologist Roy Wise later found that rats given dopamine-blocking drugs displayed precisely the opposite effects of a pleasure electrode. The rats slumped into utter indifference. They stopped eating and drinking; sweetness and all other pleasures lost their allure.

Wise proclaimed dopamine the pleasure chemical, and the scientific community followed suit. “The dopamine junctions,” he wrote in 1980, “represent a synaptic way station . . . where sensory inputs are translated into the hedonic messages we experience as pleasure, euphoria, or ‘yumminess.'”

• • •

Berridge reran his rat experiment. The results were the same. So he began to search for an explanation for why dopamine-­free animals could still savor the taste of sugar. He wondered
if Wise was wrong. (The two of them were collaborating at the time, so it was a bit awkward.)

One obstacle he faced was that, beyond its facial expressions and behavior, a rat cannot explain how it feels. While researching old pleasure electrode experiments, he found an intriguing way around that problem. Between the 1950s and 1970s, doctors at Tulane University in New Orleans had implanted electrodes in the brains of human volunteers. Most had severe forms of mental illness; researchers hoped that brain stimulation would alleviate their symptoms. (Today, a more exacting variant of this technique, deep brain stimulation, is used to treat severe depression.)

The experiments were revealing, helping psychologists map the sources of behavior and emotions in the brain's anatomy. But they were sometimes spectacularly wrong-headed. In one, psychiatrist Robert Heath implanted nine electrodes in the brain of a young man, code-named B-19, who was severely depressed and had not responded to either drugs or talk therapy. He was also gay, and one aim of the treatment was to “cure” him; therapies included viewing a stag film, and a two-hour visit from a female prostitute.

With so many curling wires dangling from his skull, B-19 looked like a cyborg, and in a way he was: he became a kind of electronic puppet pulling its own strings. Heath gave him a button to activate the electrodes. One was placed in the pleasure center. And sure enough, when a small jolt was administered there, B-19 acted just as the rats had. He kept punching the button: during one three-hour period he hit it 850 times. He reported a strange mix of feelings: self-confidence, relaxation, and arousal. When the lab technicians started to disconnect him, he begged them not to. The electrode also made him want to have sex with both men and women, leading
Heath to think he'd found a potential cure for homosexuality. After several weeks of experiments, the electrodes were removed and B-19 was released. Heath followed his progress for eleven months. “While he looks and is apparently functioning better, he still has a complaining disposition which does not permit him to readily admit his progress,” he wrote. Following his release, B-19 held a number of part-time jobs, had a ten-month sexual relationship with a married woman, and told Heath he had twice turned tricks with men to make money.

Reading these descriptions, Berridge noticed something. The electrodes were assumed to be stimulating eruptions of dopamine in B-19's brain—yet he never seemed to enjoy himself. He became sexually aroused, but never had an orgasm. He never said “oh, that feels good!” Hitting the button led only to more anticipation. Perhaps dopamine did not really create pleasure after all, Berridge thought, but rather the craving for it. Once, scientists had dismissed pleasure's importance. Now, they might be mixed up about what caused it.

Searching for alternative pleasure chemicals, Berridge looked to addictive drugs. Opioids such as morphine and heroin evoke feelings of euphoria. Perhaps the answer was the brain's own natural opioids, also known as endorphins. In the early 2000s, nearly two decades after his initial discovery, he tracked intense pleasure reactions to endorphins in two areas of a rat's brain, the nucleus accumbens and ventral pallidum. He named these “hedonic hotspots.” These tiny clumps of neurons, about the size of the head of a pin, are the only brain structures known that directly cause pleasure.

The neurons in hedonic hotspots respond to several different endorphins, suggesting that pleasure is complicated, the
result of many brain systems interacting at once. One such endorphin is orexin, a comparatively rare substance also connected to appetite, arousal, and wakefulness; another is anandamide, named for the Sanskrit word
ananda
, which means “bliss.” It plays a role not only in pleasure but pain, memory, and higher thought processes. Orexin and anandamide activate opioid and cannabinoid receptors, respectively, which also respond to heroin and marijuana.

The anatomy of pleasure bridges the visceral and the brain's higher functions, placing hedonic hotspots smack in the middle. They work something like circuit boards. There are two hotspots, as well as a “coldspot” nearby that sparks disgust. The coldspot is nestled in an area rich in dopamine neurons that inspire intense wanting: when the two were stimulated together, Berridge made a rat yearn for something that tasted terrible. Removing one hotspot reduced pleasure but didn't eliminate it, but removing the other made sweet things taste terrible. That could mean this hotspot's job is to inhibit disgust and enhance pleasure at the same time.

The simple delight of sugar dissolving on one's tongue appeared to be the product of certain neurons tucked into structures deep inside the brain percolating in a cocktail of the body's most intoxicating hormones. Yet however detailed these anatomical maps of the origins of pleasure became, they could not explain its purpose. The role of the cravings caused by dopamine was also up in the air. As he learned more, Berridge formulated a theory he hoped would fill this void. Like many behavioral models, it was blunt, reducing the vast diversity of human decisions and actions down to the shape of a triangle.

The triangle's sides are named “wanting,” “liking,” and “learning.” It can describe all behavior, but applies particularly to taste and to flavor. Wanting is a state of desire and heightened focus before food is eaten. Liking is the pleasure of a good taste, a reward for doing the work of obtaining food. Wanting and liking work in tandem to forge learning. The human brain very quickly picks up on how to gratify itself, learning where the tastiest food is and how to get it.

In the 1990s, Cambridge University neuroscientist Wolfram Schultz did a series of groundbreaking experiments that dramatized this dynamic. Schultz also showed that dopamine was the hidden hand in cravings: it is what powers “wanting.” In one test, monkeys were placed in front of a computer screen that displayed geometric patterns. One pattern flashed two seconds before sugar syrup was dispensed from a bottle; the other appeared randomly. Electrodes measured the activity of a single dopamine neuron in the monkeys' brains. At first, this neuron fired when a monkey sipped. But as the cycle repeated and the monkeys picked up on the signals, the neuron adapted. It began to fire
before
the treat arrived—­predicting a good taste was coming and sharpening the anticipation and craving for it. When kitchen smells make the mouth water, that's dopamine setting the sensory table. And if learning can be tracked in a single neuron, imagine billions of neurons in the human brain doing the same over the course of a lifetime.

Having identified building blocks of pleasure, Berridge pondered what the fleeting “goodness” in a sweet taste really was. Clearly, it was distinct from the feelings that accompany listening to a favorite song, or seeing an old friend. But deep down, these states might be the same—formed in
the same areas of the brain, reliant on the same patterns of firing hedonic hotspots and hormonal flux. Evidence from fMRI scans suggests there's something to this idea—the different forms of pleasure have patterns of brain activity that closely overlap. As humans evolved and culture made its imprint on the human brain, perhaps the ancient neural circuitry responsible for sweetness was adapted as the template for more exalted pleasures, and maybe even happiness itself. “Final happiness may be a state of liking without wanting,” Berridge said. “That may be a Buddhist sense of happiness.”

• • •

Overindulging in sugar disrupts the normal rhythms of wanting, liking, and learning. Humans evolved eating just enough food to sustain big brains and lithe, active bodies. The stomach can hold only so much, and the gut and brain engage in a continual dialogue to ensure a balance is struck. Powerful hormones excite the dopamine-sensitive parts of the brain, spurring humans to seek food when hunger strikes. Pleasure peaks at the start of a meal, when hunger is keenest, then declines—one reason why no one eats the entire contents of a sugar bowl. But persistently overdose this system, and the signals start going awry. Fructose appears to raise levels of the hormone ghrelin, for instance, which stimulates hunger; instead of satisfying, eating sugar leaves us wanting more.

Science has only begun to trace these easily corruptible pathways running between body and brain. Thanks to our expanding knowledge of taste genes, lab mice and rats can be genetically engineered with specific genetic traits for experiments. Ivan de Araujo, a neuroscientist at Yale, fed both
plain water and sugar water to a type of mouse engineered to have no taste for sweetness. They should not have been able to sense the difference, yet they strongly preferred the sugar water.

Ordinarily, the tongue's sweet receptors signal the brain that a delicious reward is on the way. With that signal absent, de Araujo suspected that the sugar was still making its presence known through an unknown back channel, making the mice crave sugar with no conscious awareness of it. To test this hypothesis, he implanted probes in the mice's brains that measured their dopamine levels; the sugar water produced a dopamine rush. Somehow, de Araujo thought, the body sensed the sugar—perhaps through taste receptors lining the gut—and signaled the brain it was there, triggering the yen for more. When the experiments were repeated with human subjects—their sweet taste blocked with a drug—they described a hazy sense of satisfaction after sipping sugar water.

These urges resist both willpower and medications. Appetite suppressants reduce hunger, but craving and pleasure are more complicated phenomena. Dopamine-blocking drugs shut down the hankering for sugar, but extinguish all motivation at the same time. A drug aimed at suppressing the pleasure of food might kill all joy along with it.

• • •

As more of sugar's insidious effects were discovered, people began getting the message. In the first few years of the 2010s, sales of soft drinks—the single largest source of dietary sugar in the United States—leveled off, and then decreased for the first time in their century-long history. Overall high-­fructose corn syrup consumption fell, too. Obesity rates plateaued,
though at high levels nutritionists still found alarming. Diabetes rates, however, continued to rise. It will take years to assess the public health toll.

The ideal solution would be a sugar substitute that perfectly mimics the taste and poses no health risks. But this is the oldest unsolved taste problem in the world. The Romans boiled crushed grapes in lead vessels to make a syrup called
sapa
, used to sweeten wine, stews, and other dishes. The active ingredient was lead acetate, also known as “sugar of lead,” created by a chemical reaction between the grape juice and the containers. It was also toxic. Some have claimed Rome fell because its entire ruling class suffered from
sapa
-induced lead poisoning (historians are skeptical of this explanation). Lead acetate was still used for centuries afterward as a wine sweetener; among its possible victims were wine-drinkers Pope Clement II, who mysteriously dropped dead in 1047, and, eight hundred years later, Beethoven.