Fat land : how Americans became the fattest people in the world (18 page)

The notion of an obesity drug for children may frighten some, particularly those who remember the poorly administered diet drugs of the past, not to mention the debacle of fen-phen in more recent years. Yet those on the leading edge of obesity treatment believe a drug is essential. "I am convinced that the drug for treating a truly obese child, which we see more and more and

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more of, will be a lifelong drug," says Francine Kaufman, the new president of the American Diabetes Association, who specializes in such cases. "But we aren't seeing that coming down the tube anytime soon."

In the tube instead are simply more drugs to treat the consequences of obesity, mainly diabetes. Whole companies have been retooled to do so. Such was the case in 1999, when Eli Lilly and Company built its new manufacturing plant. The plant is the largest factory dedicated to the production of a single drug in industry history. The drug is insulin, the sales of which are growing, at least at Lilly, at 24 percent a year.

No wonder, then, that almost every leading pharmaceutical conglomerate has like-minded ventures under way. Many have a special emphasis on pill-form treatments for non-insulin-dependent forms of diabetes. A recent advertisement for the drug Avan-dia sums up the industry attitude. Showing a photograph of an attractive elderly black man and his son, the ad proclaims, "The 20th century brought him type 2 diabetes ... the 21st century gave him insulin-sensitizing Avandia." In fact, the market segment is considered so important that any large company executive without a "diabetes portfolio" is considered hopelessly out of touch. As James Kappel, one of Lilly's public relations executives, explains, "These days, you've got to be in diabetes."

Diabetes — the growth industry for an ever expanding nation.

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At about the time that traditional inner-city populations and many suburbanites came under the sway of cheap fast foods, another demographic boon appeared on the horizon for its most aggressive purveyors. The Latino immigration surge of the mid-1980s was coming of economic age; in many large cities, from Los Angeles to New York to Chicago, they were displacing older urban populations and bringing with them new consumer demands. Almost immediately, every major fast-food company started a Spanish-language campaign. Once relegated to the "alternative buy" category, the "Spanish buy" now became a mainstream buy, with tens of millions of dollars in new ad budgets designated specifically to capture the Latin consumer.

In Los Angeles, the new Ellis Island, such efforts often became news stories in themselves. In the fall of 1999, on the same day that the Spanish-language La Opinion ran a banner story headlined diabetes, epidemia en latinos, Krispy Kreme doughnuts opened its newest store in Van Nuys, in the heart of the San Fernando Valley's burgeoning Latino population. It was, as they like to say in marketing circles, a "resonant" event, re-

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plete with around-the-block lines, celebrity news anchors, and stern cops directing traffic between freebie dunks. Everywhere the Latin flavor was pushed: "Chocolate iced custard filled" became "Rellena de crema pastelera y cubierta con chocolate." "Cinnamon apple filled" became "Rellena de manzana y canela."

With norteno music blaring, the store itself seemed to pulse with excitement.

Yet one corner of the affair seemed a decidedly placid world apart. There sat a young Anglo fellow, eyes red from overwork. It was the new store's manager and marketing director. After a few rather uninspired answers to a reporter's questions, he fielded one about strategy: Why did Krispy Kreme, with all of the pent-up demand for its profitable franchises elsewhere, decide to locate here?

"See," he said, checking his watch and brushing a crumb of choco-glaze from his fingers, "the idea is simple: accessible but not convenient."

"Accessible but not convenient?"

"Eh, yuh," he explained. "See, the idea is to make the store accessible — easy to get into and out of from the street — but just a tad away from the, eh, mainstream so as to make sure customers are pre-sold — and very intent — before they get here. We want them intent to get at least a dozen before they even think of coming in."

But why this slightly non-"mainstream" place?

"Because it's obvious . . ." He gestured to the dozens of stout doughnut enthusiasts queuing around the building. "We're looking for all the bigger families."

Bigger in size?

"Yeah." His eyes rolled, like little glazed crullers. "Bigger in size!'

Bigger in size — but why? After all, if there was ever a population of hardworking, energy-expending people in the United States, it was L.A.'s Latinos. Most of them had come from hard-

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scrabble towns in north and central Mexico and beyond to lead more comfortable — but often just as labor-intensive — lives in the City of Angels. In fact, their hard labor — and the fact that they were un-unionized — was the one thing that made them extra valuable in the constantly changing L.A. labor pool. There their services enabled the middle and upper middle classes to continue their upward, double-income ascent. Latino maids cleaned the house, Latino nannies watched the kids after school, Latino gardeners mowed the lawn and blew the leaves away. Yet if they were expending so much energy, why were they gaining so much weight? The question is a road map to an even bigger concern: How does boundary-free culture, class, free market entrepreneurism, and biology make modern man fat?

One answer might be found in what has become known as the thrifty gene theory, the notion that we, as a species, are genetically programmed to hold on to fat. The theory, first articulated by V. Neel in 1962, argues that the gene most likely implicated is the one that pushes glycogen into muscle tissue; a defect in that gene, or in another one close by, causes that glycogen instead to be stored as fat. It is also known as the insulin-resistance gene. As elegantly restated by Leif Groop, the current leading proponent of the theory, "The insulin-resistance gene has protected individuals during long periods of starving by storing energy as fat rather than as glycogen in muscle. The abundance of food in Western society has made this once protective gene a deleterious one, suggesting that these individuals are not equipped with the metabolic machinery to handle overeating."

Perhaps more important is the way that the thrifty gene expresses itself through and combines with different environmental experiences. The nutritionally poor environment of many men and women born in Mexico and Central America, for example, might accentuate the effects of the thrifty gene and its relatives. One way it might do so is through what scientists now call in utero programming. The theory holds that a pregnant woman who experiences starvation during pregnancy is more likely to

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have a child that is metabolically disposed to retain fat. Two mechanisms incline that child to do so. One is impaired fat oxidation through alterations in the gene responsible for burning fat. The result: Dietary fat gets stored rather than burned, leading to obesity in later life. The other mechanism is impaired sugar metabolism, which some scientists believe derives from an inadequately developed pancreas in the offspring of starved mothers. The consequence: not enough insulin, with excess sugars either running amok in the bloodstream or being stored as fat.

Barry Bogin, an anthropologist at the University of Michigan at Dearborn, has been watching this process unfold in two groups of Mayan immigrants from Guatemala, one in Indiantown, Florida, the other in Los Angeles, California. "What we are seeing is a mismatch between culture and metabolism," Bogin says. "We are seeing the greatest one-generation gains in height ever — but we are also seeing huge weight gain. Not because of heredity in the classic sense — genetics — but rather because of their metabolic inheritance." As Bogin sees it, that metabolic inheritance derives from a long history of cultural and political oppression, one initiated by European conquerors and now continued by their twenty-first-century descendants in urban Guatemala. Such cultural dominance has reinforced further economic exploitation of the Maya, leading to poverty and then generation after generation of children born to nutritionally deprived mothers. Those children are born with a metabolic inclination to hold on to fat, "which works fine as long as they are in a culture of scarcity," Bogin says. "But in a culture of abundance, it doesn't." Instead, they blow up. "In a strange way, you are seeing the original traumas of conquest being played out, metabolically, in the streets of Los Angeles."

Bogin also notes that the experience of the L.A. Guatemalans fits into what is known about the growth patterns of poor peoples who move to richer nations. Increase in height from generation to generation, he writes, "lags behind increases in weight and body composition. This happens because . . . height reflects health and

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nutritional history, whereas weight and body composition reflect recent events. Indeed, a child's height is a historical record of both the individual and his or her parents."

Immigrants may also suffer from what might be called the "shantytown syndrome." Studying fifty-eight pre-pubertal boys in a Sao Paolo, Brazil, slum, epidemiologists from Tufts University were able to document a slightly different source of impaired fat oxidation: childhood undernutrition. Although still somewhat speculative, the state-of-the-art explanation runs thus: Long-term undernutrition is usually accompanied by a reduction in insulin growth factor, or IGF-i. IGF-i plays an important role in stimulating hormones that accelerate fat oxidation. Therefore, any reduction in concentrations of IGF-1 may also result in decreased fat oxidation. Many first-generation immigrants from Mexico and Central America experienced just such childhood undernutrition, and therefore carry the consequential oxidation impairment to the more nutritionally dense environment of the modern American city. No IGF-i plus lots of fast food means more obese kids in places like the City of Angels.

Once here, and once fat — Krispy Kreme right in the neighborhood — the immigrant parent is much more likely to produce fat toddlers, another predictor of both childhood and adult obesity. Looking at nineteen studies of birth weight and its relationship to obesity, the British Institute of Children's Health found that "the child of obese parents is at increased risk of becoming fat early in life, and once relatively fat, he/she is more likely to be so later in adulthood." The current obesity rate for Mexican American children would seem to be testimony to that finding. Between the ages of five and eleven, 27.4 percent of Mexican American girls are obese, as are 23 percent of boys. By fourth grade the rate for girls peaks at 32.4 percent. By fifth grade boys top out at 43.4 percent.

Such, then, is one biomedical reaction to the New World, rellena de crema style.

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If a court case were ever brought to adjudicate the effects of obesity on the human body, the proverbial people's number one would come straight out of the coat pocket of Dr. Scott Loren-Selco, a neurologist at L.A.'s frenetic USC Medical Center, one of the busiest urban hospitals in the nation. Loren-Selco's pocket contains a BMI card. BMI, or body mass index, is a more sophisticated method for determining healthy weight for height, in essence dividing body weight in kilograms by height in meters squared (for a simplified method, see Appendix). Loren-Selco's card thus allows him to easily calculate whether a patient is normal weight, overweight, or obese. "And it's one of the first things I get my patients and their parents familiar with," he says. That's because an increasing number of his young patients are not only obese, but, because of it, have a disease once thought to be solely the woe of adults: type 2 diabetes.

"We are seeing it all the time now, and believe me, it is frightening," he says. "I mean, I tell them all the time that I could take them up to the diabetes ward and show them their possible future: the blind, the amputees, the endless number of people who are completely infirm because of type 2 — and who are all obese."

Loren-Selco understands why he sees more obese youth these days. "The message they are getting, especially in the immigrant population, is what they hear and see via TV — they immediately understand that this is a place about 'more,' where they can get more. It's 'Look at me! I'm just a poor kid from Xapotecas and even I can get more.' They can afford supersized burgers and fries — and so they get them. There's no one out there telling them it is wrong — certainly not the fast-food companies, and, frankly, certainly not most physicians, who still aren't trained in nutrition."

Across town, up in the endocrinology department of Children's Hospital, Dr. Francine Kaufman is also getting — and giving — the proverbial wake-up call. Children had been coming in fat and sick since the early 1990s. "As endocrinologists, all of us were aware of the changing trends, and all of us were somewhat

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involved in obesity. It was just another part of the job," she explains. "It wasn't even something a lot of us wanted to deal with, because the disease links were not as strong."

That began to change in the mid-1990s, when Kaufman began seeing children like Jason (not his real name). A typical referral from county social services, the fourteen-year-old was poor, unkempt, lacking in the most basic forms of medical care, and slipping into a morass of profound health problems. Qrie other thing: Jason weighed three hundred pounds. He had arrived at Kaufman's office with a note from his school nurse. The nurse directed Kaufman to Jason's "obviously poor" bathing habits. There were, after all, several "dirty" dark patches on the back of his neck, on his elbows, and on his knees — anywhere "dirt" might accumulate. But almost immediately Kaufman could see that Jason was not unclean at all — or at least no more dirty than the average child. The smooth, velvety dark shadings in his skinfold areas were Acanthosis nigricans, a rare skin disease that resulted from too much insulin in the blood. In the past, the disease has been manifest almost entirely in adult populations with diabetes and other severe metabolic disorders. Seeing it on Jason, "we could see that he had never been screened for diabetes, never been adequately evaluated, and here was the school nurse, telling him he had to bathe better." Here, at last, was the classic marker — a link connecting obesity, youth, and diabetes.