Fat land : how Americans became the fattest people in the world (19 page)

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 1992, 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

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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,

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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 i 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 i 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 11 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

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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

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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) —

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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 acyl-carnitine, 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

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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 hyper-insulinemia [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

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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

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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 preoccu-

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pied 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

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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