6. WHAT THE EXTRA CALORIES DO TO YOU

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 Opinión 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, replete 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 norteño 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 hardscrabble 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 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 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-i 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.

***

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 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. One 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.

By 1996, in pediatric clinics, children's wards, private practices, and teaching universities around the country, physicians were coming to a sobering new conclusion: Type 2 diabetes, a potentially crippling, lifelong chronic disease, had come home to roost among the poor, the young, and the fat. The rate of increase had been swift. In i992, for example, most pediatric diabetes centers in the United States reported only 2 to 4 percent of their diabetes patients as type 2. Two years later that figure jumped to 16 percent of new cases. By 1999 the figure in some parts of the country would zoom to nearly 45 percent of new cases. Most of the new cases were found in African American, Mexican American, and Native American youth. Just up the coast from Kaufman, in the coastal town of Ventura, 31 percent of new onset diabetes cases in children were Hispanic. As Kaufman saw it, "Something had changed."

But what? The short answer is that more kids were fat, more kids were fatter, and so more kids were developing conditions caused by excess fat. But to truly understand what had changed, one first has to understand a little about the biology of the obese body.

At the most fundamental level, the obese body is like a four-cylinder car pulling a trailer full of bricks; it is, in the simplest sense, overloaded. Its "cylinders"—the heart and its ancillary arteries and veins—are not built for pulling the extra weight, and so must work harder, straining to accommodate the load. Its fuel injection system—the pancreas, the liver, and all of the organs that process fuel—are similarly overloaded, unable to process enough energy or to get it to the proper place to be used to fire the body's key muscles. Its chassis—the skeleton—groans under the excess weight, and like a car with bad shocks, begins to jangle and bump with the most minute movements.

There, however, ends the car simile, for when it comes to diabetes, there is no mechanical analogue to the human pancreas, the central player in the drama of the disease. A small, elongated organ tucked into the abdomen, the pancreas is responsible for making insulin, and it is insulin that makes sure that nutrients get into muscle cells. In a nondiabetic body, insulin is produced in a region of the pancreas known as the islets of Langerhans, named for the late-nineteenth-century German pathologist who discovered their function. There, "beta" cells secrete the hormone into the bloodstream. Once in the bloodstream, insulin binds to receptors on the surface of tissue cells, in a sense "pushing" those little buttons like doorbells to open the cell door to nutrients in the form of glucose. (Glucose is dietary carbohydrate—sugars—resynthesized by the liver to be used by cells for fuel, or to be stored as glycogen for later use.) The cell then "burns" the fuel, using it to repair torn tissue, grow new tissue, feed critical nerve endings, and nourish any number of other critical bodily processes. In the body of a traditional diabetic, also known as a type 1 diabetic, this process is derailed because the pancreas is unable to make any insulin. As a result, the bloodstream is flooded with sugar (glucose), which proceeds to wreak havoc on nerve endings while cells are starved for fuel. Only through daily injections of synthetic insulin is the type 1 diabetic able to survive.

In a type 2 diabetic, the metabolic scenario is somewhat less straightforward. Type 2 diabetics have the same ultimate problem as the type 1 patient—they are unable to get glucose out of their blood and into their cells—but they arrive at the impasse differently. The pancreas of a type 2 may or may not initially produce enough insulin, but that is almost beside the point. The real culprit in type 2 is a phenomenon called insulin resistance, wherein cells themselves become resistant to insulin's effects. Many believe that such resistance is the result of a defect in the little receptors on the cell surface, those little doorbells. How those receptors get twisted is the matter of much debate. There is evidence, for example, that the trait may be the result of a genetic mutation; "thrifty gene" scholars have even pinpointed a specific allele—or arm—of chromosome ii as the origin of gene-based insulin resistance. Some populations—African American, Native American, and Mexican American—seem to have this gene in greater percentages than others. Genetics are probably responsible for about 50 percent of the development of insulin resistance.

The other 50 percent likely comes from so-called lifestyle factors, and of all lifestyle factors implicated in insulin resistance, none is more influential than obesity. This is not to say that all obese people are insulin-resistant, or that excess fat alone causes insulin resistance. But obesity certainly makes insulin resistance worse. The mechanism is unclear, but, as the pre-eminent scholar of the phenomenon, Stanford's Gerald Reaven, suggests, it likely relates to the fact that excess visceral fat cells make excess fatty acids, which somehow interfere with the ability of insulin to stimulate the movement of glucose into muscle cells. If you have the least inclination toward insulin resistance, "the more obese you are," Reaven writes, "the more insulin-resistant you will be."

Increasingly, scholars believe that the modern way of eating also causes enhanced insulin resistance. Consider frequent high-energy snacking, which stimulates the pancreas to oversecrete insulin, thereby exposing the liver to longer, uninterrupted bombardment by the hormone. When that happens, according to Victor Zammit, head of cell biology at the Hannah Research Institute in Ayr, Scotland, the liver begins to interpret insulin differently—as a signal to release more fats, in the form of triglycerides, into the bloodstream. Along with the excess insulin (stimulated in the first place by excess snacking) these excess triglycerides tend to make muscle more insulin-resistant. (In the doorbell analogy, it would be as if one constantly rang one's neighbor's doorbell and then ran away; eventually the neighbor would stop coming to the door.) In the final leg of their journey, the triglycerides overload fat cells, where they are supposed to be stored as future energy, and begin to spill over as fatty acids, which in turn strike at the pancreas's insulin-producing beta cells, causing insulin levels to drop and, consequently, blood sugar to spike. That kicks off the dangerous diabetic cycle.

But it is not just how often one eats that can encourage insulin resistance, it's what one eats as well, and in this regard it pays to remember one of the key accomplishments of the Butzian revolution in American food: the commodification of high-fructose corn syrup, the use of which has increased tenfold since Butz's mid-1970s reforms. For years, food technologists and academics alike knew that, in addition to its properties of sweetness and stability (which made it so useful to convenience food makers) there was something else unique about fructose. Unlike its cousin sucrose, fructose is selectively "shunted" toward the liver; it does not go through some of the critical intermediary breakdown steps that sucrose does. This was interesting, but for years no one knew exactly what it meant. Eventually, cell biologists figured out that fructose was being used in the liver as a building block of triglycerides. This it did by mimicking insulin's ability to cause the liver to release fatty acids into the bloodstream (as demonstrated by Zammit in Scotland). Bombarded by fatty acids, muscle tissue develops insulin resistance. Whether humans consume enough high-fructose syrup to activate the effect was something that eluded scientists until the year 2000, when researchers at the University of Toronto in Canada fed a high-fructose diet to Syrian golden hamsters, which have a fat metabolism remarkably similar to that of humans. In weeks, the hamsters developed high triglyceride levels and insulin resistance.

Preliminary human studies also indict concentrated fructose. Two years ago, the clinical nutritionist John Bantle at the University of Minnesota at Minneapolis fed two dozen healthy volunteers a diet that derived 17 percent of total calories from fructose — the percentage that Bantle believes about 27 million Americans eat regularly (particularly all of those fast-food "heavy users" and drinkers of 32-ounce Cokes). Bantle then measured the volunteers' blood fats and sugars, and then switched them to a diet sweetened mainly with sucrose. The results were dramatic. The fructose diet produced significantly higher triglycerides in the blood—in men about 32 percent higher—than the sucrose-sweetened diet. The fructose diets also made triglyceride levels peak faster—just after the meal, when such fats can do the most damage to artery walls. To put a point on such observations, the conservative American Journal of Clinical Nutrition published one article that bluntly (and uncharacteristically) concluded that "these deleterious changes [by dietary fructose] occur in the absence of any beneficial effect ... and these abnormalities ... appear to be greater in those individuals already at an increased risk for coronary artery disease."

The fructose trouble hardly ends there. Fructose consumption — it now constitutes 9 percent of the average individual's daily energy intake (and up to 20 percent of the average child's diet)— has lately prompted science to look at another, more controversial, theory—that fructose consumption itself may have led to increased rates of obesity, not merely through increased calories, but through a variety of complex chemical reactions it stimulates in the human body. The theory has its origins in the 1970s, when European researchers began to chart the exact cellular pathways that determine whether or not a cell burns or stores new fuel. They soon focused on two critical enzymes, acyl-CoA and acylcarnitine, which act as pathway regulators on the cell surface. Both seem to "tell" the inner cell whether to "store" or "burn" a newly arriving fat particle. Scientists then looked at the effect of different fats and sugars on these enzymes. Two elements, glycerol and fructose, emerged as principal players. When these were present in abundance, acyl-CoA and acyl-carnitine levels were depressed, thus leading the researchers to conclude that fructose and glycerol "lower the rate of fatty acid oxidation." For almost a decade however, such work was virtually ignored by American nutritional scientists, who were much more interested in dietary fats rather than dietary sugars. This was largely because the research agenda had been set by the American Heart Association, which had decided that dietary fat was the principal cause of excess, artery-clogging cholesterol.

Then, in the late 1990s, things began to change. One factor was the sheer magnitude and frequency of fructose consumption, mainly in new convenience foods, pastries, and snacks. The connection with obesity grew when, in 1999, the American Journal of Clinical Nutrition published a revealing graph, showing, on one axis, the rate of growth of new food products (principally fructose-laden convenience foods, snacks, and candy), and, on the other axis, the rate of growth of the average national BMI. Both rates increased across the same span of years at almost exactly the same incline. More research followed. Older research was revived and given a second look. A 1993 study from the U.K. showed another pathway and mechanism implicating fructose and obesity. Reviewing studies of animal and human models, the University of London veterinary scientist P. A. Mayes narrated how fructose consumption led to increased production in the liver of an enzyme called pyruvate dehydrogenase, or PDH. PDH is another chemical gateway that tells a cell whether to burn fatty acids or sugars; the more that is present at the cell surface, the more the cell will tend to burn sugar instead of fat. "Long-term absorption of fructose," Mayes concluded, "causes enzyme adaptations that increase lipogenesis [fat formation] and VLDL [bad cholesterol] formation, leading to triglyceridemia [too many triglycerides in the blood], decreased glucose tolerance, and hyperinsulinemia [too much insulin in the blood]." By 1995 a far-sighted team of researchers from the University of California at Berkeley, studying how certain sugars alter how the body selects fuels to burn, concluded basically the same thing: Long-term dietary changes involving simple sugars—as had happened in two decades with fructose—"contribute to [overall] changes in fat oxidation." Overuse of fructose, these and other studies were saying, was skewing the national metabolism toward fat storage.

Still, nutritionists involved in public health pronouncements remained reluctant to single out one specific kind of sugar; most of their careers had been made, after all, in demonizing dietary fat. Nonetheless, in 2001, one high-visibility group from the Department of Medicine at Children's Hospital in Boston took the leap. In a brilliant methodological tactic, researchers under Dr. David Ludwig singled out childhood consumption of soda pop and obesity as their target. Soda is, ninety-nine out of a hundred times, nothing but high-fructose corn syrup and carbonated water, with a few flavoring agents thrown in for brand distinction. The researchers tracked 548 ethnically diverse Massachusetts schoolchildren (average age eleven) for nineteen months, looking at the association between their weight at the beginning of the study, intake of soda, and weight at the end of the study period. The results were revealing. For one thing, 57 percent increased their intake over the nineteen-month period. The calories from just one extra soft drink a day gave a child a 60 percent greater chance of becoming obese. One could even link specific amounts of soda to specific amounts of weight gain. Each daily drink added .18 points to a child's BMI. This, the researchers noted, was regardless of what else they ate or how much they exercised. "Consumption of sugar[HFCS]-sweetened drinks," they concluded, "is associated with obesity in children."

The reaction by the food industry was predictable, with many of its underwritten scientific advisory boards issuing proclamations that fructose was a natural product of Mother Nature. It was, they inevitably pointed out, made from good old American corn. But none of those organizations has yet refuted the growing scientific concern that, when all is said and done, fructose—as produced by modern food processors and used by the American consumer—is about the furthest thing from natural that one can imagine, let alone eat.

Although not as intensively studied as fructose, palm oil and palm kernel oil, the other great legacies (along with cheap soybean oil) of the Butz years, have also rendered their share of obesity-related woes. Both are implicated in insulin resistance. As saturated fats—fats rich in fatty acids—both tend to raise total and LDL, or "bad," cholesterol, thereby contributing to atherosclerosis and coronary heart disease. (A highly publicized campaign in the late 1980s by the businessman Ira Sokolow against the use of palm oil for french-frying led to a marked decrease in usage.) Palm oil's impact on insulin effectiveness, on its ability to stimulate glucose use by cells, is less clear. One study by researchers in the Netherlands demonstrated that palm oil was only half as effective as sunflower seed oil in fostering glucose uptake. In another study by the same group, groups of lab rats were fed diets containing different kinds of oils (sunflower seed oil, palm oil, olive oil, linseed oil, cocoa butter, and coconut oil). The researchers then looked at the level of insulin response by fat cells in each group. The result: Compared to the other oils, cocoa butter, coconut oil, and palm oil were negatively correlated to insulin response. No one can yet tell if this effect is due to something particular to all tropical oils, or if the effect is simply a reaction to all saturated fats, but one thing is certain: There are far better fats and oils to use as an industrial oil than palm oil and its relatives. Which is certainly something to keep in mind as palm oil's proponents attempt, as they have recently, to revive its use by promoting its "healthful" amounts of vitamin A.

 

Regardless of how one arrives at his or her insulin resistance—and there are an estimated 60 million Americans who have it—the path that follows the condition is almost always a painful one, eventually leading to full-blown type 2 diabetes. And because insulin resistance often goes undetected—the pancreas can delay its main effects by pumping out extra insulin before eventually wearing out its capacity to do so—one may be suffering from near-type 2 damage long before the condition is officially diagnosed. Too much sugar in the blood becomes the catalyst for a dirge of woes that can eventually render the sufferer all but helpless.

The obese diabetic may first notice strange things happening to his or her feet; they may tingle, or they may be numb. When they are bruised or scratched, they may take a long time to heal. This is because excess sugar in the blood has damaged vital nerve endings and, in the worst case, caused atherosclerosis, leading to reduced blood flow to the limbs. The consequent numbness can mask a severe injury, which can become infected, eventually leading to gangrene and amputation. This happens more often than one might suspect, particularly as the disease progresses into middle and late middle age.

Now move up the legs. Behind the knees one may develop Acanthosis nigricans, the dark, velvety patches that Dr. Kaufman saw on young Jason. Too much insulin in the blood causes that. Muscle tissue on the calves and thighs, starved of fuel because it has become so insulin-resistant, may atrophy. The diabetic may, then, be losing muscle as he or she gains fat, the worst of all possible situations.

It is likely, however, that the obese diabetic will be preoccupied with other, more painful woes. Because the obese tend to excrete excess cholesterol, they are also more likely to form gallstones. In adult women, obesity raises the chances of contracting such twofold. In children, obesity accounts for somewhere between 8 and 33 percent of gallstones. This may seem like a rather abstract development—until the body decides to pass the stones, causing biliary colic. In that case, as the Merck Manual puts it, there is nothing abstract about it at all: "In contrast to other types of colic, biliary colic is constant, with pain progressively rising to a plateau and falling gradually, lasting up to several hours. Nausea and vomiting are often associated." Elsewhere in the abdomen, the obese diabetic may contract liver steatosis—fatty liver disease. Although by itself not life-threatening, fatty livers have been shown to lead to tissue scarring and eventually to cirrhosis, particularly if the patient continues to gain weight. Obese children are also at risk for steatohepatitis, with the most severe cases leading, again, to cirrhosis.

Menstrual and other sex hormone-related conditions increase in proportion to weight too. Obese girls tend to experience earlier menarche, often before age ten. As one ages, obesity can inculcate patterns of late or absent menstruation. About 40 to 60 percent of adult women who contract polycystic ovary syndrome—large but benign ovarian cysts—are overweight or obese. The syndrome often brings with it acne, Acanthosis nigricans, and hirsutism (excess hairiness), the latter in such abundance as to require its own regimen of treatment.

Excess blood sugar and insulin continue to damage other parts of the body. For the same reasons that high blood sugar causes foot problems, it causes numbness in hands, arms, and legs. Then there are the eyes, perhaps the most delicate of diabetes' targets. With the disease out of control, and with a bad diet repeatedly jacking up blood sugar and blood fat levels, blood sugar damages the small blood vessels of the retina, the part of the eye that is sensitive to light. The broken vessels can leak blood into the eyes, form deposits, and/or cause the retina to grow new, much more fragile vessels, which bleed even more easily. When they begin to bleed into the vitreous humor (a clear, jelly-like substance that fills the center of the eye) the obese diabetic will get blurred vision, leading to double vision and, eventually, blindness. About 80 percent of people who have diabetes for fifteen years or more have some damage to blood vessels in the retina.

Numb limbs, darkened skin, painful gallstones, hair sprouting from embarrassing places, fading vision—such is the lot of the obese diabetic. And that is just the beginning, for any biography of an obese body would not be complete without chapters on nondiabetic medical consequences. Even if one does not become a full-blown diabetic, insulin resistance, combined with an ongoing poor diet and too many visceral fat cells, can lead to the triple threat of coronary artery disease (CAD), hypertension, and stroke.

CAD proceeds directly from atherosclerosis, a thickening of the artery walls due to the repeated presence of lipids—blood fats; these come from diet, but are also multiplied via the insulin-resistant patient's propensity to produce too much compensatory insulin, which in turn sparks the liver to spew fatty acids into the bloodstream. (A new study shows that structural changes in the artery walls that lead to hardening begin as early as age twelve.) Hypertension—high blood pressure due to constricted blood vessels—has more complex and still many unknown causes, but two emergent theories, again put forth by Stanford's Gerald Reaven, go something like this: First, hyperinsulinemia causes the kidneys to retain salt and water, thereby boosting total blood volume and its consequent pressure against artery walls. Next come changes in the blood vessels themselves. Here insulin plays the pivotal role again. Because the hormone acts on the central nervous system, it can encourage the arteries to decrease in diameter. Insulin also catalyzes the action of catecholamines, which act, in part, to decrease the diameter of blood vessels, again pushing up blood pressure. (Hypertension is nine times more frequent in obese children; 20 percent of obese children between five and eleven already have it.) With clotted, constricted, and overloaded arteries, the stage is set for all kinds of vascular mischief, one of the most deadly of which is stroke. Stroke happens when all of these conditions cause the vessels of the human brain to become blocked, depriving the organ of much needed oxygen and nutrients and causing it, eventually, to cease functioning.

The brain suffers from obesity in other ways too, responding with a condition known as Pseudotumor cerebri. As the name suggests, this is a brain tumor-like condition caused when excess abdominal weight presses down upon the lungs and the heart, causing increased pressure on the vein returning blood from the brain. The most common symptoms are headaches, vomiting, blurred vision, and double vision. Obesity occurs in 30 to 80 percent of children with pseudotumor. The chances of a child getting the condition increase by twenty times when body weight exceeds 20 percent above the ideal.

Then there are the orthopedic problems. First comes the obvious: arthritic joints caused by simply carrying too much weight. Next is a condition known as slipped capital femoral epiphysis—a slipped hip. Obese children succumb to it much more often, and at substantially younger ages, than the nonobese. Its consequences can be painful and chronic and eventually require surgical insertion of a screw in the hip. The same can be said of Blount's disease, also known as Tibia vara. In Blount's, the legs respond to early weight excess by becoming bowed, and contrary to popular conceptions about bowed legs, this is not merely a cosmetic inconvenience. Consider a recent case report, detailed by J. Richard Bower, the chief of orthopedic surgery at the Alfred I. Du Pont Institute: "The patient is a 14 and one half year old black male with a one year history of worsening left knee pain. He states that the pain began in both knees and was intermittent.... Over the past six months the pain is more isolated to the left knee and has become constant in nature. Within the past two weeks the constant pain has become bad enough to limit his activities. He is unable to attend school or walk more than several hundred feet because of the pain. The pain is now affecting his sleep.... The adolescent is morbidly obese." As are 80 percent of children with Blount's.

Now drones the true dirge of the obese child—respiratory diseases. These come in three forms. The first, Pickwickian syndrome, is named after the ever somnolent Joe the Fat Boy in Dickens's Pickwick Papers. The syndrome starts when large amounts of abdominal fat cause the child to breathe in a rapid, shallow fashion, with increasing intervals of breathlessness. This leads to oxygen deprivation, chronic sleepiness, and, if untreated, heart failure. Excess fat tissue in the throat and uvula is also the direct cause of obstructive sleep apnea in obese children, a third of whom display the main symptoms of apathy, listlessness, nighttime sleeplessness, and daytime somnolence. More troubling are the condition's effects on learning. According to a report in the International Journal of Obesity, "Obese children with obstructive sleep apnea demonstrate clinically significant decrements in learning and memory function."

Lastly there is the condition known as allergic asthma. For the past three decades, epidemiologists have watched a progressive rise in this wheezing condition, particularly among children between five and eighteen. The two principal theories about its origin—increased time spent around or near indoor allergens and the rise in childhood antibiotic use—have recently been joined by a new theory of causation: the general decline in childhood physical activity. In this scenario, lack of the strengthening effects of exercise leads to weakened lungs, making it easier for wheezing reactions to set in. A study by the Respiratory Sciences Center at the University of Arizona showed that females who became overweight or obese between six and eleven years of age were seven times more likely to develop new asthma symptoms than those who were normal weight.

Obesity makes for special problems when fat girls grow up to become fat mothers. Women who are overweight or obese before becoming pregnant are much more likely to develop gestational diabetes and hypertension of pregnancy, also known as preeclampsia; they will inevitably need longer and more intensive hospitalization. A mother's excessive pre-pregnancy weight also greatly increases her chances of having a baby that is stillborn or that will die shortly after birth. If the child survives, he or she is 30 to 40 percent more likely to present with a variety of birth defects, ranging from spina bifida to heart malformations to defects in the abdominal wall. Folic acid supplements are less likely to prevent such defects in the offspring of the obese, who are at increased risk of becoming obese themselves, thereby setting in motion the vicious cycle once more.

As if all of this were not enough, the obese child who becomes an obese adult will also have an increased risk of cancer. In early 2001 the American Cancer Society, after years of deliberation, issued a special statement on the connection in its annual Cancer Facts and Figures. Obesity, the society declared, was "linked to an increased risk of breast cancer after menopause and to cancer of the endometrium, ovaries, colon, prostate and gall bladder." Again, much of the problem derives from excess visceral fat cells, which, among other things, play a key role in converting estrogen to estradiol, a more active form of the hormone that can promote tumor growth. If the obese individual is insulin-resistant, compensatory oversecretion of insulin will cause overproduction of insulin-like growth factor, related, in turn, to growth factors that bring about colon, breast, and prostate cancer. Cancer, the obsession of twentieth-century medicine, has entered the new millennium as the special burden of the obese.

As Fran Kaufman had observed, something had indeed changed.

 

Outside of the medical consequences to the individual, what are the economic consequences to the nation if obesity is merely incorporated into the American way of life rather than resisted?

There are, first and foremost, the premature deaths of more than 280,000 Americans every year, the figure the American Medical Association now believes reflects the number of obesity-related mortalities. There is the $100 billion annual price tag for the care and treatment of diabetics, the majority of new cases being a direct result of excess weight. That boils down to one in every ten dollars dedicated to health care. In terms of federal resources, diabetes alone commands one in every four Medicare dollars. These are considered to be conservative estimates. Most policy experts on the subject believe that diabetes is subject to the classic epidemiological "rule of halves"; because of its overwhelming residence at lower social addresses, and because one can have the disease for long periods of time without feeling sick, only half of all diabetics are ever diagnosed. Of those, only half are ever treated. And of those only half ever have their disease managed effectively.

Obesity takes its toll on our daily quality of life too. Between 1988 and 1994 the number of days of lost work due to obesity increased by 50 percent—to 39 million days, worth $3.9 billion. There were also 239 million restricted activity days due to obesity, 89.5 million bed rest days, and 62.6 million physician visits, the last equivalent to an 88 percent rise over 1988. As A. M. Wolfe and G. A. Colditz of the University of Virginia concluded in a study of such costs among a population of 88,000 U.S. residents, "The economic and personal health costs of overweight and obesity are enormous and compromise the health of the United States" (emphasis added). As a recent RAND/University of Chicago report noted, "More Americans are obese than smoke, use illegal drugs, or suffer from ailments unrelated to obesity."

How will the average person feel obesity's economic pinch? To figure that out, four researchers from the independent Policy Analysis Inc. (PAI) set up a sophisticated model of a hypothetical HMO with 1 million members. Using reference data from a large managed health care plan in the Pacific Northwest, the researchers then projected the number of cases of eight diseases for which obesity is an established risk factor (coronary heart disease, hypertension, hypercholesterolemia, gall bladder disease, stroke, type 2 diabetes, osteoarthritis of the knee, and endometrial cancer). The results were mind-boggling, even to jaded public health types. In a population of 1 million, the PAI researchers found, "obesity would account for 132,900 cases of hypertension (45 percent of all cases), 58,500 cases of type 2 diabetes (85 percent), 51,000 cases of hypercholesterolemia (18 percent), and 16,500 cases of coronary heart disease (35 percent)." The total costs of obesity to the HMO? $345.9 million annually, or 41 percent of the total for the eight diseases studied—"substantial," as the researchers put it.

And what will happen when people who take care of themselves start to understand why their own health care bill keeps skyrocketing? "We believe the effect will be like that of secondhand smoke," says James O. Hill, of the University of Colorado and the dean of American obesity studies. "When people who are fit really begin to understand this, it will be a catalyst for one of two things, though likely both: anger, and then a demand for change." Hill has been studying the phenomenon in Pueblo, Colorado, where groups of patients, health providers, academics, physicians, and policy makers are trying to come up with a way to involve HMOs more directly in treating and preventing obesity. "The main thing we see is real shock when people digest this. They get very worked up—and why not? They are taking care of themselves. But they also want to know: What can we do besides just throw more money at this?"

One approach would be for HMOs to get more proactively involved in identifying obesity-related problems within their contracted populations. An enlightened HMO might sponsor a free blood sugar testing clinic, with employees who test high being counseled to schedule more complete workups in the future. But what then? Not a few fat people's rights organizations would argue that such an approach would merely legitimize discrimination against the obese, giving them a medical stigma to go with their aesthetic stigma. (Yes, this may sound crazy, but such concerns are a fact of life in large organizations, particularly large governmental organizations, where obesity rates run particularly high.) Moreover, mainstream (read: middle) America remains in deep denial about obesity; it will likely be some time until the culture connects the proverbial dots and demands such testing. As Gerry Oster, one of the authors of the PAI study, says, "We have a long long way to go until the average person gets a clue about the connection. I am not representative at all of the typical attitude toward obesity. None of my friends are obese; we are coastal professionals involved in health care research. But go to the Mall of America in Minneapolis—I'd bet the obesity rate you see there is 75 percent or more." A culture that condones obesity, whether consciously or unconsciously, undermines any attempts to convince people to pare down.

 

Yet not taking such basic preventive measures merely encourages more rampant obesity, which, in turn, fuels its own kind of social sorting, one based on both aesthetics and social class. The aspiring classes of the country tilt toward thinness as a social goal. Perusing the pages of any "New Economy" magazine of the 1990s, one was pressed to find a single example of an obese CEO, let alone an obese venture capitalist. Ditto today's heroes in Fortune or Forbes. The operative notion is simple: If one can't control one's own contours, how can one be trusted to control someone else's money?

Even the Clinton-Lewinsky scandal had a strong taint of upper-class anti-fatism to it. As Jane Gallop, a distinguished professor of English at the University of Wisconsin at Milwaukee, commented in the New York Times, "There's a moment in the Barbara Walters interview where Monica relates that he [Clinton] would always leave his shirt untucked because of his belly, and you just feel that was one of the ways where Monica and Bill get connected. If the right wing in this country is still really moralistic about sex, the left is moralistic about food—that's where the new style of moralism about control is. Well-educated people are supposed to be in control of the amount of body fat they have. The people who are disgusted by Clinton's fat and by Monica's aren't the right wing, they're the ones who wanted a yuppie president with the right amount of body fat at the helm."

Although one might quibble with her left-right dialectics (after all, it is George W. Bush who has the right body fat, not to mention a pulse lower than that of Seabiscuit), Gallop clearly is on to one thing: When it comes to fat, the affluent are afraid. Very afraid. They will do anything not to be affiliated with it. In the upper classes, fat is seen as the great cheat—a barrier to performance, a denier of rewards delayed, a mark of the uncontrolled, primal fellow supposedly left behind in the individual's arduous upward economic march. To be affiliated with being fat would put the affluent person on the wrong side of the stigma, where the dynamic would seem to cut the other way—fat attracting fat.

Fat attracting fat! Johannes Hebebrand, the German psychiatrist who was so taken aback by how unashamed obese Americans seem to be, has been studying that side of the stigma for more than a decade. "We got very interested in this area some time ago, when we saw that negative impressions about fat people—as indicated in various surveys and attitude tests—showed a huge jump in just ten years. It led us to ask: If people feel stigmatized, will they be more likely to mate with other stigmatized people, in this case other fat people?" he says. "The other factor was the huge jump in the obesity rate itself, and the fact that everyone was saying it had to be entirely an environmental issue, because twenty years was too short of a time for genetic mutations to appear. We started to think that maybe that was not entirely true. Maybe environment—via assortative mating—was accelerating genetic expression of obesity."

To find out if that were the case, Hebebrand and his fellows at the University of Marburg, Germany, examined the parents of 471 extremely obese children and adolescents. The researchers took down three key pieces of data: the parents' current measured height, the parents' current self-measured height, and the parents' recalled weights and heights at ages twenty and thirty, the period when most couples meet and marry. They then referenced these measures against BMI averages for the general population. When they charted the cross-references, they found a high degree of assortative mating; obese children tended to have parents who mated when they themselves were obese. Although the results are only suggestive—Hebebrand was unable to show that the rate of assortative mating itself has increased over time—his finding falls in line with what is already known about obese children and obese parents. It is this: Obese parents influence their children's fatness both through genetics and through environment. "It is not exactly a straight line," Hebebrand says. "There are all kinds of other factors going on here. Take the case of the thinner person marrying the fatter person, who soon drags the thinner person down into his or her habits. He watches ten hours of TV and she begins to do the same, and over time she becomes obese too. In this case it was not the genetic expression of obesity from assortative mating that makes for fat kids. It's the environment that both the parents produce."

In all of this—fat attracting fat, stigma causing assortative mating, fat producing fat—there glimmers just a touch of the old eugenicist impulse. Yet in this case, recognizing such a dynamic might help prevent a eugenic reality, for however parents become obese, one thing is indisputable: Fat parents are more likely—much more likely—to raise fat children, who are in turn more likely to be fat adults, who are then more likely to continue the daisy chain until, as James Hill fears, all Americans are overweight or obese. And that day is not far away...

 

Let us now spend an imaginary day with a typical American, circa 2050, when overweight and obesity are the norm, and when the social divisions are not between the slim and the fat but between the obese and the not so obese. In other words, a lot like today, only intensified by a factor of one hundred.

Our average guy arises late in the morning, later than he had planned. He has slept poorly. The night before, the CPAP (for continuously pressurized air pathway) machine that provides an extra forceful flow of air to aid with his sleep apnea had been louder than usual. Looking in the mirror, he takes in his visage: Across the bridge of his nose and under his eyes rises a freshet of new acne, the nightly legacy of the sticky plastic face mask he must wear in order to remain hooked up to the CPAP machine. "Shit," he mutters.

He takes a shower, shaves, dresses. He curses at his ever too small pants and shirt—hadn't he just purchased a larger size a few months ago?—and then turns to the mirror again. He examines the dark circles under his eyes and the Acanthosis nigricans on his neck, then decides to cover up the latter with his wife's face powder. From his desk he picks up his blood sugar meter and, in the first of a half-dozen tests he will administer throughout the day, pricks his finger, draws blood, and measures his glucose level. He then injects his thigh with the first of several doses of insulin. Running late, he decides that, despite the worsening pain in his arthritic knee, he will forgo his pain medication, and walks out to the kitchen.

He cannot have his favorite breakfast, pancakes, because his blood sugar will soar if he eats more than one. (And what is the use of that? he reasons.) He drinks a cup of black coffee, has some oatmeal with nonfat milk and artificial sweetener, kisses his wife, and leaves for work.

In traffic, his blood pressure soars. Did he take the medication for that today? He cannot remember. The cell phone beeps; it is his wife reminding him that he has to take his son Jonny to the endocrinologist today. Only nine, the boy is already forty pounds overweight, and just last week he had another fainting spell at recess. It may have been from hypoglycemia. Whatever the cause, the school nurse sent home an embarrassing ultimatum: Get Jonny checked or she would have to notify social services.

Finally our average guy arrives at work. The office is humming; business is good. But, again, the new sales charts underscore that, as a salesman, our man is not what he used to be. Getting in and out of the car to make sales calls, always arduous even when he was not obese, is now something to be avoided altogether. The two-hour drop in his afternoon energy level doesn't exactly help either. Nor does his aching knee. He checks his blood sugar and begins the afternoon round of phone calls. He is glad that he ordered the large-type phone pad, since his eyesight too is not what it once was.

At around four, a marked silence falls outside his office door. His officemates burst in with a birthday cake and a song. His assistant gets out a knife and begins serving slices of the cake with ice cream. She offers him a plate, and he demurs. She insists. He refuses again, but feels ashamed to reveal why he cannot eat such a sugary treat, and so eventually relents. An hour later he is flushed, sweaty, and dizzy. He vows never to do such a stupid thing again.

Outside, the cool air dries his sweat-beaded brow. He gets in his car and drives over to day care to pick up Jonny. When he gets there his son is crying. "They ... they used me as a dodgeball target again!" he explains. "They ... they call me earthquake boy because I'm so..." Jonny doesn't need to finish the sentence.

"Aren't there other... heavy kids in your class? What do they do when..."

His son cuts him off. "It's just that I'm the biggest," he blurts out.

It is a long, uncomfortable drive.

At the doctor's, the boy fares better than he thought he would. "I'm thinking that the fainting may be more from stress—from all the teasing and harassment—than from his blood sugar," the doctor says. "But you better get that hip checked out ... When did he start walking like that?" He writes out a referral to a specialist in pediatric bone disease. "Just in case," he says, not very convincingly.

At home, waiting for dinner, he opens the mail. There is a notice from his HMO—again—telling him that his rates have gone up. Again. Also, the co-pay for medications has jumped; given the fact that he pays upward of $200 in co-payments a month already, it makes him worry: What would he do if he ever lost his job, or even if the company scaled back its health coverage? He shudders to recall a nightmare he had earlier in the week, one in which he was being told by his physician that "amputating today is not what it used to be—amputees can live full, long lives..." He decides to pay more attention to the chronic numbness in his left foot.

Dinner, since it is diabetically correct, is not worth eating, but he does so anyway, if just to spend some time with his wife. She, too, has weight-related woes; though not yet a full-blown diabetic, she nonetheless feels the limitations of being obese. Her energy level is low. She seems to sweat endlessly. Her gynecologist has called her back for more x-rays and a discussion of whether she should have surgery to remove the large but (so far) benign ovarian cyst she has had for the past two years.

Later, while the family is watching TV, he sneaks into the kitchen and eats handful after handful of the cookies he stashed behind the coffee tin the evening before. The momentary pleasure is followed by a rush of guilt, then nausea, then clammy sweating. He relaxes for a while longer, resolves never to do that again, and decides to turn in early.

In bed, he sets the CPAP machine on low, puts in his earplugs so he doesn't have to listen to the thing chug and puff all night, and gets ready to put on the mask. Shit, he thinks. Perhaps if he swabs it with alcohol first he will not wake up with another crop of unsightly red zits.

They are, after all, more than a little embarrassing, particularly at age thirty-five.