فصل 1

1

THE FATTEST MAN ON THE ISLAND

Stout but not quite obese, and boasting a prominent belly, Yutala would have been an unremarkable-looking man in many places. He would not have stood out on the streets of New York, Paris, or Nairobi. Yet on his native island of Kitava, off the coast of New Guinea, Yutala was quite unusual. He was the fattest man on the island. In 1990, researcher Staffan Lindeberg traveled to the far-flung island to study the diet and health of a culture scarcely touched by industrialization. Rather than buying food in grocery stores or restaurants like we do, Kitavans used little more than digging sticks to tend productive gardens of yams, sweet potatoes, taro, and cassava. Seafood, coconuts, fruits, and leafy vegetables completed their diet. They moved their bodies daily and rose with the sun. And they did not suffer from detectable levels of obesity, diabetes, heart attacks, or stroke—even in old age.

As extraordinary as this may sound to a person living in a modern society beset by obesity and chronic disease, it’s actually typical of nonindustrialized societies living similarly to how our distant ancestors might have lived. These societies have their own health problems, such as infectious disease and accidents, but they appear remarkably resistant to the disorders that kill us and sap our vigor in affluent nations.

As it turns out, Yutala wasn’t living on Kitava at the time of Lindeberg’s study; he was only visiting. He had left the island fifteen years earlier to become a businessman in Alotau, a small city on the eastern tip of Papua New Guinea. When Lindeberg examined him, Yutala was nearly fifty pounds heavier than the average Kitavan man of his height and twelve pounds heavier than the next heaviest man. He was also extraordinary in another respect: He had the highest blood pressure of any Kitavan examined by Lindeberg. Living in a modern environment had caused Yutala to develop a modern body.

Yutala is a harbinger of the health impacts of industrialization. His departure from a traditional diet and lifestyle, and subsequent weight gain, form a scenario that has played out in countless cultures around the globe—including our own culture, our own families, and our own friends. In the United States, we have a tremendous amount of information about the diet, lifestyle, and weight changes that accompanied this cultural transition. This will provide us with valuable clues as we piece together the reasons why our brains drive us to overeat, despite our best intentions. Let’s start by examining how our weight has changed over the last century.

THE COST OF PROGRESS

In New Guinea, as in many other places around the globe, industrialization has triggered an explosion of obesity and chronic disease. If we look back far enough, we can see traces of the same process happening in the United States.

In 1890, the United States was a fundamentally different place from what it is today. Farmers made up 43 percent of the workforce, and more than 70 percent of jobs involved manual labor. Refrigerators, supermarkets, gas and electric stoves, washing machines, escalators, and televisions didn’t exist, and motor vehicle ownership was reserved for engineers and wealthy eccentrics. Obtaining and preparing food demanded effort, and life itself was exercise.

How common was obesity among our American forebears? To find out, researchers Lorens Helmchen and Max Henderson pored through the medical records of more than twelve thousand middle-aged white Civil War veterans and used their height and weight measurements to calculate a figure called the body mass index (BMI). BMI is basically a measure of weight that is corrected for height so we can compare weights between people of different statures. It’s a simple measure that’s commonly used to classify people as lean, overweight, or obese (a BMI below 25 is classified as lean; 25 to 29.9 is overweight, and 30 and above is obese). When Helmchen and Henderson crunched the numbers, they found something truly remarkable: Prior to the turn of the twentieth century, fewer than one out of seventeen middle-aged white men was obese.

The researchers then calculated the prevalence of obesity in the same demographic between 1999 and 2000 using data from the US Centers for Disease Control and Prevention. They found that it started at 24 percent in early middle age and increased sharply to 41 percent by retirement age. Side-by-side comparison of the data from 1890 to 1900 and 1999 to 2000 yields a striking contrast.

This suggests that obesity was much less common in the United States before the turn of the twentieth century, just as it remains uncommon in traditionally living societies today. Although obesity has existed among the wealthy for thousands of years—as demonstrated by the portly 3,500-year-old mummy of the Egyptian queen Hatshepsut—in all of human history, it has probably never been as common as it is today.

Let’s take a closer look at the last half century, because that’s the period over which our data are the most reliable—and during which these numbers have changed most dramatically. In 1960, one out of seven US adults had obesity. By 2010, that number had increased to one out of three. The prevalence of extreme obesity increased even more remarkably over that time period, from one out of 111 to one out of 17. Ominously, the prevalence of obesity in children also increased nearly fivefold. Most of these changes occurred after 1978 and happened with dizzying speed.

Public health authorities call this the “obesity epidemic,” and it’s having a profound impact on health and well-being in the United States and throughout the affluent world. The latest research suggests that we may be gravely underestimating the health impacts of obesity, as up to one-third of all deaths among older US adults is linked to excess weight. Diabetes rates are soaring, as are orthopedic problems caused by obesity. Nearly two hundred thousand Americans per year are having their digestive tracts surgically restricted or rerouted to lose weight. Clothing is now available in staggering sizes such as XXXXXXXXL.

Why are we so much fatter than we used to be? The answer lies in what we’ve been eating and how it relates to the fat we carry, which we’ll explore shortly. But we first have to understand how food delivers energy to our bodies.

THE CALORIE IS BORN

Contrary to popular belief, the term calorie was not invented by SnackWell’s. Rather, it was coined in the early 1800s and was used by scientists to measure energy in all its different forms by the same metric: as heat, light, motion, or the potential energy contained in chemical bonds. These chemical bonds are found in bread, meat, beer, and most other foods, which release their potential energy as heat and light when burned, just like wood or gasoline.

In 1887, Wilbur Atwater, the father of modern nutrition science, described how the potential energy in food fuels the furnace of the human body: The same energy from the sun is stored in the protein and fats and carbohydrates of food, and the physiologists to-day are telling us how it is transmuted into the heat that warms our bodies and into strength for our work and thought.

Recognizing the power of energy as a way to understand our bodies, Atwater’s team was the first to exhaustively measure the calorie content of different foods by burning them in his energy-measuring “calorimeters.” When you see a calorie value on the side of your box of cereal, it was calculated using formulas Atwater developed by measuring the calorie content of food and adjusting it for the intricacies of human digestion and metabolism. (The values are actually in kilocalories, or thousands of calories, which is denoted by capitalizing the word Calorie, a convention begun by Atwater.) Atwater and his colleagues also constructed a giant live-in calorimeter to measure the combustion of food by the human body. This calorimeter was large enough to provide a modest living space for experiments lasting multiple days. Atwater’s system was so effective that it was able to demonstrate with greater than 99 percent accuracy that the energy entering a weight-stable person as food is equal to the energy leaving the body. In other words, in a person neither gaining nor losing weight, the number of calories consumed is equal to the number burned. This statement can be rearranged as the energy balance equation:

Change in body energy = energy in − energy out

Energy enters the body as food, and it leaves as heat after we’ve used it to do metabolic housekeeping, pump blood and breathe, digest food, and move our bodies. We also use it to build lean tissues, such as muscle and bone, during growth. Any energy that’s left over after the body has used what it needs is stored as body fat, technically called adipose tissue. Adipose tissue is the major energy storage site of the body, and it has an almost unlimited capacity. When you eat more calories than you burn, the excess calories are primarily shunted into your adipose tissue. Your adiposity, or body fatness, increases. It really is as simple as that, although as we’ll see in later chapters, the implications are not as straightforward as they initially appear.

Atwater also discovered that chemical energy from different types of foods, including those rich in carbohydrate, fat, protein, and alcohol, is effectively interchangeable in the body: Roughly speaking, all calories are the same as far as the human furnace is concerned. More recent research has also supported the idea that the fat, carbohydrate, and protein content of foods has little influence on adiposity beyond the calories they supply. We know this because when researchers strictly control total calorie intake, varying the fat, carbohydrate, and protein content of the diet has no appreciable impact on adiposity—whether in the context of weight loss, weight maintenance, or weight gain. This undermines the commonly held belief that certain nutrients, like carbohydrate or fat, are more fattening than what their calorie content would suggest. Some foods are nevertheless more fattening than others, but this appears to be primarily because they coax us to eat more calories, not because they have a special effect on our metabolic rate. With this in mind, we can adapt the energy balance equation to describe long-term changes in adiposity: Change in adiposity = food calories in − calories out

To gain fat, you must eat more calories, burn fewer calories, or both. To lose fat, you must eat fewer calories, burn more calories, or both. It’s a simple concept, although applying it to weight loss can be surprisingly difficult, as many people know all too well.

If this principle is true, then we should expect to see that Americans began eating more calories, and/or burning fewer calories, as our waistlines expanded. Let’s have a look.

CALORIES IN: HOW OUR CALORIE INTAKE HAS CHANGED

Measuring calorie intake in an entire country is a challenging task. Yet researchers have so far managed to do it in three different ways. The first way is to measure food production, adjust for the amount that’s being exported and imported, try to account for loss due to food waste, and see how many calories are left per person. The second way is simply to ask a representative sample of people what they eat and tally up the calories. The third way is to mathematically model the relationship between body weight and calorie intake, and use that model to calculate the change in calorie intake that should be required to produce the observed increase in weight.

I’ve graphed calorie intake estimates from all three methods in figure 3. As you can see, the methods yield different estimates, but they all agree that our calorie intake has increased substantially over the period of time that we gained weight the most rapidly (218–367 additional Calories per day between 1978 and 2006). The third method, pioneered by National Institutes of Health researcher Kevin Hall and highlighted in black on the graph, probably comes the closest to capturing the true increase in daily calorie intake over the course of the obesity epidemic: 218 Calories. Remarkably, this increase is single-handedly sufficient to explain the obesity epidemic that developed over the same period of time, without having to invoke changes in physical activity or anything else.

Right about now, you might be putting on your skeptic hat. One pound of body fat contains about 3,500 Calories, so if we’re really overeating by 218 Calories per day, shouldn’t we be gaining a pound of fat every sixteen days—twenty-three pounds per year—and requiring a forklift to get around after a decade or two? Actually, despite the popularity of this type of back-of-the-envelope math among popular media sources, public health authorities, doctors, and even some researchers, that’s not how adiposity works. Hall and his colleagues have shown that this way of estimating changes in adiposity is way off target—and the consequences of this error have important implications for how we think about weight gain and weight loss.

The primary problem with this way of thinking is that it doesn’t acknowledge the fact that as your body size changes, your body’s energy needs change too. To illustrate the principle, think of your adipose tissue as a bank account. If you start out with $10,000 in savings, an income of $1,000 a month, and expenditures of $1,000 a month, in a year, your account will still contain $10,000. Now, imagine you get a raise and your earnings climb to $2,000 a month. At first, your lifestyle remains the same and you only spend $1,000 a month, saving the extra $1,000 per month. But gradually, you start to think it would be nice to have that new computer or fancy pair of shoes. You move into a nicer apartment. Your lifestyle expands, and your expenditures creep up. Six months after your raise, you’re spending $1,500 per month, and after a year, you’re spending the full $2,000 a month. Over this year, your bank account has been accumulating money, but at a gradually slowing rate, until accumulation stops when your expenditures match your income. Your account balance plateaus at about $16,000, and it remains there until your income or expenditures change.

And so it is for adiposity. When your calorie intake increases, your body weight increases, and this extra tissue burns calories. Gradually, as your body enlarges, your calorie expenditure comes to match your extra calorie intake, and you reach a weight plateau. You’re no longer eating more calories than you’re burning, so your weight and adiposity stabilize at a higher level. The same plateau effect happens in reverse when a person cuts her calorie intake.

What are the practical implications of this? An important one is that it takes a larger change in calorie intake to gain—or lose—weight than most people realize. Making small changes to your diet, such as cutting out one slice of toast per day, will lead to correspondingly small changes in adiposity that don’t continue to accrue indefinitely. The new, evidence-based rule of thumb is that you must eat ten fewer Calories per day for every pound you want to lose. Yet it takes several years to arrive at a new stable weight, so most people will want to start with a larger calorie deficit to reach their target weight more quickly and then use the ten-Calorie rule of thumb to maintain the loss.

This offers a partial explanation for that scourge of conscientious dieters everywhere: the dreaded weight-loss plateau. This is where a person diligently cuts her calorie intake and successfully loses weight, but her weight loss stalls before she reaches her goal, even though she continues to follow her formerly successful diet. This phenomenon is real, and Hall’s research offers two explanations for it. First, as a person loses weight, her smaller body needs less fuel, the calorie deficit gradually closes, and weight loss stalls. And second, weight loss ramps up her appetite, making it harder to maintain the calorie deficit (I’ll explain why this happens in later chapters). To restart weight loss during a plateau, she must reestablish a calorie deficit, although that’s easier said than done.

Three independent methods suggest that our calorie intake increased substantially over the course of the obesity epidemic, and this increase is sufficient to account for the weight we gained. Simply stated, we gained weight because we ate more.

Now, let’s step back for a moment. We’ve been focusing on recent history because that’s the time period over which we have the most complete information about adiposity. But what about the first half of the twentieth century? In figure 4, I’ve graphed our calorie intake over the last century, based on food disappearance data from the US Department of Agriculture (the second method of estimating calorie intake). These data are crude, but they serve to illustrate broad trends over time.

As you can see, we ate more calories in 1909 than we did in 1960. Yet as far as we know, there was no obesity epidemic in 1909. Why not?

CALORIES OUT: HOW OUR PHYSICAL ACTIVITY HAS CHANGED

This brings us to the second determinant of adiposity: the amount of energy leaving the body. Aside from metabolic housekeeping, pumping blood and air, and digesting food, another important thing we do with energy is to contract our muscles so we can walk, weed our crops, bale our hay, milk our cows, knead our dough, wash our laundry by hand, and put things together in a factory. As it turns out, we used to do those things a lot more a century ago than we do today. In other words, we ate a lot because we needed the energy to fuel our relatively high level of physical activity.

This is a critical point. In 1909, our high calorie intake was appropriate for our high calorie needs. As our lifestyles gradually became more mechanized over the course of the next half century, physical activity declined substantially. Fewer of us were working the fields with plows and hoes, and more of us were sitting behind a steering wheel, as demonstrated by the massive increase in automobile registrations shown in figure 5. Until 1913, fewer than one out of one hundred Americans had an automobile. Today, there are eight automobiles for every ten of us.

As we became a more sedentary nation, calorie intake declined appropriately until about 1960. People were working up less of an appetite, so they ate less.

Then, around 1978, something changed: We started eating a lot more calories—and our calorie intake continued to increase over the next twenty years, reaching historically unprecedented levels. Yet we remained sedentary. The obesity rate rose so quickly that public health authorities didn’t realize what was happening until an epidemic was upon us.

A NATION OUT OF BALANCE

When calorie expenditure decreases and calorie intake increases, the energy balance equation leaves only one possible outcome: fat gain. We gained fat as we ate more calories than we needed to remain lean, given our physical activity level. In other words, we overate.

For most of human history, including the majority of the twentieth century in the United States, nearly everyone was able to approximately match their calorie intake to their calorie needs without even thinking about it. Yet mysteriously, since then, something has caused our calorie intake to uncouple from our true needs. Something pushed us to overeat.

What drove us to overeat? If we can answer that question, we’ll empower ourselves to do something about it. Let’s begin to answer it by asking another question: What’s the most effective way to cause overeating?

ONE WEIRD TRICK TO MAKE A RAT OVEREAT

Obesity research has a long, rich history of fattening rodents for science. In the 1970s, researchers were looking for a better way to fatten their rats so they could study the development and impacts of obesity more efficiently. In the early days, researchers would simply add fat to standard rodent chow. This worked, but it often took months to produce a portly rat—making rodent obesity research a costly and time-consuming endeavor.

One fateful day when Anthony Sclafani, now the director of the Feeding Behavior and Nutrition Laboratory at Brooklyn College, was a graduate student, he happened to place a rat onto a lab bench where a fellow student had left a bowl of Froot Loops cereal. The rat waddled over and began to eat it heartily. This was surprising because rats are typically cautious with unfamiliar foods. Watching the rat greedily devouring human food, it occurred to Sclafani that foods marketed for people might be more fattening than the high-fat rodent chow he was currently using.

To see if he could design a faster and more effective way to fatten rats, Sclafani went to the supermarket and bought a variety of calorie-dense “palatable supermarket foods,” including Froot Loops, sweetened condensed milk, chocolate chip cookies, salami, cheese, bananas, marshmallows, milk chocolate, and peanut butter. When Sclafani placed these foods into the rats’ cages, along with the obligatory standard rodent pellets and water, the rats immediately gorged on the human food, losing interest in their boring pellets. On this diet, they gained weight at an unprecedented rate. In a few short weeks, the rats were obese, and neither exercise nor an enriched environment were able to prevent it (although exercise did attenuate it). Sclafani named this the “supermarket diet,” although most researchers now call it the “cafeteria diet.” Sclafani’s study was published in 1976, and to this day, the cafeteria diet remains the most effective way to get a normal rat or mouse to overeat—far more effective than diets that are simply high in fat and/or sugar.

This leads us to a disturbing conclusion: Palatable human food is the most effective way to cause a normal rat to spontaneously overeat and become obese, and its fattening effect cannot be attributed solely to its fat or sugar content. If that’s true, then what does this food do to humans?

ONE WEIRD TRICK TO MAKE A HUMAN OVEREAT

In the early 1990s, Eric Ravussin, currently director of the Nutrition Obesity Research Center at the Pennington Biomedical Research Center in Baton Rouge, and his team were looking for a better way to measure calorie and nutrient intake in humans. This turns out to be a surprisingly difficult task. At the time, a number of studies had reported that people with obesity eat about the same number of calories as lean people, leading some researchers to question the role of calorie intake in obesity. The catch was that the data were all self-reported. In other words, researchers asked people to describe what they had eaten and then tallied up the resulting calories. This method does have its advantages; in particular, it provides a snapshot of what people eat in their everyday lives.

It also has disadvantages, which became apparent when researchers began to use more accurate methods of measuring calorie intake. These experiments indicated that people with obesity consistently eat more calories than lean people—after factoring in height, gender, and physical activity (as explained previously, the fact that they have to eat more calories to maintain weight is due to their larger tissue mass). This suggested that the self-reported calorie intake data were wrong in a very misleading way. Today, we know from a variety of lines of evidence that this is indeed the case: People are notoriously bad at describing what, and particularly how much, they eat. Ravussin knew he couldn’t use this method if he wanted accurate results.

A more rigorous approach is to lock people inside a research facility called a metabolic ward and feed them a carefully controlled diet in which every morsel of food is precisely quantified by researchers. This is an extremely accurate way to measure food intake, but it’s also unnatural. People don’t get to choose what they eat, so their food intake may not reflect their normal eating habits. The results of these studies are very reliable but may lack real-world validity.

Ravussin and his team wanted an intermediate method, one that had the accuracy of the metabolic ward but allowed people to select their own diets, replicating everyday life as much as possible. Their solution was to install enormous U-Select-It 3007 vending machines inside a metabolic ward, each containing a variety of entrées, snacks, and beverages. The foods in the vending machines were not chosen at random—“We were screening what people liked and disliked,” explains Ravussin—and only included foods that were tempting. The menu included things like french toast and sausages with syrup, chicken pot pie, chocolate-vanilla swirl Jell-O pudding, cheesecake, nacho cheese Doritos, M&M’s, Shasta cola, and a few apples for the health nuts (no Froot Loops, sadly)—in other words, mostly “palatable human foods” similar to those Sclafani used in his rat study. Ten male volunteers were locked up with the vending machines for seven days with the freedom to select when and what they ate. To monitor their food intake, each person had to enter an ID code when he withdrew food and return all uneaten food to the research staff for weighing.

The experiment was a success: Ravussin’s team was able to accurately measure food intake in people who were selecting their own food, and at the same time take a number of other informative metabolic measurements. Yet during the course of the study, something remarkable dawned on Ravussin: The volunteers were overeating tremendously. “People were on average eating almost double the amount they needed,” he recalls. To be precise, the volunteers averaged 173 percent of their normal calorie needs, overeating from day one until the end of the experiment. Over the course of the seven-day study, the men gained an average of five pounds each.

Over the next three years, Ravussin’s team published two additional “human cafeteria diet” studies. These studies tested the vending machine setup with men, women, lean people, people with obesity, Caucasians, and Native Americans. In each case, volunteers locked in a metabolic ward with a variety of free, tasty foods overate substantially, without being asked to overeat. Ravussin named this phenomenon opportunistic voracity.

These findings are particularly remarkable because it’s normally quite difficult to get people to overeat substantially for more than a few days (imagine yourself eating twice as much food at each meal!). In other settings, researchers coax their volunteers to overeat using enticements such as money, and even then, volunteers have to force down the extra food against a growing sense of queasiness and impending stomach rupture. Yet in Ravussin’s study, his volunteers overate cheerfully without even being asked to, suggesting that the environment he created had the peculiar ability to sweep aside our natural limits on eating.

ENTER THE BRAIN

Just as Yutala gained weight when he left the traditional diet and lifestyle of his native island of Kitava, Americans gained weight as our own way of life evolved. Our current food environment shares many parallels with Sclafani’s and Ravussin’s cafeteria diet studies. To understand why we overeat when we’re placed in such environments, and why we do so without having any conscious intention or desire to overeat, we must turn to the organ that controls all behavior, including eating: the brain.