Showing posts with label Nutrition. Show all posts
Showing posts with label Nutrition. Show all posts

Thursday, March 1, 2012

Are Your Friends Making You Fat?


Are Your Friends Making You Fat?

Published: September 10, 2009
EILEEN BELLOLI KEEPS very good track of her friends. Belloli, who is 74, was born in Framingham, Mass., which is where she met her future husband, Joseph, when they were both toddlers. (“I tripped her and made her cry,” recalls Joseph, a laconic and beanpole-tall 76-year-old.) The Bellolis never left Framingham, a comfortable, middle-class town 25 miles west of Boston — he became a carpenter and, later, a state industrial-safety official; and after raising four children, she taught biology at a middle school. Many of her friends from grade school never left Framingham, either, so after 60 years, she still sees a half dozen of them every six weeks.
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I visited the Bellolis at their home in Framingham last month, and when I asked Eileen about her old friends, she jumped up from her rose-colored rocking chair, ran to her cabinet and pulled down a binder filled with class photos and pictures from her school reunions. Every five years, she told me, she helps organize a reunion, and each time they manage to collect a group of about 30 students she has known since elementary and junior high school. She opened the binder and flipped through the pictures, each one carefully laminated, with a label on the back listing each classmate’s name. “I’m a Type A personality,” she said.
As I leafed through the binder, I could see that the Bellolis and their friends stayed in very good health over the years. As they aged, they mostly remained trim, even as many other Framingham residents succumbed to obesity. The fattening of America annoys Eileen — “people are becoming more and more accustomed to not taking responsibility for their actions,” she said — and she particularly prides herself on remaining active. Almost every day she does a three-mile circuit inside the local mall with her husband and a cluster of friends, though she speed walks so rapidly that some gripe about her breakneck pace. Her one vice used to be smoking, usually right after her teaching day ended. “I would take myself to Friendly’s with a book, and I would sit there and have two cups of coffee and two cigarettes,” she said. At the time, her cigarette habit didn’t seem like a problem; most of her friends also smoked socially. But in the late 1980s, a few of them began to quit, and pretty soon Eileen felt awkward holding a cigarette off to one side when out at a restaurant. She quit, too, and within a few years nobody she knew smoked anymore.
In the reunion photos, there is only one person who visibly degrades in health as the years pass: a boyish-faced man sporting mutton-chop sideburns. When he was younger, he looked as healthy as the rest of the crowd. But each time he showed up for the reunion, he had grown steadily heavier, until the 2003 photograph, when he looked straightforwardly obese, the only one of his size in the entire picture. Almost uniquely among the crowd, he did not remain friends with his old classmates. His only point of contact was the reunions, which he kept attending until he didn’t show up last year. It turned out he’d died.
The man’s story struck me as particularly relevant because Eileen and Joseph are part of a scientific study that might actually help explain his fate. The Bellolis are participants in the Framingham Heart Study, the nation’s most ambitious project to understand the roots of heart disease. Founded in 1948 by the National Heart Institute, the study has followed more than 15,000 Framingham residents and their descendants, bringing them in to a doctor’s office every four years, on average, for a comprehensive physical. Each time the Bellolis are examined, every aspect of their health is quantified and collected: heart rate, weight, blood levels and more. Over the decades, the Framingham study has yielded a gold mine of information about risk factors for heart disease; it was instrumental, for instance, in identifying the positive role of “good” cholesterol.
But two years ago, a pair of social scientists named Nicholas Christakis and James Fowler used the information collected over the years about Joseph and Eileen and several thousand of their neighbors to make an entirely different kind of discovery. By analyzing the Framingham data, Christakis and Fowler say, they have for the first time found some solid basis for a potentially powerful theory in epidemiology: that good behaviors — like quitting smoking or staying slender or being happy — pass from friend to friend almost as if they were contagious viruses. The Framingham participants, the data suggested, influenced one another’s health just by socializing. And the same was true of bad behaviors — clusters of friends appeared to “infect” each other with obesity, unhappiness and smoking. Staying healthy isn’t just a matter of your genes and your diet, it seems. Good health is also a product, in part, of your sheer proximity to other healthy people. By keeping in close, regular contact with other healthy friends for decades, Eileen and Joseph had quite possibly kept themselves alive and thriving. And by doing precisely the opposite, the lone obese man hadn’t.
FOR DECADES, SOCIOLOGISTS and philosophers have suspected that behaviors can be “contagious.” In the 1930s, the Austrian sociologist Jacob Moreno began to draw sociograms, little maps of who knew whom in friendship or workplace circles, and he discovered that the shape of social connection varied widely from person to person. Some were sociometric “stars,” picked by many others as a friend, while others were “isolates,” virtually friendless. In the 1940s and 1950s, social scientists began to analyze how the shape of a social network could affect people’s behavior; others examined the way information, gossip and opinion flowed through that network. One pioneer was Paul Lazarsfeld, a sociologist at Columbia University, who analyzed how a commercial product became popular; he argued it was a two-step process, in which highly connected people first absorbed the mass-media ads for a product and then mentioned the product to their many friends. (This concept later bloomed in the 1990s and in this decade with the rage for “buzz marketing” — the attempt to identify thought-leaders who would spread the word about a new product virally.) Lazarsfeld also studied how political opinions flowed through friendship circles; he would ask a group of friends to identify the most influential members of their group, then map out how a political view or support for a candidate spread through and around those individuals.
By the 1980s and 1990s, alarmed by the dangers of smoking among young Americans, health care workers began to do the same work on groupings of teenagers to discover exactly how each individual was influenced to pick up the habit. The language of contagion is part of pop culture today, thanks in part to the influence of Malcolm Gladwell’s best-selling book “The Tipping Point.” It’s now common to speak of social changes as epidemics (like the “obesity epidemic”) and to talk about “superconnectors” who are so promiscuously well linked that they exert an outsize influence in society, ushering trends into existence almost single-handedly.
Yet the truth is, scientists have never successfully demonstrated that this is really how the world works. None of the case studies directly observed the contagion process in action. They were reverse-engineered later, with sociologists or marketers conducting interviews to try to reconstruct who told whom about what — which meant that people were potentially misrecalling how they were influenced or whom they influenced. And these studies focused on small groups of people, a few dozen or a few hundred at most, which meant they didn’t necessarily indicate much about how a contagious notion spread — if indeed it did — among the broad public. Were superconnectors truly important? How many times did someone need to be exposed to a trend or behavior before they “caught” it? Certainly, scientists knew that a person could influence an immediate peer — but could that influence spread further? Despite our pop-cultural faith in social contagion, no one really knew how it worked.
Sociologists began hunting for ongoing, real-life situations in which better data could be found. A 2000 study of dorm mates at Dartmouth College by the economist Bruce Sacerdote found that they appeared to infect each other with good and bad study habits — such that a roommate with a high grade-point average would drag upward the G.P.A. of his lower-scoring roommate, and vice versa. A 2006 Princeton study found that having babies appeared to be contagious: if your sibling has a child, you’re 15 percent more likely to have one yourself in the next two years. These were tantalizing findings, but again, each was too narrow to really indicate whether and how the effect worked in the mass public. What was needed was something more ambitious, some way of mapping out the links between thousands of real-life people for years — decades, even — to see whether, and how, behaviors spread.
NICHOLAS CHRISTAKIS BEGAN taking a new look at this question in 2000 after an experience visiting terminally ill patients in the working-class neighborhoods of Chicago. Christakis is a medical doctor and sociologist at Harvard; back then, he was posted at the University of Chicago and, at the age of 38, he had made a name for himself studying the “widowhood effect,” the well-known propensity of spouses to die soon after their partners’ deaths. One of his patients was a terminally ill elderly woman with dementia who lived with her daughter as her main caregiver. The daughter was exhausted from caring for her mother for months; the daughter’s husband, in turn, was becoming ill from coping with his wife’s extreme stress. One night after visiting the dying mother, Christakis arrived back at his office and got a phone call from a friend of the husband, asking for help, explaining that he, too, was feeling overwhelmed by the situation. The mother’s sickness had, in effect, spread outward “across three degrees of separation,” Christakis told me. “This illness affects the daughter, who spreads to the husband, who spreads to the friend, the guy who calls me up,” he added. He began talking to colleagues, wondering how he could further study the phenomenon.
In 2002, a common friend introduced him to James Fowler, at the time a Harvard political-science graduate student. Fowler was researching the question of whether the decision to vote in elections could spread virally from one person to another. Christakis and Fowler agreed that social contagion was an important area of inquiry and decided the only way to settle the many unanswered questions surrounding it was to find or compile a huge data set, one that tracked thousands of people. At first, they figured they would mount their own survey. They asked for $25 million from the National Institutes of Health to track 31,000 adults for six years, but the N.I.H. said they had to find some preliminary evidence first. So they went on the hunt for an existing collection of data. They weren’t optimistic. While several large surveys of adult health exist, medical researchers have no tradition of thinking about social networks, so they rarely bother to collect data on who knows whom — which means there’s no way to track whether behaviors are spreading from person to person. Christakis and Fowler examined study after study, discarding each one.
Christakis knew about the Framingham Heart Study and arranged a visit to the town to learn more. The study seemed promising: he knew it had been underway for more than 50 years and had followed more than 15,000 people, spanning three generations, so in theory, at least, it could offer a crucial moving picture. But how to track social connections? During his visit, Christakis asked one of the coordinators of the study how she and her colleagues were able to stay in contact with so many people for so long. What happened if a family moved away? The woman reached under her desk and pulled out a green sheet. It was a form that staff members used to collect information from every participant each time they came in to be examined — and it asked them to list all their family and at least one of their friends. “They asked you, ‘Who is your spouse, who are your children, who are your parents, who are your siblings, where do they live, who is your doctor, where do you work, where do you live, who is a close friend who would know where to find you in four years if we can’t find you?” Christakis said. “And they were writing all this stuff down.” He felt a jolt of excitement: he and Fowler could use these thousands of green forms to manually reconstruct the social ties of Framingham — who knew whom, going back decades.
Over the next few years, Christakis and Fowler managed a team that painstakingly sifted through the records. When they were done, they had a map of how 5,124 subjects were connected, tracing a web of 53,228 ties between friends and family and work colleagues. Next they analyzed the data, beginning with tracking patterns of how and when Framingham residents became obese. Soon they had created an animated diagram of the entire social network, with each resident represented on their computer screens as a dot that grew bigger or smaller as he or she gained or lost weight over 32 years, from 1971 to 2003. When they ran the animation, they could see that obesity broke out in clusters. People weren’t just getting fatter randomly. Groups of people would become obese together, while other groupings would remain slender or even lose weight.
And the social effect appeared to be quite powerful. When a Framingham resident became obese, his or her friends were 57 percent more likely to become obese, too. Even more astonishing to Christakis and Fowler was the fact that the effect didn’t stop there. In fact, it appeared to skip links. A Framingham resident was roughly 20 percent more likely to become obese if the friend of a friend became obese — even if the connecting friend didn’t put on a single pound. Indeed, a person’s risk of obesity went up about 10 percent even if a friend of a friend of a friend gained weight.
“People are connected, and so their health is connected,” Christakis and Fowler concluded when they summarized their findings in a July 2007 article in The New England Journal of Medicine, the first time the prestigious journal published a study of how social networks affect health. Or as Christakis and Fowler put it in “Connected,” their coming book on their findings: “You may not know him personally, but your friend’s husband’s co-worker can make you fat. And your sister’s friend’s boyfriend can make you thin.”
Obesity was only the beginning. Over the next year, the sociologist and the political scientist continued to analyze the Framingham data, finding more and more examples of contagious behavior. Smoking, they discovered, also appeared to spread socially — in fact, a friend taking up smoking increased your chance of lighting up by 36 percent, and if you had a three-degrees-removed friend who started smoking, you were 11 percent more likely to do the same. Drinking spread socially, as did happiness and even loneliness. And in each case one’s individual influence stretched out three degrees before it faded out. They termed this the “three degrees of influence” rule about human behavior: We are tied not just to those around us, but to others in a web that stretches farther than we know.
WHEN I FIRST MET Christakis and Fowler last spring, at a downtown Manhattan cafe, they seemed like a living example of their theory: even their conversational style appeared to be contagious, each of them bursting in in the middle of a sentence to complete the other’s thought. Christakis, an intense and jovial man with bristling eyebrows and a booming voice, wore a suit with no tie and sipped a coffee. Fowler, who is 39, looked like a boyish wunderkind, wearing a T-shirt and jeans and a constant broad smile. In the two years since they published their first work, they had become relatively famous and highly controversial. People — and late-night comics — were drawn to a theory that seemed to offer a scientific basis for some exquisitely calculating behavior, like avoiding your friends if they get fat. (Or avoiding your friends merely because some of their friends’ friends gained a couple of pounds.) Newspapers splashed Christakis and Fowler’s obesity findings across front pages, and the study penetrated into corners of the popular culture generally untouched by social-science research. “My favorite was the ‘Cathy’ cartoon,” Fowler told me; in it, Cathy and two friends sit in a restaurant, chatting about the obesity paper; when the waiter comes, each woman points to another and says, “She’ll have a small dry salad and a cup of water.”
Fowler told me their work had inspired him to lose five pounds and to listen to upbeat music before he arrives home from work so he will be in a good mood when he greets his family. “I try to get myself in a mental space where I’ll be happy,” he says. “Because I know that I’m not just having an impact on my son, I’m potentially having an impact on my son’s best friend’s mother.”
But how, exactly, could obesity or happiness spread through so many links? Between one immediate peer and another, some contagious behaviors — like smoking — seem pretty commonsensical. If lots of people around you are smoking, there’s going to be peer pressure for you to start, whereas if nobody’s smoking, you’ll be more likely to stop. But the simple peer-pressure explanation doesn’t work as well with happiness or obesity: we don’t often urge people around us to eat more or implore them to be happier. (In any case, simply telling someone to be happier or unhappier isn’t likely to work.) Instead, Christakis and Fowler hypothesize that these behaviors spread partly through the subconscious social signals that we pick up from those around us, which serve as cues to what is considered normal behavior. Scientists have been documenting this phenomenon; for example, experiments have shown that if a person is seated next to someone who’s eating more, he will eat more, too, unwittingly calibrating his sense of what constitutes a normal meal. Christakis and Fowler suspect that as friends around us become heavier, we gradually change our mental picture of what “obese” looks like and give ourselves tacit permission to add pounds. With happiness, the two argue that the contagion may be even more deeply subconscious: the spread of good or bad feelings, they say, might be driven partly by “mirror neurons” in the brain that automatically mimic what we see in the faces of those around us — which is why looking at photographs of smiling people can itself often lift your mood.
“In some sense we can begin to understand human emotions like happiness the way we might study the stampeding of buffalo,” Christakis said. “You don’t ask an individual buffalo, ‘Why are you running to the left?’ The answer is that the whole herd is running to the left. Similarly, you can see pockets of unhappy and happy people clustered in the network. They don’t even know each other necessarily,” but their moods rise and fall together.
The subconscious nature of emotional mirroring might explain one of the more curious findings in their research: If you want to be happy, what’s most important is to have lots of friends. Historically, we have often thought that having a small cluster of tight, long-term friends is crucial to being happy. But Christakis and Fowler found that the happiest people in Framingham were those who had the most connections, even if the relationships weren’t necessarily deep ones.
The reason these people were the happiest, the duo theorize, is that happiness doesn’t come only from having deep, heart-to-heart talks. It also comes from having daily exposure to many small moments of contagious happiness. When you frequently see other people smile — at home, in the street, at your local bar — your spirits are repeatedly affected by your mirroring of their emotional state. Of course, the danger of being highly connected to lots of people is that you’re at risk of encountering many people when they are in bad moods. But Christakis and Fowler say their findings show that the gamble of increased sociability pays off, for a surprising reason: Happiness is more contagious than unhappiness. According to their statistical analysis, each additional happy friend boosts your good cheer by 9 percent, while each additional unhappy friend drags you down by only 7 percent. So by this logic, adding more links to your network should — mathematically — add to your store of happiness. “If you’re at the center of a network, you are going to be more susceptible to anything that spreads through it,” Fowler said. “And if happiness is spreading more reliably, then on average you’re going to be catching happy waves more often than you catch sad waves.”
The Framingham findings also suggest that different contagious behaviors spread in different ways. For example, co-workers did not seem to transmit happiness to one another, while personal friends did. But co-workers did transmit smoking habits; if a person at a small firm stopped smoking, his or her colleagues had a 34 percent better chance of quitting themselves. The difference is based in the nature of workplace relationships, Fowler contends. Smokers at work tend to cluster together outside the building; if one of them stops smoking, it reduces the conviviality of the experience. (If you’re the last smoker outside on a freezing afternoon, your behavior can seem completely ridiculous even to yourself.) But when it comes to happiness, Fowler said, “people are both cooperative and competitive at work. So when one person gets a raise, it might make him happy, but it’ll make other people jealous.”
Obesity had its own quirk: Spouses didn’t appear to have as big an effect on each other as friends. If a male Framingham subject had a male friend who became fat, his risk doubled, but if his wife became obese, his risk was increased by only 37 percent. This, Christakis and Fowler say, is because when it comes to body image, we compare ourselves primarily to people of the same sex (and in the Framingham study, all spouses were of the opposite sex). In fact, different-sexed friends didn’t transmit any obesity to one another at all. If a man became fat, his female friends were completely unaffected, and vice versa. Similarly, siblings of the same sex had a bigger impact on one another’s weight than siblings of the opposite sex.
When it came to drinking, Christakis and Fowler found a different kind of gender effect. Framingham women were considerably more influential than Framingham men. A woman who began drinking heavily increased the heavy-drinking risk of those around her, whereas heavy-drinking men had less effect on other people. Why? In the age of frat-party binge drinking, you might imagine that hard-partying men are the most risky people to be around. But Fowler says he suspects women are more influential precisely because they tend to drink less. When a woman starts drinking heavily, he says, it sends a strong signal to those around her that it’s O.K. to start boozing too.
Christakis and Fowler’s strangest finding is the idea that a behavior can skip links — spreading to a friend of a friend without affecting the person who connects them. If the people in the middle of a chain are somehow passing along a social contagion, it doesn’t make sense, on the face of it, that they wouldn’t be affected, too. The two researchers say they don’t know for sure how the link-jumping works. But they theorize that people may be able to pass along a social signal without themselves acting on it. If your friends at work become obese, even if you don’t gain weight yourself, you might become more accepting of obesity as a normal state — and unconsciously transmit that signal to your family members, who would then feel a sort of permission to gain weight themselves, knowing they wouldn’t face any sort of censure from you.
Christakis and Fowler postulate that our ability to affect people three degrees away from us may have evolutionary roots — and so may the very shape of human social networks. Tribal groups that were tightly connected were likely more able to pass along positive behaviors than those that weren’t. Christakis and Fowler say social contagion could even help explain the existence of altruism: if we can pass on altruism to distant points in a network, it would help explain why altruistic people aren’t simply constantly taken advantage of by other members of their community. Last year, to test this theory, they conducted a laboratory experiment in which participants played a “cooperation game.” Each participant was asked to share a sum of money with a small group and could choose to be either generous or selfish. Christakis and Fowler found that if someone was on the receiving end of a generous exchange, that person would become more generous to the next set of partners — until the entire larger group was infected, as it were, with altruistic behavior, which meant the altruist would benefit indirectly.
CHRISTAKIS AND FOWLER’S work has produced a variety of reactions from other scientists. Many health care experts are thrilled. After years of observing patients, they suspected that behaviors spread socially; now there was data that appeared to prove it. “It was an aha! moment,” James O. Hill, a pioneering obesity researcher at the University of Colorado, Denver, said about the time in 2007 when he read the researchers’ first obesity paper. Tom Valente, the director of the master’s of public health program at the University of Southern California and an early investigator of the role of social networks in smoking behavior, was similarly excited. “The Christakis and Fowler work is fantastic,” he told me. Among public-health practitioners, he said, their theories have “had amazing acceptance.”
But many of those who study networks are more cautious in their reactions. Unlike medical experts, these scientists specialize in the study of networks themselves — anything ranging from neighborhoods linked via the power grid to teenagers linked on Facebook — and they are familiar with the difficulty of ascertaining cause and effect in such complex constructs. As they point out, the Framingham study has found intriguing correlations in people’s behavior. Christakis and Fowler can show what appear to be waves of obesity or smoking moving across the map. But that doesn’t prove social contagion is causing the spread.
There are at least two other possible explanations. One is “homophily,” the tendency of people to gravitate toward others who are like them. People who are gaining weight might well prefer to hang out with others who are also gaining weight, just as people who are happy might seek out others who are happy. The other possible explanation is that the shared environment — and not social contagion — might be causing the people of Framingham to change in groups. If a McDonald’s opens up in a Framingham neighborhood, it could cause a cluster of people living nearby to gain weight or become slightly happier (or sadder, depending on what they think about McDonald’s). The cluster of people would appear as though they are sharing a contagious form of behavior, but it would be an illusion.
Because of the confounding factors, as they are called, of homophily and the environment, many social scientists find themselves caught in an emotional bind when it comes to Christakis and Fowler’s work. As Alex Pentland, former academic head of the M.I.T.Media Lab and an expert in unconscious social signals, told me, “You couldn’t prove what they say, but I happen to believe it.” I heard precisely the same thing from many of Pentland’s peers. They have all long suspected that human behavior is widely contagious; they just don’t think Christakis and Fowler have proved their case.
One of Christakis and Fowler’s most prominent critics is Jason Fletcher, an assistant professor of public health at Yale University. Last year, he and an economist named Ethan Cohen-Cole published two papers arguing that Christakis and Fowler had not successfully stripped out all possible homophily effects from their calculations. Fletcher initially wanted to replicate Christakis and Fowler’s analysis of the data, but he didn’t have access to their source; Christakis and Fowler have not published their network data, arguing that doing so would violate the privacy rights of the participants in the Framingham Heart Study. Faced with that obstacle, Fletcher and his colleague decided instead to test Christakis and Fowler’s mathematical techniques on a different set of data: the Add Health study, a federal-government project that tracked the health of 90,118 students at 144 high schools and middle schools between 1994 and 2002. Among the questionnaires the researchers distributed was one that asked students to list up to 10 of their friends. This allowed Fletcher to build maps of how the friends at each school were linked, school by school, giving them a set of small social networks upon which to test Christakis and Fowler’s math. (Before they stumbled upon the Framingham data, Christakis and Fowler themselves had considered using the Add Health surveys to look for social contagion. But they decided the data sets were too limited — each of the schools had only several hundred students interlinked — to produce results in which they could have confidence. They also wanted to study adults, figuring that the peer effects among teenagers are qualitatively different.)
When Fletcher analyzed the student cliques using statistical tools that he says are similar to those used by Christakis and Fowler, he found that social contagion indeed existed. But the behaviors and conditions that were apparently contagious were entirely implausible: they included acne, height and headaches. How could you become taller by hanging around with taller people? This, Fletcher concluded, called into doubt whether Christakis and Fowler’s statistical techniques really removed homophily or environmental effects — and he says this means the Framingham results are just as dubious. When I spoke to Fletcher, he said that he, too, believes social-contagion effects are real. “We are on board with the idea that they exist and they’re important,” he added. But he simply isn’t impressed by Christakis and Fowler’s evidence.
Other scientists have pointed out another important limitation in Christakis and Fowler’s work, which is that their map showing connections between the people of Framingham is necessarily incomplete. When the Framingham participants checked in every four years, they were asked to list all their family members — but only one person they considered a close friend. This could arguably mean that those eerie three-degree effects might be an illusion. For example, if John lists Allison as his friend, and Allison lists Robert as her friend, and Robert lists Samantha as his friend, then Christakis and Fowler could conclude that John is three links away from Samantha. But what if John and Samantha actually know each other from church, but didn’t have a way to indicate this on the Framingham forms? Then if John and Samantha both become slightly fatter, it might look like a social contagion is spreading through three social ties, via Allison and Robert, when in fact it’s only spreading through one link, via church.
When I raised this concern with Christakis and Fowler, they agreed that their map of friendships isn’t perfect. “This is a general problem with our study and with any similar study,” Christakis said. But he said he believes their map of the Framingham connections has far fewer holes than critics charge. When he and Fowler tallied up the green sheets, they often were able to deduce relationships between two people who didn’t explicitly list each other as acquaintances — reducing the number of false three-degree links. (One helpful fact was that many participants listed more than one friend, despite the instructions on the green sheets.) “We are not overreaching our data,” Christakis insisted.
He and Fowler also acknowledged that it is impossible to completely remove the problems of homophily and environmental effects. This doesn’t mean they agree with Fletcher; in fact, they point out that in his height-and-acne paper, he used a somewhat looser mathematical model, one that makes it easier to produce spurious correlations between people — which is why, they say, Fletcher found that acne and height were contagious. When they ran their own statistical technique on the Add Health data, they found that obesity followed precisely the same three-degree pattern of contagion as they found in Framingham.
And Christakis and Fowler point to two other findings to bolster their case for social contagion over environmental effects. One is that in the Framingham study, obesity seemed to be able to jump from friend to friend even over great distances. When people moved away, their weight gain still appeared to influence friends back in Massachusetts. In such cases, the local environment couldn’t be making both gain weight, Christakis and Fowler say.
Their other finding is more intriguing and arguably more significant: They discovered that behaviors appear to spread differently depending on the type of friendship that exists between two people. In the Framingham study, people were asked to name a close friend. But the friendships weren’t always symmetrical. Though Steven might designate Peter as his friend, Peter might not think of Steven the same way; he might never designate Steven as a friend. Christakis and Fowler found that this “directionality” mattered greatly. According to their data, if Steven becomes obese, it has no effect on Peter at all, because he doesn’t think of Steven as a close friend. In contrast, if Peter gains weight, then Steven’s risk of obesity rises by almost 100 percent. And if the two men regard each other as mutual friends, the effect is huge — either one gaining weight almost triples the other’s risk. In Framingham, Christakis and Fowler found this directionality effect even among people who lived and worked very close to each other. And that, they argue, means it can’t be the environment that is making people in Framingham fatter, since the environment ought to affect each of these friends equally.
“If a McDonald’s opens up nearby, it should make both of us gain weight simultaneously,” Christakis adds. “It shouldn’t matter whether I nominate you as a friend or you nominate me.” In fact, though, the directionality effect seems to matter very much, and that fact, in turn, buttresses the case for social contagion.
Duncan Watts, a social-network pioneer and a researcher for Yahoo, has reservations about some of Christakis and Fowler’s findings — for example, he thinks the fact that most of the Framingham participants listed only one friend “really casts some doubt” on the three-degrees theory. But he told me that the directionality effect is one finding that none of Christakis and Fowler’s critics have been able to rebut. It is, for him, the strongest evidence that the Framingham results aren’t just caused by the environment or by people flocking to others like them. “I don’t see how that can be explained any other way,” he said.
IF YOU LOOK AT A CHART showing the change in smoking rates in the United States since the 1970s, it is a picture of early public-health success that soon tails off. In 1970, the smoking rate for adults was 37 percent. It fell to 33 percent by 1980 and then fell even more precipitously between 1980 and 1990. But after that, the rate at which people quit smoking began to slow. Between 2004 and 2005, in fact, the smoking rate stayed steady; on balance, nobody quit smoking those years. Antismoking forces successfully pushed the number of smokers down to one in five people, but they now seem stuck. Smoking-cessation experts have debated why it has become so hard to get the final holdouts to quit. Perhaps, some said, it was because the average cost of a pack of cigarettes remains largely unchanged nationally since 2002.
But there might be another, hidden reason: the shape of a smoker’s social ties. When Christakis and Fowler mapped out the way Framingham people quit smoking during roughly the same period — 1971 to 2003 — they found that the decline was not evenly distributed across the town. Instead, clusters of friends all quit smoking at the same time, in a group. It was like a ballroom emptying out one table at a time. But this meant that by 2003, the remaining smokers were also not evenly distributed: instead, they existed in isolated, tightly knit clusters of like-minded nicotine fiends. Worse, those clusters had migrated to the edges of the social network, where they were less interlinked with the mass of Framingham participants. In their everyday social lives, Christakis and Fowler say, the town’s remaining smokers are thus mostly surrounded by people who still smoke, and they rarely have strong connections with nonsmokers. Nonsmoking may be contagious, but the smokers don’t appear to be close to anyone from whom they could catch the behavior.
The federal government has officially set a goal of reducing the number of smokers in the country to 12 percent of the population by 2010. But the very shape of our social networks is working against that goal, Fowler says, and this poses a potential public-health challenge. Meanwhile, public-health strategists who want to counteract obesity face the opposite problem. Since the country is gradually becoming more and more obese, when individual people do lose weight, they are more likely to be surrounded by people who are still heavy. If it’s true that obesity can affect people even three links away, that may be one reason that people have such trouble keeping weight off. Even if they form a weight-loss group to lose weight with their close friends, they will still be influenced by obese people two or three links away — people they barely know. “We know that people are wildly successful in losing weight and wildly unsuccessful in keeping it off,” Hill, the obesity researcher, says; he believes Framingham offers an important explanation of why this is.
In essence, Christakis and Fowler’s work suggests a new way to think about public health. If they’re right, public-health initiatives that merely address the affected individuals are doomed to failure. To really grapple with bad behaviors that spread, you have to simultaneously focus on individuals who are so distant they don’t even realize they’re affecting one another. Hill says this is possible with obesity. Last year, he collaborated with David Bahr, a physicist at Regis University in Denver, to construct a computer model of society that replicates the way obesity spreads. They created a simulation of hundreds of thousands of individuals, each programmed to influence one another in precisely the same way that Christakis and Fowler documented in Framingham. To test whether their model accurately mimicked reality, they seeded it with a few obese people and set it running. The virtual society slowly became obese in the same pattern and at the same rate as Framingham. If they could accurately copy the way Framingham became obese, they figured, they could then use the model to test different ways that the spread might be halted. They began trying different experiments — like focusing on specific individuals and seeing whether or not they could use them to create a counterepidemic of skinniness.
One solution jumped out at them. In theory, the best way to fight obesity, the model predicted, isn’t to urge people to diet with a cluster of close friends. It is to encourage them to skip a link and to diet with friends of friends. That way, in your immediate social network, everyone would be surrounded on at least one side by people who are actively losing weight, and this would in turn influence those other links to begin losing weight themselves. When Hill and Bahr ran the simulation with this sort of staggered dieting, it worked: the virtual society began slimming down, and the obesity epidemic reversed itself. “It’s like you have bridging dams to try and stop the flow,” Bahr told me. (Bahr also found that the obesity epidemic could be reversed quickly, with only 1 percent of the entire population losing weight, so long as the dieters were placed in precisely the right spots. “You don’t need a lot of people, but you do need the right ones,” he said.)
In reality, of course, this sort of intervention would be quite difficult to pull off. You would have to figure out some way to persuade friends of friends to form dieting groups together. But other scientists have used Christakis and Fowler’s work to inspire more potentially practical public-health projects, some of which are now being implemented. Nathan Cobb, a smoking-cessation expert and researcher at the Schroeder Institute for Tobacco Research and Policy Studies, is designing an application that Facebook users can install on their pages when they’re trying to quit smoking. The application will publicly display how long they’ve gone without cigarettes, whether they are using a nicotine patch and how much money they have saved by not smoking. The idea, Cobb says, is to take your invisible, internal battle to quit smoking and make it visible so that it can influence your friends (and friends of friends) who are still puffing away.
IT’S TEMPTING TO think, confronted by Christakis and Fowler’s work, that the best way to improve your life is to simply cut your ties to people with bad behavior. And obviously this is possible; people change their friends often, sometimes abruptly. But reshaping your social network may be more challenging than altering your behavior. There’s also compelling evidence in their research that we do not have as much control as we might think we do over the way we’re linked to other people: our location in a social network, say, or how many of our friends know each other. These patterns in our life are relatively stable, and they might, weirdly, be partly innate.
Christakis and Fowler first noticed this effect when they examined their happiness data. They discovered that people who were deeply enmeshed in friendship circles were usually much happier than “isolates,” those with few ties. But if an isolate did manage to find happiness, she did not suddenly develop more ties and migrate to a position where she was more tightly connected to others. The reverse was also true: if a well-connected person became unhappy, he didn’t lose his ties and become an isolate. Your level of connectedness appears to be more persistent than even your overall temperament. “If you picked up someone who’s well connected and dropped them into another network, they’d migrate toward the center,” Christakis said. Your place in the network affects your happiness, in other words, but your happiness doesn’t affect your place in the network.
Christakis and Fowler began to wonder if a person’s connectedness is to some degree fated from birth — a product, at least in part, of DNA. To test the idea, they conducted a study of twins. Using the Add Health school data, they located more than 500 sets of twins and analyzed where they were located in their friendship clusters. Employing statistical techniques traditionally used to parse out how much of twins’ lifestyles are attributable to their genes as opposed to their environment, they found that almost half — 46 percent — of the difference between two twins’ levels of connectedness could be explained by DNA. “On average,” they wrote, “a person with five friends has different genes than a person with one friend.” More oddly still, twins also tended to have the same “transitivity”: their friendship groupings had a strikingly similar degree of interlinking, which is the number of friends who knew one another. By and large, the people who were most tightly clustered in Framingham tended to be better off — healthier, happier and even wealthier. (Several other economic studies have also found that better-connected people make more money.) But if half the reason these people were so well positioned is related to the accident of DNA, then you could consider connectedness a new form of inequality: lucky and unlucky cards, dealt out at birth.
Social-network science ultimately offers a new perspective on an age-old question: to what extent are we autonomous individuals? “If someone does a good thing merely because they’re copying others, or they do something bad merely because they’re copying others, what credit do they deserve, or what blame do they deserve?” Christakis asks. “If I quit smoking because everyone around me quits smoking, what credit do I get” for demonstrating self-control? If you’re one of the people who are partly driven by his DNA to hang out on the periphery of society, well, that’s also where the smokers are, which means you are also more likely to pick up their habit.
To look at society as a social network — instead of a collection of individuals — can lead to some thorny conclusions. In a column published last fall in The British Medical Journal, Christakis wrote that a strictly utilitarian point of view would suggest we should give better medical care to well-connected individuals, because they’re the ones more likely to pass on the benefits contagiously to others. “This conclusion,” Christakis wrote, “makes me uneasy.”
Yet there is also, the two scientists argue, something empowering about the idea that we are so entwined. “Even as we are being influenced by others, we can influence others,” Christakis told me when we first met. “And therefore the importance of taking actions that are beneficial to others is heightened. So this network thing can cut both ways, subverting our ability to have free will, but increasing, if you will, the importance of us having free will.”
As Fowler pointed out, if you want to improve the world with your good behavior, math is on your side. For most of us, within three degrees we are connected to more than 1,000 people — all of whom we can theoretically help make healthier, fitter and happier just by our contagious example. “If someone tells you that you can influence 1,000 people,” Fowler said, “it changes your way of seeing the world.”

Clive Thompson, a contributing writer for the magazine, writes frequently about technology and science.


LETTERS

Is Happiness Catching?

Published: September 24, 2009
Someone dubbed the theory of social contagion the “High-School Cafeteria Theory”: if you hang out with the “right” crowd, you’ll do O.K.; if you hang out with the “wrong” crowd, you won’t. The problem is that the idea of social contagion reifies a metaphor. You can catch a virus without free will; you can’t “catch” smoking without it. Mirror neurons activate feelings and impulses; free will keeps them going. Thank God Copernicus, Freud, Einstein, Columbus and Emily Dickinson were not unduly influenced by this theory.

Related

Are Your Friends Making You Fat? (September 13, 2009)

ELIZABETH STRINGER
New York
Clive Thompson writes that Nicholas Christakis and James Fowler “suspect that as friends around us become heavier, we gradually change our mental picture of what ‘obese’ looks like.” In a forthcoming article in Obesity, we find that perceptions of what it means to be overweight became more lenient in the United States from 1988 to 2004, a period during which the population grew significantly heavier. The share of overweight (but not obese) individuals ages 17 to 74 who described themselves as “overweight” fell by 6 percentage points between two surveys conducted, respectively, during the periods 1988-94 and 1999-2004.
The decline in overweight self-perception was roughly equivalent for women and men, and is not explained by changes in population characteristics, such as age and racial composition, between the survey periods. The findings agree with the notion that we judge our weight in relation to others around us rather than according to fixed standards.
MARY A. BURKE
Senior Economist
CARL NADLER
Research Assistant
Federal Reserve Bank of Boston

FRANK HEILAND
Assistant Professor
School of Public Affairs
Baruch College
New York

Your article on the research of social-network science brings new meaning to the old saying “Tell me who your friends are, and I’ll tell you who you are.” Ultimately, we are all products of our environment, some of us more than others.
As highly social and adaptable creatures, we do conform to our immediate environment as shaped by those we spend lots of time with and thus share similar ideas.
This is an evolutionary advantage that enabled our early ancestors to cooperate with each other, form immediate communes and collectively survive the natural harshness of their existence. This is indeed a primitive and core behavior and, without it, none of us would be here today.
MICHAEL HADJIARGYROU
Associate Professor of Biomedical Engineering, Genetics and Orthopedics
Stony Brook University
Stony Brook, N.Y.

Friday, April 29, 2011

Is Sugar Toxic?

April 13, 2011

Is Sugar Toxic?

On May 26, 2009, Robert Lustig gave a lecture called “Sugar: The Bitter Truth,” which was posted on YouTube the following July. Since then, it has been viewed well over 800,000 times, gaining new viewers at a rate of about 50,000 per month, fairly remarkable numbers for a 90-minute discussion of the nuances of fructose biochemistry and human physiology.
Lustig is a specialist on pediatric hormone disorders and the leading expert in childhood obesity at the University of California, San Francisco, School of Medicine, which is one of the best medical schools in the country. He published his first paper on childhood obesity a dozen years ago, and he has been treating patients and doing research on the disorder ever since.
The viral success of his lecture, though, has little to do with Lustig’s impressive credentials and far more with the persuasive case he makes that sugar is a “toxin” or a “poison,” terms he uses together 13 times through the course of the lecture, in addition to the five references to sugar as merely “evil.” And by “sugar,” Lustig means not only the white granulated stuff that we put in coffee and sprinkle on cereal — technically known as sucrose — but also high-fructose corn syrup, which has already become without Lustig’s help what he calls “the most demonized additive known to man.”
It doesn’t hurt Lustig’s cause that he is a compelling public speaker. His critics argue that what makes him compelling is his practice of taking suggestive evidence and insisting that it’s incontrovertible. Lustig certainly doesn’t dabble in shades of gray. Sugar is not just an empty calorie, he says; its effect on us is much more insidious. “It’s not about the calories,” he says. “It has nothing to do with the calories. It’s a poison by itself.”
If Lustig is right, then our excessive consumption of sugar is the primary reason that the numbers of obese and diabetic Americans have skyrocketed in the past 30 years. But his argument implies more than that. If Lustig is right, it would mean that sugar is also the likely dietary cause of several other chronic ailments widely considered to be diseases of Western lifestyles — heart disease, hypertension and many common cancers among them.
The number of viewers Lustig has attracted suggests that people are paying attention to his argument. When I set out to interview public health authorities and researchers for this article, they would often initiate the interview with some variation of the comment “surely you’ve spoken to Robert Lustig,” not because Lustig has done any of the key research on sugar himself, which he hasn’t, but because he’s willing to insist publicly and unambiguously, when most researchers are not, that sugar is a toxic substance that people abuse. In Lustig’s view, sugar should be thought of, like cigarettes and alcohol, as something that’s killing us.
This brings us to the salient question: Can sugar possibly be as bad as Lustig says it is?
It’s one thing to suggest, as most nutritionists will, that a healthful diet includes more fruits and vegetables, and maybe less fat, red meat and salt, or less of everything. It’s entirely different to claim that one particularly cherished aspect of our diet might not just be an unhealthful indulgence but actually be toxic, that when you bake your children a birthday cake or give them lemonade on a hot summer day, you may be doing them more harm than good, despite all the love that goes with it. Suggesting that sugar might kill us is what zealots do. But Lustig, who has genuine expertise, has accumulated and synthesized a mass of evidence, which he finds compelling enough to convict sugar. His critics consider that evidence insufficient, but there’s no way to know who might be right, or what must be done to find out, without discussing it.
If I didn’t buy this argument myself, I wouldn’t be writing about it here. And I also have a disclaimer to acknowledge. I’ve spent much of the last decade doing journalistic research on diet and chronic disease — some of the more contrarian findings, on dietary fat, appeared in this magazine —– and I have come to conclusions similar to Lustig’s.
The history of the debate over the health effects of sugar has gone on far longer than you might imagine. It is littered with erroneous statements and conclusions because even the supposed authorities had no true understanding of what they were talking about. They didn’t know, quite literally, what they meant by the word “sugar” and therefore what the implications were.
So let’s start by clarifying a few issues, beginning with Lustig’s use of the word “sugar” to mean both sucrose — beet and cane sugar, whether white or brown — and high-fructose corn syrup. This is a critical point, particularly because high-fructose corn syrup has indeed become “the flashpoint for everybody’s distrust of processed foods,” says Marion Nestle, a New York University nutritionist and the author of “Food Politics.”
This development is recent and borders on humorous. In the early 1980s, high-fructose corn syrup replaced sugar in sodas and other products in part because refined sugar then had the reputation as a generally noxious nutrient. (“Villain in Disguise?” asked a headline in this paper in 1977, before answering in the affirmative.) High-fructose corn syrup was portrayed by the food industry as a healthful alternative, and that’s how the public perceived it. It was also cheaper than sugar, which didn’t hurt its commercial prospects. Now the tide is rolling the other way, and refined sugar is making a commercial comeback as the supposedly healthful alternative to this noxious corn-syrup stuff. “Industry after industry is replacing their product with sucrose and advertising it as such — ‘No High-Fructose Corn Syrup,’ ” Nestle notes.
But marketing aside, the two sweeteners are effectively identical in their biological effects. “High-fructose corn syrup, sugar — no difference,” is how Lustig put it in a lecture that I attended in San Francisco last December. “The point is they’re each bad — equally bad, equally poisonous.”
Refined sugar (that is, sucrose) is made up of a molecule of the carbohydrate glucose, bonded to a molecule of the carbohydrate fructose — a 50-50 mixture of the two. The fructose, which is almost twice as sweet as glucose, is what distinguishes sugar from other carbohydrate-rich foods like bread or potatoes that break down upon digestion to glucose alone. The more fructose in a substance, the sweeter it will be. High-fructose corn syrup, as it is most commonly consumed, is 55 percent fructose, and the remaining 45 percent is nearly all glucose. It was first marketed in the late 1970s and was created to be indistinguishable from refined sugar when used in soft drinks. Because each of these sugars ends up as glucose and fructose in our guts, our bodies react the same way to both, and the physiological effects are identical. In a 2010 review of the relevant science, Luc Tappy, a researcher at the University of Lausanne in Switzerland who is considered by biochemists who study fructose to be the world’s foremost authority on the subject, said there was “not the single hint” that H.F.C.S. was more deleterious than other sources of sugar.
The question, then, isn’t whether high-fructose corn syrup is worse than sugar; it’s what do they do to us, and how do they do it? The conventional wisdom has long been that the worst that can be said about sugars of any kind is that they cause tooth decay and represent “empty calories” that we eat in excess because they taste so good.
By this logic, sugar-sweetened beverages (or H.F.C.S.-sweetened beverages, as the Sugar Association prefers they are called) are bad for us not because there’s anything particularly toxic about the sugar they contain but just because people consume too many of them.
Those organizations that now advise us to cut down on our sugar consumption — the Department of Agriculture, for instance, in its recent Dietary Guidelines for Americans, or the American Heart Association in guidelines released in September 2009 (of which Lustig was a co-author) — do so for this reason. Refined sugar and H.F.C.S. don’t come with any protein, vitamins, minerals, antioxidants or fiber, and so they either displace other more nutritious elements of our diet or are eaten over and above what we need to sustain our weight, and this is why we get fatter.
Whether the empty-calories argument is true, it’s certainly convenient. It allows everyone to assign blame for obesity and, by extension, diabetes — two conditions so intimately linked that some authorities have taken to calling them “diabesity” — to overeating of all foods, or underexercising, because a calorie is a calorie. “This isn’t about demonizing any industry,” as Michelle Obama said about her Let’s Move program to combat the epidemic of childhood obesity. Instead it’s about getting us — or our children — to move more and eat less, reduce our portion sizes, cut back on snacks.
Lustig’s argument, however, is not about the consumption of empty calories — and biochemists have made the same case previously, though not so publicly. It is that sugar has unique characteristics, specifically in the way the human body metabolizes the fructose in it, that may make it singularly harmful, at least if consumed in sufficient quantities.
The phrase Lustig uses when he describes this concept is “isocaloric but not isometabolic.” This means we can eat 100 calories of glucose (from a potato or bread or other starch) or 100 calories of sugar (half glucose and half fructose), and they will be metabolized differently and have a different effect on the body. The calories are the same, but the metabolic consequences are quite different.
The fructose component of sugar and H.F.C.S. is metabolized primarily by the liver, while the glucose from sugar and starches is metabolized by every cell in the body. Consuming sugar (fructose and glucose) means more work for the liver than if you consumed the same number of calories of starch (glucose). And if you take that sugar in liquid form — soda or fruit juices — the fructose and glucose will hit the liver more quickly than if you consume them, say, in an apple (or several apples, to get what researchers would call the equivalent dose of sugar). The speed with which the liver has to do its work will also affect how it metabolizes the fructose and glucose.
In animals, or at least in laboratory rats and mice, it’s clear that if the fructose hits the liver in sufficient quantity and with sufficient speed, the liver will convert much of it to fat. This apparently induces a condition known as insulin resistance, which is now considered the fundamental problem in obesity, and the underlying defect in heart disease and in the type of diabetes, type 2, that is common to obese and overweight individuals. It might also be the underlying defect in many cancers.
If what happens in laboratory rodents also happens in humans, and if we are eating enough sugar to make it happen, then we are in trouble.
The last time an agency of the federal government looked into the question of sugar and health in any detail was in 2005, in a report by the Institute of Medicine, a branch of the National Academies. The authors of the report acknowledged that plenty of evidence suggested that sugar could increase the risk of heart disease and diabetes — even raising LDL cholesterol, known as the “bad cholesterol”—– but did not consider the research to be definitive. There was enough ambiguity, they concluded, that they couldn’t even set an upper limit on how much sugar constitutes too much. Referring back to the 2005 report, an Institute of Medicine report released last fall reiterated, “There is a lack of scientific agreement about the amount of sugars that can be consumed in a healthy diet.” This was the same conclusion that the Food and Drug Administration came to when it last assessed the sugar question, back in 1986. The F.D.A. report was perceived as an exoneration of sugar, and that perception influenced the treatment of sugar in the landmark reports on diet and health that came after.
The Sugar Association and the Corn Refiners Association have also portrayed the 1986 F.D.A. report as clearing sugar of nutritional crimes, but what it concluded was actually something else entirely. To be precise, the F.D.A. reviewers said that other than its contribution to calories, “no conclusive evidence on sugars demonstrates a hazard to the general public when sugars are consumed at the levels that are now current.” This is another way of saying that the evidence by no means refuted the kinds of claims that Lustig is making now and other researchers were making then, just that it wasn’t definitive or unambiguous.
What we have to keep in mind, says Walter Glinsmann, the F.D.A. administrator who was the primary author on the 1986 report and who now is an adviser to the Corn Refiners Association, is that sugar and high-fructose corn syrup might be toxic, as Lustig argues, but so might any substance if it’s consumed in ways or in quantities that are unnatural for humans. The question is always at what dose does a substance go from being harmless to harmful? How much do we have to consume before this happens?
When Glinsmann and his F.D.A. co-authors decided no conclusive evidence demonstrated harm at the levels of sugar then being consumed, they estimated those levels at 40 pounds per person per year beyond what we might get naturally in fruits and vegetables — 40 pounds per person per year of “added sugars” as nutritionists now call them. This is 200 calories per day of sugar, which is less than the amount in a can and a half of Coca-Cola or two cups of apple juice. If that’s indeed all we consume, most nutritionists today would be delighted, including Lustig.
But 40 pounds per year happened to be 35 pounds less than what Department of Agriculture analysts said we were consuming at the time — 75 pounds per person per year — and the U.S.D.A. estimates are typically considered to be the most reliable. By the early 2000s, according to the U.S.D.A., we had increased our consumption to more than 90 pounds per person per year.
That this increase happened to coincide with the current epidemics of obesity and diabetes is one reason that it’s tempting to blame sugars — sucrose and high-fructose corn syrup — for the problem. In 1980, roughly one in seven Americans was obese, and almost six million were diabetic, and the obesity rates, at least, hadn’t changed significantly in the 20 years previously. By the early 2000s, when sugar consumption peaked, one in every three Americans was obese, and 14 million were diabetic.
This correlation between sugar consumption and diabetes is what defense attorneys call circumstantial evidence. It’s more compelling than it otherwise might be, though, because the last time sugar consumption jumped markedly in this country, it was also associated with a diabetes epidemic.
In the early 20th century, many of the leading authorities on diabetes in North America and Europe (including Frederick Banting, who shared the 1923 Nobel Prize for the discovery of insulin) suspected that sugar causes diabetes based on the observation that the disease was rare in populations that didn’t consume refined sugar and widespread in those that did. In 1924, Haven Emerson, director of the institute of public health at Columbia University, reported that diabetes deaths in New York City had increased as much as 15-fold since the Civil War years, and that deaths increased as much as fourfold in some U.S. cities between 1900 and 1920 alone. This coincided, he noted, with an equally significant increase in sugar consumption — almost doubling from 1890 to the early 1920s — with the birth and subsequent growth of the candy and soft-drink industries.
Emerson’s argument was countered by Elliott Joslin, a leading authority on diabetes, and Joslin won out. But his argument was fundamentally flawed. Simply put, it went like this: The Japanese eat lots of rice, and Japanese diabetics are few and far between; rice is mostly carbohydrate, which suggests that sugar, also a carbohydrate, does not cause diabetes. But sugar and rice are not identical merely because they’re both carbohydrates. Joslin could not know at the time that the fructose content of sugar affects how we metabolize it.
Joslin was also unaware that the Japanese ate little sugar. In the early 1960s, the Japanese were eating as little sugar as Americans were a century earlier, maybe less, which means that the Japanese experience could have been used to support the idea that sugar causes diabetes. Still, with Joslin arguing in edition after edition of his seminal textbook that sugar played no role in diabetes, it eventually took on the aura of undisputed truth.
Until Lustig came along, the last time an academic forcefully put forward the sugar-as-toxin thesis was in the 1970s, when John Yudkin, a leading authority on nutrition in the United Kingdom, published a polemic on sugar called “Sweet and Dangerous.” Through the 1960s Yudkin did a series of experiments feeding sugar and starch to rodents, chickens, rabbits, pigs and college students. He found that the sugar invariably raised blood levels of triglycerides (a technical term for fat), which was then, as now, considered a risk factor for heart disease. Sugar also raised insulin levels in Yudkin’s experiments, which linked sugar directly to type 2 diabetes. Few in the medical community took Yudkin’s ideas seriously, largely because he was also arguing that dietary fat and saturated fat were harmless. This set Yudkin’s sugar hypothesis directly against the growing acceptance of the idea, prominent to this day, that dietary fat was the cause of heart disease, a notion championed by the University of Minnesota nutritionist Ancel Keys.
A common assumption at the time was that if one hypothesis was right, then the other was most likely wrong. Either fat caused heart disease by raising cholesterol, or sugar did by raising triglycerides. “The theory that diets high in sugar are an important cause of atherosclerosis and heart disease does not have wide support among experts in the field, who say that fats and cholesterol are the more likely culprits,” as Jane E. Brody wrote in The Times in 1977.
At the time, many of the key observations cited to argue that dietary fat caused heart disease actually support the sugar theory as well. During the Korean War, pathologists doing autopsies on American soldiers killed in battle noticed that many had significant plaques in their arteries, even those who were still teenagers, while the Koreans killed in battle did not. The atherosclerotic plaques in the Americans were attributed to the fact that they ate high-fat diets and the Koreans ate low-fat. But the Americans were also eating high-sugar diets, while the Koreans, like the Japanese, were not.
In 1970, Keys published the results of a landmark study in nutrition known as the Seven Countries Study. Its results were perceived by the medical community and the wider public as compelling evidence that saturated-fat consumption is the best dietary predictor of heart disease. But sugar consumption in the seven countries studied was almost equally predictive. So it was possible that Yudkin was right, and Keys was wrong, or that they could both be right. The evidence has always been able to go either way.
European clinicians tended to side with Yudkin; Americans with Keys. The situation wasn’t helped, as one of Yudkin’s colleagues later told me, by the fact that “there was quite a bit of loathing” between the two nutritionists themselves. In 1971, Keys published an article attacking Yudkin and describing his evidence against sugar as “flimsy indeed.” He treated Yudkin as a figure of scorn, and Yudkin never managed to shake the portrayal.
By the end of the 1970s, any scientist who studied the potentially deleterious effects of sugar in the diet, according to Sheldon Reiser, who did just that at the U.S.D.A.’s Carbohydrate Nutrition Laboratory in Beltsville, Md., and talked about it publicly, was endangering his reputation. “Yudkin was so discredited,” Reiser said to me. “He was ridiculed in a way. And anybody else who said something bad about sucrose, they’d say, ‘He’s just like Yudkin.’ ”
What has changed since then, other than Americans getting fatter and more diabetic? It wasn’t so much that researchers learned anything particularly new about the effects of sugar or high-fructose corn syrup in the human body. Rather the context of the science changed: physicians and medical authorities came to accept the idea that a condition known as metabolic syndrome is a major, if not the major, risk factor for heart disease and diabetes. The Centers for Disease Control and Prevention now estimate that some 75 million Americans have metabolic syndrome. For those who have heart attacks, metabolic syndrome will very likely be the reason.
The first symptom doctors are told to look for in diagnosing metabolic syndrome is an expanding waistline. This means that if you’re overweight, there’s a good chance you have metabolic syndrome, and this is why you’re more likely to have a heart attack or become diabetic (or both) than someone who’s not. Although lean individuals, too, can have metabolic syndrome, and they are at greater risk of heart disease and diabetes than lean individuals without it.
Having metabolic syndrome is another way of saying that the cells in your body are actively ignoring the action of the hormone insulin — a condition known technically as being insulin-resistant. Because insulin resistance and metabolic syndrome still get remarkably little attention in the press (certainly compared with cholesterol), let me explain the basics.
You secrete insulin in response to the foods you eat — particularly the carbohydrates — to keep blood sugar in control after a meal. When your cells are resistant to insulin, your body (your pancreas, to be precise) responds to rising blood sugar by pumping out more and more insulin. Eventually the pancreas can no longer keep up with the demand or it gives in to what diabetologists call “pancreatic exhaustion.” Now your blood sugar will rise out of control, and you’ve got diabetes.
Not everyone with insulin resistance becomes diabetic; some continue to secrete enough insulin to overcome their cells’ resistance to the hormone. But having chronically elevated insulin levels has harmful effects of its own — heart disease, for one. A result is higher triglyceride levels and blood pressure, lower levels of HDL cholesterol (the “good cholesterol”), further worsening the insulin resistance — this is metabolic syndrome.
When physicians assess your risk of heart disease these days, they will take into consideration your LDL cholesterol (the bad kind), but also these symptoms of metabolic syndrome. The idea, according to Scott Grundy, a University of Texas Southwestern Medical Center nutritionist and the chairman of the panel that produced the last edition of the National Cholesterol Education Program guidelines, is that heart attacks 50 years ago might have been caused by high cholesterol — particularly high LDL cholesterol — but since then we’ve all gotten fatter and more diabetic, and now it’s metabolic syndrome that’s the more conspicuous problem.
This raises two obvious questions. The first is what sets off metabolic syndrome to begin with, which is another way of asking, What causes the initial insulin resistance? There are several hypotheses, but researchers who study the mechanisms of insulin resistance now think that a likely cause is the accumulation of fat in the liver. When studies have been done trying to answer this question in humans, says Varman Samuel, who studies insulin resistance at Yale School of Medicine, the correlation between liver fat and insulin resistance in patients, lean or obese, is “remarkably strong.” What it looks like, Samuel says, is that “when you deposit fat in the liver, that’s when you become insulin-resistant.”
That raises the other obvious question: What causes the liver to accumulate fat in humans? A common assumption is that simply getting fatter leads to a fatty liver, but this does not explain fatty liver in lean people. Some of it could be attributed to genetic predisposition. But harking back to Lustig, there’s also the very real possibility that it is caused by sugar.
As it happens, metabolic syndrome and insulin resistance are the reasons that many of the researchers today studying fructose became interested in the subject to begin with. If you want to cause insulin resistance in laboratory rats, says Gerald Reaven, the Stanford University diabetologist who did much of the pioneering work on the subject, feeding them diets that are mostly fructose is an easy way to do it. It’s a “very obvious, very dramatic” effect, Reaven says.
By the early 2000s, researchers studying fructose metabolism had established certain findings unambiguously and had well-established biochemical explanations for what was happening. Feed animals enough pure fructose or enough sugar, and their livers convert the fructose into fat — the saturated fatty acid, palmitate, to be precise, that supposedly gives us heart disease when we eat it, by raising LDL cholesterol. The fat accumulates in the liver, and insulin resistance and metabolic syndrome follow.
Michael Pagliassotti, a Colorado State University biochemist who did many of the relevant animal studies in the late 1990s, says these changes can happen in as little as a week if the animals are fed sugar or fructose in huge amounts — 60 or 70 percent of the calories in their diets. They can take several months if the animals are fed something closer to what humans (in America) actually consume — around 20 percent of the calories in their diet. Stop feeding them the sugar, in either case, and the fatty liver promptly goes away, and with it the insulin resistance.
Similar effects can be shown in humans, although the researchers doing this work typically did the studies with only fructose — as Luc Tappy did in Switzerland or Peter Havel and Kimber Stanhope did at the University of California, Davis — and pure fructose is not the same thing as sugar or high-fructose corn syrup. When Tappy fed his human subjects the equivalent of the fructose in 8 to 10 cans of Coke or Pepsi a day — a “pretty high dose,” he says —– their livers would start to become insulin-resistant, and their triglycerides would go up in just a few days. With lower doses, Tappy says, just as in the animal research, the same effects would appear, but it would take longer, a month or more.
Despite the steady accumulation of research, the evidence can still be criticized as falling far short of conclusive. The studies in rodents aren’t necessarily applicable to humans. And the kinds of studies that Tappy, Havel and Stanhope did — having real people drink beverages sweetened with fructose and comparing the effect with what happens when the same people or others drink beverages sweetened with glucose — aren’t applicable to real human experience, because we never naturally consume pure fructose. We always take it with glucose, in the nearly 50-50 combinations of sugar or high-fructose corn syrup. And then the amount of fructose or sucrose being fed in these studies, to the rodents or the human subjects, has typically been enormous.
This is why the research reviews on the subject invariably conclude that more research is necessary to establish at what dose sugar and high-fructose corn syrup start becoming what Lustig calls toxic. “There is clearly a need for intervention studies,” as Tappy recently phrased it in the technical jargon of the field, “in which the fructose intake of high-fructose consumers is reduced to better delineate the possible pathogenic role of fructose. At present, short-term-intervention studies, however, suggest that a high-fructose intake consisting of soft drinks, sweetened juices or bakery products can increase the risk of metabolic and cardiovascular diseases.”
In simpler language, how much of this stuff do we have to eat or drink, and for how long, before it does to us what it does to laboratory rats? And is that amount more than we’re already consuming?
Unfortunately, we’re unlikely to learn anything conclusive in the near future. As Lustig points out, sugar and high-fructose corn syrup are certainly not “acute toxins” of the kind the F.D.A. typically regulates and the effects of which can be studied over the course of days or months. The question is whether they’re “chronic toxins,” which means “not toxic after one meal, but after 1,000 meals.” This means that what Tappy calls “intervention studies” have to go on for significantly longer than 1,000 meals to be meaningful.
At the moment, the National Institutes of Health are supporting surprisingly few clinical trials related to sugar and high-fructose corn syrup in the U.S. All are small, and none will last more than a few months. Lustig and his colleagues at U.C.S.F. — including Jean-Marc Schwarz, whom Tappy describes as one of the three best fructose biochemists in the world — are doing one of these studies. It will look at what happens when obese teenagers consume no sugar other than what they might get in fruits and vegetables. Another study will do the same with pregnant women to see if their babies are born healthier and leaner.
Only one study in this country, by Havel and Stanhope at the University of California, Davis, is directly addressing the question of how much sugar is required to trigger the symptoms of insulin resistance and metabolic syndrome. Havel and Stanhope are having healthy people drink three sugar- or H.F.C.S.-sweetened beverages a day and then seeing what happens. The catch is that their study subjects go through this three-beverage-a-day routine for only two weeks. That doesn’t seem like a very long time — only 42 meals, not 1,000 — but Havel and Stanhope have been studying fructose since the mid-1990s, and they seem confident that two weeks is sufficient to see if these sugars cause at least some of the symptoms of metabolic syndrome.
So the answer to the question of whether sugar is as bad as Lustig claims is that it certainly could be. It very well may be true that sugar and high-fructose corn syrup, because of the unique way in which we metabolize fructose and at the levels we now consume it, cause fat to accumulate in our livers followed by insulin resistance and metabolic syndrome, and so trigger the process that leads to heart disease, diabetes and obesity. They could indeed be toxic, but they take years to do their damage. It doesn’t happen overnight. Until long-term studies are done, we won’t know for sure.
One more question still needs to be asked, and this is what my wife, who has had to live with my journalistic obsession on this subject, calls the Grinch-trying-to-steal-Christmas problem. What are the chances that sugar is actually worse than Lustig says it is?
One of the diseases that increases in incidence with obesity, diabetes and metabolic syndrome is cancer. This is why I said earlier that insulin resistance may be a fundamental underlying defect in many cancers, as it is in type 2 diabetes and heart disease. The connection between obesity, diabetes and cancer was first reported in 2004 in large population studies by researchers from the World Health Organization’s International Agency for Research on Cancer. It is not controversial. What it means is that you are more likely to get cancer if you’re obese or diabetic than if you’re not, and you’re more likely to get cancer if you have metabolic syndrome than if you don’t.
This goes along with two other observations that have led to the well-accepted idea that some large percentage of cancers are caused by our Western diets and lifestyles. This means they could actually be prevented if we could pinpoint exactly what the problem is and prevent or avoid that.
One observation is that death rates from cancer, like those from diabetes, increased significantly in the second half of the 19th century and the early decades of the 20th. As with diabetes, this observation was accompanied by a vigorous debate about whether those increases could be explained solely by the aging of the population and the use of new diagnostic techniques or whether it was really the incidence of cancer itself that was increasing. “By the 1930s,” as a 1997 report by the World Cancer Research Fund International and the American Institute for Cancer Research explained, “it was apparent that age-adjusted death rates from cancer were rising in the U.S.A.,” which meant that the likelihood of any particular 60-year-old, for instance, dying from cancer was increasing, even if there were indeed more 60-years-olds with each passing year.
The second observation was that malignant cancer, like diabetes, was a relatively rare disease in populations that didn’t eat Western diets, and in some of these populations it appeared to be virtually nonexistent. In the 1950s, malignant cancer among the Inuit, for instance, was still deemed sufficiently rare that physicians working in northern Canada would publish case reports in medical journals when they did diagnose a case.
In 1984, Canadian physicians published an analysis of 30 years of cancer incidence among Inuit in the western and central Arctic. While there had been a “striking increase in the incidence of cancers of modern societies” including lung and cervical cancer, they reported, there were still “conspicuous deficits” in breast-cancer rates. They could not find a single case in an Inuit patient before 1966; they could find only two cases between 1967 and 1980. Since then, as their diet became more like ours, breast cancer incidence has steadily increased among the Inuit, although it’s still significantly lower than it is in other North American ethnic groups. Diabetes rates in the Inuit have also gone from vanishingly low in the mid-20th century to high today.
Now most researchers will agree that the link between Western diet or lifestyle and cancer manifests itself through this association with obesity, diabetes and metabolic syndrome — i.e., insulin resistance. This was the conclusion, for instance, of a 2007 report published by the World Cancer Research Fund and the American Institute for Cancer Research — “Food, Nutrition, Physical Activity and the Prevention of Cancer.”
So how does it work? Cancer researchers now consider that the problem with insulin resistance is that it leads us to secrete more insulin, and insulin (as well as a related hormone known as insulin-like growth factor) actually promotes tumor growth.
As it was explained to me by Craig Thompson, who has done much of this research and is now president of Memorial Sloan-Kettering Cancer Center in New York, the cells of many human cancers come to depend on insulin to provide the fuel (blood sugar) and materials they need to grow and multiply. Insulin and insulin-like growth factor (and related growth factors) also provide the signal, in effect, to do it. The more insulin, the better they do. Some cancers develop mutations that serve the purpose of increasing the influence of insulin on the cell; others take advantage of the elevated insulin levels that are common to metabolic syndrome, obesity and type 2 diabetes. Some do both. Thompson believes that many pre-cancerous cells would never acquire the mutations that turn them into malignant tumors if they weren’t being driven by insulin to take up more and more blood sugar and metabolize it.
What these researchers call elevated insulin (or insulin-like growth factor) signaling appears to be a necessary step in many human cancers, particularly cancers like breast and colon cancer. Lewis Cantley, director of the Cancer Center at Beth Israel Deaconess Medical Center at Harvard Medical School, says that up to 80 percent of all human cancers are driven by either mutations or environmental factors that work to enhance or mimic the effect of insulin on the incipient tumor cells. Cantley is now the leader of one of five scientific “dream teams,” financed by a national coalition called Stand Up to Cancer, to study, in the case of Cantley’s team, precisely this link between a specific insulin-signaling gene (known technically as PI3K) and tumor development in breast and other cancers common to women.
Most of the researchers studying this insulin/cancer link seem concerned primarily with finding a drug that might work to suppress insulin signaling in incipient cancer cells and so, they hope, inhibit or prevent their growth entirely. Many of the experts writing about the insulin/cancer link from a public health perspective — as in the 2007 report from the World Cancer Research Fund and the American Institute for Cancer Research — work from the assumption that chronically elevated insulin levels and insulin resistance are both caused by being fat or by getting fatter. They recommend, as the 2007 report did, that we should all work to be lean and more physically active, and that in turn will help us prevent cancer.
But some researchers will make the case, as Cantley and Thompson do, that if something other than just being fatter is causing insulin resistance to begin with, that’s quite likely the dietary cause of many cancers. If it’s sugar that causes insulin resistance, they say, then the conclusion is hard to avoid that sugar causes cancer — some cancers, at least — radical as this may seem and despite the fact that this suggestion has rarely if ever been voiced before publicly. For just this reason, neither of these men will eat sugar or high-fructose corn syrup, if they can avoid it.
“I have eliminated refined sugar from my diet and eat as little as I possibly can,” Thompson told me, “because I believe ultimately it’s something I can do to decrease my risk of cancer.” Cantley put it this way: “Sugar scares me.”
Sugar scares me too, obviously. I’d like to eat it in moderation. I’d certainly like my two sons to be able to eat it in moderation, to not overconsume it, but I don’t actually know what that means, and I’ve been reporting on this subject and studying it for more than a decade. If sugar just makes us fatter, that’s one thing. We start gaining weight, we eat less of it. But we are also talking about things we can’t see — fatty liver, insulin resistance and all that follows. Officially I’m not supposed to worry because the evidence isn’t conclusive, but I do.
Gary Taubes (gataubes@gmail.com) is a Robert Wood Johnson Foundation independent investigator in health policy and the author of “Why We Get Fat.” Editor: Vera Titunik (v.titunik-MagGroup@nytimes.com).