Most of my favorite factoids about obesity are historical ones, and they don’t make it into the new, four-part HBO documentary on the subject, The Weight of the Nation. Absent, for instance, is the fact that the very first childhood-obesity clinic in the United States was founded in the late 1930s at Columbia University by a young German physician, Hilde Bruch. As Bruch later told it, her inspiration was simple: she arrived in New York in 1934 and was “startled” by the number of fat kids she saw—“really fat ones, not only in clinics, but on the streets and subways, and in schools.”
What makes Bruch’s story relevant to the obesity problem today is that this was New York in the worst year of the Great Depression, an era of bread lines and soup kitchens, when 6 in 10 Americans were living in poverty. The conventional wisdom these days—promoted by government, obesity researchers, physicians, and probably your personal trainer as well—is that we get fat because we have too much to eat and not enough reasons to be physically active. But then why were the PC- and Big Mac–-deprived Depression-era kids fat? How can we blame the obesity epidemic on gluttony and sloth if we easily find epidemics of obesity throughout the past century in populations that barely had food to survive and had to work hard to earn it?
These seem like obvious questions to ask, but you won’t get the answers from the anti-obesity establishment, which this month has come together to unfold a major anti-fat effort, including The Weight of the Nation, which begins airing May 14 and “a nationwide community-based outreach campaign.” The project was created by a coalition among HBO and three key public-health institutions: the nonprofit Institute of Medicine, and two federal agencies, the Centers for Disease Control and Prevention and the National Institutes of Health. Indeed, it is unprecedented to have the IOM, CDC, and NIH all supporting a single television documentary, says producer John Hoffmann. The idea is to “sound the alarm” and motivate the nation to act.
At its heart is a simple “energy balance” idea: we get fat because we consume too many calories and expend too few. If we could just control our impulses—or at least control our environment, thereby removing temptation—and push ourselves to exercise, we’d be fine. This logic is everywhere you look in the official guidelines, commentary, and advice. “The same amount of energy IN and energy OUT over time = weight stays the same,” the NIH website counsels Americans, while the CDC site tells us, “Overweight and obesity result from an energy imbalance.”
The problem is, the solutions this multi-level campaign promotes are the same ones that have been used to fight obesity for a century—and they just haven’t worked. “We are struggling to figure this out,” NIH Director Francis Collins conceded to Newsweek last week. When I interviewed CDC obesity expert William Dietz back in 2001, he told me that his primary accomplishment had been getting childhood obesity “on the map.” “It’s now widely recognized as a major health problem in the United States,” he said then—and that was 10 years and a few million obese children ago.
There is an alternative theory, one that has also been around for decades but that the establishment has largely ignored. This theory implicates specific foods—refined sugars and grains—because of their effect on the hormone insulin, which regulates fat accumulation. If this hormonal-defect hypothesis is true, not all calories are created equal, as the conventional wisdom holds. And if it is true, the problem is not only controlling our impulses, but also changing the entire American food economy and rewriting our beliefs about what constitutes a healthy diet.
Oddly, this nutrient-hormone-fat interaction is not particularly controversial. You can find it in medical textbooks as the explanation for why our fat cells get fat. But the anti-obesity establishment doesn’t take the next step: that fat fat cells lead to fat humans. In their eyes, yes, insulin regulates how much fat gets trapped in your fat cells, and the kinds of carbohydrates we eat today pretty much drive up your insulin levels. But, they conclude, while individual cells get fat that way, the reason an entire human gets fat has nothing to do with it. We’re just eating too much.
I’ve been arguing otherwise. And one reason I like this hormonal hypothesis of obesity is that it explains the fat kids in Depression-era New York. As the extreme situation of exceedingly poor populations shows, the problem could not have been that they ate too much, because they didn’t have enough food available. The problem then—as now, across America—was the prevalence of sugars, refined flour, and starches in their diets. These are the cheapest calories, and they can be plenty tasty without a lot of preparation and preservation. And the biology suggests that they are literally fattening—they make us fat, while other foods (fats, proteins, and green leafy vegetables) don’t.
Photograph by Dwight Eschliman
If this hypothesis is right, then the reason the anti-obesity efforts championed by the IOM, the CDC, and the NIH haven’t worked and won’t work is not because we’re not listening, and not because we just can’t say no, but because these efforts are not addressing the fundamental cause of the problem. Like trying to prevent lung cancer by getting smokers to eat less and run more, it won’t work because the intervention is wrong.
The authority figures in obesity and nutrition are so fixed on the simplistic calorie-balance idea that they’re willing to ignore virtually any science to hold on to it.
The first and most obvious mistake they make is embracing the notion that the only way foods can influence how fat we get is through the amount of energy—calories—they contain. The iconic example here is sugar, or rather sugars, since we’re talking about both sucrose (the white, granulated stuff we sprinkle on cereal) and high-fructose corn syrup. “What’s the single best thing I can do for me and my family?” asks one obese mother in The Weight of the Nation. The answer she’s given is “stop drinking sugar-sweetened beverages.” But the official wisdom—that all we need know is that a calorie is a calorie is a calorie—doesn’t explain why that might be so.
Left unsaid is the fact that sucrose and high-fructose corn syrup have a unique chemical composition, a near 50-50 combination of two different carbohydrates: glucose and fructose. And while glucose is metabolized by virtually every cell in the body, the fructose (also found in fruit, but in much lower concentrations) is metabolized mostly by liver cells. From there, the chain of metabolic events has been worked out by biochemists over 50 years: some of the fructose is converted into fat, the fat accumulates in the liver cells, which become resistant to the action of insulin, and so more insulin is secreted to compensate. The end results are elevated levels of insulin, which is the hallmark of type 2 diabetes, and the steady accumulation of fat in our fat tissue—a few tens of calories worth per day, leading to pounds per year, and obesity over the course of a few decades.
Last fall, researchers at the University of California, Davis, published three studies—two of humans, one of rhesus monkeys—confirming the deleterious effect of these sugars on metabolism and insulin levels. The message of all three studies was that sugars are unhealthy—not because people or monkeys consumed too much of them, but because, well, they do things to our bodies that the other nutrients we eat simply don’t do.
The second fallacy is the belief that physical activity plays a meaningful role in keeping off the pounds—an idea that the authorities just can’t seem to let go of, despite all evidence to the contrary. “We don’t walk, we don’t bike,” says University of North Carolina economist Barry Popkin in The Weight of the Nation. If we do exercise regularly, the logic goes, then we’ll at least maintain a healthy weight (along with other health benefits), which is why the official government recommendations from the USDA are that we should all do 150 minutes each week of “moderate intensity” aerobic exercise. And if that’s not enough to maintain a healthy weight or lose the excess, then, well, we should do more.
So why is the world full of obese individuals who do exercise regularly? Arkansas construction workers in The Weight of the Nation, for instance, do jobs that require constant lifting and running up ladders with “about 50 to 60 pounds of tools”—and an equal amount of excess fat. They’re on-camera making the point about how the combination is exhausting. “By the time the day’s over,” one tells us, “your feet are killing you; your legs are cramping. You can’t last as long as you used to.” If physical activity helps us lose weight or even just maintain it, how did these hardworking men get so fat?
There are two obvious reasons why this idea that working out makes you skinny or keeps you skinny is likely to be just wrong. One is that it takes a significant amount of exercise to burn even a modest amount of calories. Run three miles, says Cornell University researcher Brian Wansink in the documentary, and you’ll burn up roughly the amount of calories in a single candy bar. And this brings up the second reason: you’re likely to be hungrier after strenuous exercise than before and so you’re more likely to eat that candy bar’s worth of calories after than before. (When the American Heart Association and the American College of Sports Medicine jointly published physical-activity guidelines back in 2007, they described the evidence that exercise can even prevent us from growing fatter as “not particularly compelling,” which was a kind way to put it.)
Finally, the anti-obesity establishment embraces the idea that what are really missing from our diet are fresh fruits and vegetables—that these are the sine qua non of a healthy diet—and that meat, red meat in particular, is a likely cause of obesity. Since the mid-1970s, health agencies have waged a campaign to reduce our meat consumption, for a host of reasons: it causes colon cancer or heart disease (because of the saturated fat) and now because it supposedly makes us fat as well. The lowly cheeseburger is consistently targeted as a contributor to both obesity and diabetes.
But when David Wallinga of the Institute for Agriculture and Trade Policy tells us in The Weight of the Nation that the USDA has established the cause of the obesity epidemic and it’s “an increase in our calorie consumption over the last 30, 35 years,” he also tells us where those calories come from: a quarter come from added sugars, a quarter from added fats (“most of which are from soy”), and “almost half is from refined grains, mainly corn starches, wheat, and the like.” What Wallinga doesn’t say is that the same USDA data clearly shows that red-meat consumption peaked in this country in the mid-1970s, before the obesity epidemic started. It’s been dropping ever since, consistent with a nation that has been doing exactly what health authorities have been telling it to do.
Frank Siteman / Science Faction-Corbis
At the moment, the government efforts to curb obesity and diabetes avoid the all-too-apparent fact, as Hilde Bruch pointed out more than half a century ago, that exhorting obese people to eat less and exercise more doesn’t work, and that this shouldn’t be an indictment of their character but of the value of the advice. By institutionalizing this advice as public-health policy, we waste enormous amounts of money and effort on programs that might make communities nicer places to live—building parks and making green markets available—but that we have little reason to believe will make anyone thinner. When I asked CDC Director Thomas Frieden about this, he pointed to two recent reports, from Massachusetts and New York, documenting small but real decreases in childhood-obesity levels. He then admitted that they had no idea why this had happened. “I’m doing everything I can do,” he said, “to assure that we rigorously monitor the efforts underway so we can try to understand what works and what doesn’t.”
If the latest research is any indication, sugar may have been the primary problem all along. Back in the 1980s, the FDA gave sugar a free pass based on the idea that the evidence wasn’t conclusive. While the government spent hundreds of millions trying to prove that salt and saturated fat are bad for our health, it spent virtually nothing on sugar. Had it targeted sugar then, instead of waiting for an obesity and diabetes epidemic for motivation, our entire food culture and the options that go with it might have changed as they did with low-fat and low-salt foods.
So what should we eat? The latest clinical trials suggest that all of us would benefit from fewer (if any) sugars and fewer refined grains (bread, pasta) and starchy vegetables (potatoes). This was the conventional wisdom through the mid-1960s, and then we turned the grains and starches into heart-healthy diet foods and the USDA enshrined them in the base of its famous Food Guide Pyramid as the staples of our diet. That this shift coincides with the obesity epidemic is probably not a coincidence. As for those of us who are overweight, experimental trials, the gold standard of medical evidence, suggest that diets that are severely restricted in fattening carbohydrates and rich in animal products—meat, eggs, cheese—and green leafy vegetables are arguably the best approach, if not the healthiest diet to eat. Not only does weight go down when people eat like this, but heart disease and diabetes risk factors are reduced. Ethical arguments against meat-eating are always valid; health arguments against it can no longer be defended.
If The Weight of the Nation accomplishes anything, it’s communicating the desperation of obese Americans trying to understand their condition and, even more, of lean (or relatively lean) parents trying to cope with the obesity of their offspring. Lack of will isn’t their problem. It’s the absence of advice that might actually work. If our authorities on this subject could accept that maybe their fundamental understanding of the problem needs to be rethought, we and they might begin to make progress. Clearly the conventional wisdom has failed so far. We can hold onto it only so long.
Everyone knows some people who can eat ice cream, cake, and whatever else they want and still not gain weight. At the other extreme are people who seem to gain weight no matter how little they eat. Why? What are the causes of obesity? What allows one person to remain thin without effort but demands that another struggle to avoid gaining weight or regaining the pounds he or she has lost previously?
On a very simple level, your weight depends on the number of calories you consume, how many of those calories you store, and how many you burn up. But each of these factors is influenced by a combination of genes and environment. Both can affect your physiology (such as how fast you burn calories) as well as your behavior (the types of foods you choose to eat, for instance). The interplay between all these factors begins at the moment of your conception and continues throughout your life.
The calorie equation
The balance of calories stored and burned depends on your genetic makeup, your level of physical activity, and your resting energy expenditure (the number of calories your body burns while at rest). If you consistently burn all of the calories that you consume in the course of a day, you will maintain your weight. If you consume more energy (calories) than you expend, you will gain weight.
Excess calories are stored throughout your body as fat. Your body stores this fat within specialized fat cells (adipose tissue) — either by enlarging fat cells, which are always present in the body, or by creating more of them. If you decrease your food intake and consume fewer calories than you burn up, or if you exercise more and burn up more calories, your body will reduce some of your fat stores. When this happens, fat cells shrink, along with your waistline.
To date, more than 400 different genes have been implicated in the causes of overweight or obesity, although only a handful appear to be major players. Genes contribute to obesity in many ways, by affecting appetite, satiety (the sense of fullness), metabolism, food cravings, body-fat distribution, and the tendency to use eating as a way to cope with stress.
The strength of the genetic influence on weight disorders varies quite a bit from person to person. Research suggests that for some people, genes account for just 25% of the predisposition to be overweight, while for others the genetic influence is as high as 70% to 80%. Having a rough idea of how large a role genes play in your weight may be helpful in terms of treating your weight problems.
How much of your weight depends on your genes?
Genes are probably a significant contributor to your obesity if you have most or all of the following characteristics:
- You have been overweight for much of your life.
- One or both of your parents or several other blood relatives are significantly overweight. If both of your parents have obesity, your likelihood of developing obesity is as high as 80%.
- You can't lose weight even when you increase your physical activity and stick to a low-calorie diet for many months.
Genes are probably a lower contributor for you if you have most or all of the following characteristics:
- You are strongly influenced by the availability of food.
- You are moderately overweight, but you can lose weight when you follow a reasonable diet and exercise program.
- You regain lost weight during the holiday season, after changing your eating or exercise habits, or at times when you experience psychological or social problems.
These circumstances suggest that you have a genetic predisposition to be heavy, but it's not so great that you can't overcome it with some effort.
At the other end of the spectrum, you can assume that your genetic predisposition to obesity is modest if your weight is normal and doesn't increase even when you regularly indulge in high-calorie foods and rarely exercise.
People with only a moderate genetic predisposition to be overweight have a good chance of losing weight on their own by eating fewer calories and getting more vigorous exercise more often. These people are more likely to be able to maintain this lower weight.
What are thrifty genes?
When the prey escaped or the crops failed, how did our ancestors survive? Those who could store body fat to live off during the lean times lived, and those who couldn't, perished. This evolutionary adaptation explains why most modern humans — about 85% of us — carry so-called thrifty genes, which help us conserve energy and store fat. Today, of course, these thrifty genes are a curse rather than a blessing. Not only is food readily available to us nearly around the clock, we don't even have to hunt or harvest it!
In contrast, people with a strong genetic predisposition to obesity may not be able to lose weight with the usual forms of diet and exercise therapy. Even if they lose weight, they are less likely to maintain the weight loss. For people with a very strong genetic predisposition, sheer willpower is ineffective in counteracting their tendency to be overweight. Typically, these people can maintain weight loss only under a doctor's guidance. They are also the most likely to require weight-loss drugs or surgery.
The prevalence of obesity among adults in the United States has been rising since the 1970s. Genes alone cannot possibly explain such a rapid rise. Although the genetic predisposition to be overweight varies widely from person to person, the rise in body mass index appears to be nearly universal, cutting across all demographic groups. These findings underscore the importance of changes in our environment that contribute to the epidemic of overweight and obesity.
Environmental causes of obesity
Genetic factors are the forces inside you that help you gain weight and stay overweight; environmental factors are the outside forces that contribute to these problems. They encompass anything in our environment that makes us more likely to eat too much or exercise too little. Taken together, experts think that environmental factors are the driving force for the dramatic increase in obesity.
Environmental influences come into play very early, even before you're born. Researchers sometimes call these in-utero exposures "fetal programming." Babies of mothers who smoked during pregnancy are more likely to become overweight than those whose mothers didn't smoke. The same is true for babies born to mothers who had diabetes. Researchers believe these conditions may somehow alter the growing baby's metabolism in ways that show up later in life.
After birth, babies who are breast-fed for more than three months are less likely to have obesity as adolescents compared with infants who are breast-fed for less than three months.
Childhood habits often stick with people for the rest of their lives. Kids who drink sugary sodas and eat high-calorie, processed foods develop a taste for these products and continue eating them as adults, which tends to promote weight gain. Likewise, kids who watch television and play video games instead of being active may be programming themselves for a sedentary future.
Many features of modern life promote weight gain. In short, today's "obesogenic" environment encourages us to eat more and exercise less. And there's growing evidence that broader aspects of the way we live — such as how much we sleep, our stress levels, and other psychological factors — can affect weight as well.
The food factor
According to the Centers for Disease Control and Prevention (CDC), Americans are eating more calories on average than they did in the 1970s. Between 1971 and 2000, the average man added 168 calories to his daily fare, while the average woman added 335 calories a day. What's driving this trend? Experts say it's a combination of increased availability, bigger portions, and more high-calorie foods.
Practically everywhere we go — shopping centers, sports stadiums, movie theaters — food is readily available. You can buy snacks or meals at roadside rest stops, 24-hour convenience stores, even gyms and health clubs. Americans are spending far more on foods eaten out of the home: In 1970, we spent 27% of our food budget on away-from-home food; by 2006, that percentage had risen to 46%.
In the 1950s, fast-food restaurants offered one portion size. Today, portion sizes have ballooned, a trend that has spilled over into many other foods, from cookies and popcorn to sandwiches and steaks. A typical serving of French fries from McDonald's contains three times more calories than when the franchise began. A single "super-sized" meal may contain 1,500–2,000 calories — all the calories that most people need for an entire day. And research shows that people will often eat what's in front of them, even if they're already full. Not surprisingly, we're also eating more high-calorie foods (especially salty snacks, soft drinks, and pizza), which are much more readily available than lower-calorie choices like salads and whole fruits. Fat isn't necessarily the problem; in fact, research shows that the fat content of our diet has actually gone down since the early 1980s. But many low-fat foods are very high in calories because they contain large amounts of sugar to improve their taste and palatability. In fact, many low-fat foods are actually higher in calories than foods that are not low fat.
The exercise equation
The government's current recommendations for exercise call for an hour of moderate to vigorous exercise a day. But fewer than 25% of Americans meet that goal.
Our daily lives don't offer many opportunities for activity. Children don't exercise as much in school, often because of cutbacks in physical education classes. Many people drive to work and spend much of the day sitting at a computer terminal. Because we work long hours, we have trouble finding the time to go to the gym, play a sport, or exercise in other ways.
Instead of walking to local shops and toting shopping bags, we drive to one-stop megastores, where we park close to the entrance, wheel our purchases in a shopping cart, and drive home. The widespread use of vacuum cleaners, dishwashers, leaf blowers, and a host of other appliances takes nearly all the physical effort out of daily chores.
The trouble with TV: Sedentary snacking
The average American watches about four hours of television per day, a habit that's been linked to overweight or obesity in a number of studies. Data from the National Health and Nutrition Examination Survey, a long-term study monitoring the health of American adults, revealed that people with overweight and obesity spend more time watching television and playing video games than people of normal weight. Watching television more than two hours a day also raises the risk of overweight in children, even in those as young as three years old.
Part of the problem may be that people are watching television instead of exercising or doing other activities that burn more calories (watching TV burns only slightly more calories than sleeping, and less than other sedentary pursuits such as sewing or reading). But food advertisements also may play a significant role. The average hour-long TV show features about 11 food and beverage commercials, which encourage people to eat. And studies show that eating food in front of the TV stimulates people to eat more calories, and particularly more calories from fat. In fact, a study that limited the amount of TV kids watched demonstrated that this practice helped them lose weight — but not because they became more active when they weren't watching TV. The difference was that the children ate more snacks when they were watching television than when doing other activities, even sedentary ones.
Stress and related issues
Obesity experts now believe that a number of different aspects of American society may conspire to promote weight gain. Stress is a common thread intertwining these factors. For example, these days it's commonplace to work long hours and take shorter or less frequent vacations. In many families, both parents work, which makes it harder to find time for families to shop, prepare, and eat healthy foods together. Round-the-clock TV news means we hear more frequent reports of child abductions and random violent acts. This does more than increase stress levels; it also makes parents more reluctant to allow children to ride their bikes to the park to play. Parents end up driving kids to play dates and structured activities, which means less activity for the kids and more stress for parents. Time pressures — whether for school, work, or family obligations — often lead people to eat on the run and to sacrifice sleep, both of which can contribute to weight gain.
Some researchers also think that the very act of eating irregularly and on the run may contribute to obesity. Neurological evidence indicates that the brain's biological clock — the pacemaker that controls numerous other daily rhythms in our bodies — may also help to regulate hunger and satiety signals. Ideally, these signals should keep our weight steady. They should prompt us to eat when our body fat falls below a certain level or when we need more body fat (during pregnancy, for example), and they should tell us when we feel satiated and should stop eating. Close connections between the brain's pacemaker and the appetite control center in the hypothalamus suggest that hunger and satiety are affected by temporal cues. Irregular eating patterns may disrupt the effectiveness of these cues in a way that promotes obesity.
Similarly, research shows that the less you sleep, the more likely you are to gain weight. Lack of sufficient sleep tends to disrupt hormones that control hunger and appetite. In a 2004 study of more than 1,000 volunteers, researchers found that people who slept less than eight hours a night had higher levels of body fat than those who slept more, and the people who slept the fewest hours weighed the most.
Stress and lack of sleep are closely connected to psychological well-being, which can also affect diet and appetite, as anyone who's ever gorged on cookies or potato chips when feeling anxious or sad can attest. Studies have demonstrated that some people eat more when affected by depression, anxiety, or other emotional disorders. In turn, overweight and obesity themselves can promote emotional disorders: If you repeatedly try to lose weight and fail, or if you succeed in losing weight only to gain it all back, the struggle can cause tremendous frustration over time, which can cause or worsen anxiety and depression. A cycle develops that leads to greater and greater obesity, associated with increasingly severe emotional difficulties.
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