Sex Sleep Eat Drink Dream (8 page)

Midday

Think in the morning.
Act in the noon.

WILLIAM BLAKE

4. THE TEETH OF NOON

Y
OUR MEETING HAS EATEN
into the lunch hour. Breakfast was skimpy, and now, five hours later, it's getting harder to attend to the matter at hand as your thoughts turn inexorably to the sushi buffet at your favorite Japanese restaurant or the hearty ham sandwich stashed in your lunchbox. The fifteenth-century Venetian surgeon Alessandro Benedetti asserted that nature had relegated the stomach to a site distant from the brain, fencing it off with the diaphragm, "in order not to disturb the rational part of the mind with its importunity." Nature, it would seem, failed in its mission.

What does the mind look like while pondering unagi or honey-baked ham? Where does the craving originate, in the belly or the brain? One would assume clues could be found in people who think incessantly of food. Not long ago, two Swiss researchers, neuropsychologist Marianne Regard and neurologist Theodor Landis, conducted a brain imaging study of such people, a group of patients afflicted with a benign eating disorder the scientists termed gourmand syndrome.

The syndrome was first identified by the team in two patients who developed obsessions with food after suffering stroke damage to their right frontal lobes. Before their illnesses, both patients had been average eaters with no particular food preferences. After his stroke, one patient could think of nothing but tasty food served in a fine restaurant. "It is time for a real hearty dinner," he wrote in his hospital diary, "a good sausage with hash browns or some spaghetti Bolognese, or risotto and a breaded cutlet, nicely decorated, or a scallop of game in cream sauce with 'Spätzle' (a swiss and southern german specialty). Always just eat and drink!" The second patient experienced similar cravings and a yen for food shopping, cooking, and selecting restaurants. He also got a thrill out of recounting special meals: "The creamy pastry slips from the foil, like a mermaid," he wrote. "I take a bite. From now on, it will be more difficult to put me under stress."

To follow up on their observations, the Swiss researchers scanned the brains of thirty-six other passionate eaters and discovered that thirty-four of them had lesions in their right frontal lobes. The scientists were quick to say that their findings do not point to this right-hand corner of the brain as a food-contemplation area, but rather an area possibly involved in impulse control and obsessions of all sorts.

Still, I found the mania curiously familiar and wondered whether it's possible to experience this sort of frontal-lobe activity in varying degrees. I admit to more than a smidgeon of the syndrome myself, a tendency to think too often of food and to remember meals in inordinate detail: the artichokes stuffed with shrimp served on a deck in Fresno, the fried catfish dished up with collard greens in a juke joint in the Delta, a root beer float gratefully inhaled on a lakeshore at my first sleep-away camp. (Letters home from this camp were a litany of complaints about the food, save one: "I may seem happy in this letter but it's only because we had French toast this morning.")

My husband once ate a meal in Julia Child's kitchen and can recall only that he was served "some sort of chicken"—a failure of culinary consciousness I simply can't fathom.

The sort of intense preoccupation with food suffered (or enjoyed) by people with gourmand syndrome may lie at the extreme end of the scale, but all of us fixate on food when we haven't had it for a while. Scientists probing the normal species of hunger have recently zeroed in on centers in the brain devoted to its control.

Don Quixote called hunger "
la mejor salsa del mundo,
" the world's best sauce. The
Oxford English Dictionary
defines it as "that uneasy or painful sensation caused by the want of food." Hunger often involves an aching or growling stomach, but it can also elicit weakness, dry mouth, and—sorry, Dottore Benedetti—headaches and loss of concentration. Hunger pangs peak at midday, even in the absence of external time cues. (A pang, incidentally, is quite different from a growl or rumble, known as borborygmus. The latter arises from the muscular activity of the stomach and small intestine, whether empty or full—the noise is just louder when there's no meal to muffle it.)

It was once believed that the drive to eat originated solely in the stomach. However, the great nineteenth-century neuroscientist Charles Sherrington observed that hunger persists even in those who have had their stomachs surgically removed. Now the finger is definitely pointing elsewhere in our anatomy. A recent neuroimaging study found plenty of "disturbance" in the brain in response to hunger. Oddly enough, the areas of activity differed somewhat in men and women. Researchers at the National Institutes of Health used
PET
scans to look at brain activity in twenty-two men and twenty-two women after they had fasted for thirty-six hours and again after they consumed a liquid meal to satisfy their hunger. When they were fasting, all of the subjects showed more abundant blood flow in the hypothalamus, a brain region known to regulate the basic physiological response to hunger. But the hungry men showed more activity in the paralimbic areas of the brain, which govern emotion, than did the famished women; and when sated, in an area of the prefrontal cortex associated with processing reward. This suggested to the researchers that men may experience more reward from eating than women do. I doubt this, though my experience is admittedly limited.

Hunger is one thing; appetite, the desire to eat, quite another. While the two often coincide, we all know that appetite can easily occur in the absence of hunger. Many of us have the desire to eat long before our stomachs feel hollow because food looks or smells good. Or because it's noon and time for lunch and someone has served us up a plate of broiled trout. Or because we're bored and want the stimulus of hazelnut cake. What is the physiological loop that translates into the craving for crisp pita chips and hummus with a light sheen of olive oil?

What we have learned about the biology of appetite in the past ten years pours into a large pot indeed. You may have thought you were in control of your own food impulses at a given moment, but new science suggests that a complex mix of chemical messengers is in fact dictating your dietary decisions.

When endocrinologists at Harvard reviewed all the molecules that regulate appetite, turning it up or down, signaling "eat" or "don't eat," they found dozens of chemical messengers lurking in mouth, stomach, intestines, liver, bloodstream. Some of these couriers act rapidly, from meal to meal, controlling appetite and satiety for any single dining experience. Others exert their effect over the long term, keeping track of the body's fat supplies and telling the brain when they're running low so that it can step up appetite. The long-term signals may spur the production of short-term "I'm hungry" messages or quash them. You're probably unaware of these chemical fluctuations, but they direct your behavior, either driving you toward that lunch buffet or letting you get on with your work.

Two brain regions read this soup of signals, and a sophisticated crosstalk between them determines the outcome. The recipient of the short-term signals for any particular meal is the hindbrain, or caudal brainstem. The umpire of signals relating to the long-haul need for food is the hypothalamus, especially an arc-like cluster of five thousand or so neurons known as the arcuate nucleus. As early as 1912, postmortem exams of very obese subjects revealed lesions in the hypothalamus, suggesting that this part of the brain might be important in regulating appetite. Researchers lately confirmed that the arcuate nucleus integrates and adjudicates the sometimes conflicting messages from a staggering array of hormones, nutrients, and nerves to decide which way to make the body feel, like eating or not. It also determines how to adjust metabolism—the set of chemical reactions by which the body extracts energy from food or stores and uses it for all of its activities—to shift it up or down, to waste or conserve energy.

One of the star players among the "hormones of hunger" is ghrelin (pronounced GREL-lin, from the Old English
ghre,
to grow), a small peptide secreted primarily by the stomach and upper small intestine, which acts on the brain as a potent appetite stimulant. Volunteers injected with ghrelin get very hungry and eat 30 percent more than they normally would.

David Cummings and his colleagues at the University of Washington see ghrelin as a "saginary" hormone (from the Latin
saginare,
to fatten)—the product of a thrifty gene that evolved to help animals consume and store fat well, thereby increasing their chances of survival during times of famine. When the researchers measured circulating ghrelin thirty-eight times during a twenty-four-hour period, they found that levels of the hormone rise and fall dramatically over the course of a day. Before meals, levels go up precipitously, by nearly 80 percent, peaking when the stomach is empty, just before each meal, and then plummeting to trough amounts an hour after eating.

"The empty stomach, however, is not the trigger for pre-meal ghrelin surge," says Cummings; instead, it's the brain anticipating a meal. If you're accustomed to having four meals a day at regular times, you'll experience four ghrelin spikes, one before each expected meal. If you're used to two meals, there will be two spikes. As the number of scheduled meals decreases, so does the number of surges, but the size of each surge increases, as does the sensation of hunger and the amount of food eaten at each meal.

Certain hormones oppose the actions of ghrelin, among them leptin. Not long ago, this hormone made a big splash in the press as a possible magic bullet for treating obesity. Produced by fat cells, leptin is made and released into the blood in proportion to the amount of body fat one is carrying; from the blood it travels to the hypothalamus, which responds by modulating appetite and metabolic rate. The more fat you possess, the more leptin is made by your cells. Leptin appears to be the body's way of telling the brain whether fat stores are sufficient so that it can match caloric intake to caloric expenditure—a feat it's remarkably good at: For most people, intake exceeds expenditure by less than 1 percent. (Even this small difference, however, can lead to added pounds over the long term.)

When leptin levels fall, the brain reads this as a warning sign of deprivation and sends out signals to the body to ratchet up appetite and make metabolism more efficient, reducing the expenditure of energy until the lost weight is recovered. With weight loss, and the accompanying decrease of leptin levels, the hypothalamus sends neural signals to the hindbrain to render it less sensitive to short-acting satiety signals from the gut, explains David Cummings. "Consequently it takes more food at a given meal to make a person feel full, so one tends to eat more at each meal until the original body weight is regained. In this way, the long-acting signals ultimately govern food intake at individual meals." Indeed, this is what makes dieting, and especially keeping weight off, so difficult. The body has this sophisticated mechanism for protecting against weight loss.

Leptin has worked as a therapy for obesity only in rare instances, for people who genetically lack the hormone. In other cases of obesity, resistance to leptin may develop, and raising levels further is not very effective. Still, it is one powerful hormone. Studies in mice suggest that during neonatal development, leptin molds the circuitry of the brain, strengthening pathways that suppress appetite and weakening those that stimulate it. Taking in too much or too little food at this critical stage of infancy may actually change the way the circuits are shaped, affecting appetite and how the body responds to fat in adulthood. In fact, say researchers, leptin's molding of the appetite circuitry early in life may be the biological underpinning of what's known as body-weight set-point—a kind of memory for the weight range the body wants to maintain throughout life. You can move around in this set-point range through diet and exercise, but you can't change its parameters.

So here's an angle on appetite: Your desire for an early lunch on a Wednesday in June may ultimately have its roots in the distant days of infancy.

Whatever its origins, your body's cry for food will not be silenced, so you suggest a lunch break and hop in a taxi with colleagues to go to a nearby salad bar. What do you choose? Fresh greens? Fried chicken? Marinated tomatoes with fresh mozzarella?

What we opt to eat, and why, is nearly as complex a matter as appetite itself. Experience, childhood associations, legacies from our deep past, all play powerfully into food selection. The underlying drive for certain sweet, salty, and umami flavors is rooted in the need for basics, for calories and essential nutrients. The sour we pick only selectively, avoiding the strong acidity or tartness of unripe or spoiled fruit. The bitter we shun, with good reason. In perusing that salad bar, I would pass quickly over the potatoes with fresh mint—a learned aversion. Some twenty years ago, my husband made a potato salad with mint, garlic, and olive oil. Unfortunately, the potatoes he used were spoiled, and the strong dressing disguised the bitter taste of solanine, a poisonous alkaloid made when potatoes "green" in response to overexposure to light. I ate the salad with gusto and ended up sick as a dog. Two decades later, I still can't contemplate revisiting this dish.

Nausea—hunger's antithesis—is a potent protective tool. Just what causes the sick head and roiling stomach remains an enigma. But most of us have experienced the sensation at one time or another, from a bad batch of tuna, too much alcohol, tobacco, or salt water, illness, disgust, unpleasant smells, medication, pregnancy, or motion sickness (the word "nausea," in fact, derives from the Greek
naus,
for ship). So powerful is the sensation that mothers often remember the discomfort of morning sickness long after they've forgotten the pain of childbirth. As nausea goes from bad to worse, the salivary glands flow, the heart races, blood pressure drops, blood vessels in the skin constrict, and we grow pale and clammy. At the same time, electrical activity in the stomach shifts, causing its muscles to relax. The esophagus contracts, the upper small intestine empties its contents into the stomach; then, in one giant contraction coordinated by the brain, the abdominal muscles and diaphragm squeeze, exerting pressure on the stomach lying between them, and the retching begins.