Three years ago, in a documentary that was equal parts witty and disturbing, Morgan Spurlock took viewers along on his month-long McDonald’s binge. For 30 days, every food or beverage that entered his mouth came from the fast-food franchise. And every time a clerk asked if he wanted to super-size—bump up the size of the fries and drink in his order—he did. This gave rise to the feature’s title: Super Size Me.
The film was intended to explore the economic and health ramifications of the nation’s love affair with fast food. And Spurlock sandwiched in plenty of facts and mini-interviews with physicians, nutritionists, and economists between video segments of him biting into burgers, fries, and more.
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However, the initially trim and healthy Spurlock paid a big personal price to make this riveting picture: He gained about a pound a day, and in just 3 weeks exhibited symptoms of fatty liver disease, a condition that can ultimately kill. At the start of the film, doctors had given Spurlock—and his liver—a clean bill of health.
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Admittedly, most people don’t subsist on a diet of fast food alone. However, much of the nation does partake of such sweet, high-salt, and high-fat fare on a regular basis. So, it’s possible that Spurlock’s self-experimentation just compressed into 1 month what many people experience gradually over the decades. At a minimum, Spurlock’s film raised a host of troubling questions about the potential risks of fast food and its relationship to the nation’s collective waistline—one that just keeps getting fatter and fatter.
In reviewing Super Size Me, Chicago Sun-Times movie critic Richard Roeper said: “Whether you’re a fast-food junkie or a vegan, this movie provides a bounty of food for thought.”
It certainly provided food for thought to Brent Tetri. Indeed, he told Science News Online, Spurlock’s film—and apparent flirtation with diet-induced fatty-liver disease—”inspired” Tetri to investigate just how potent a liver poison fast-food meals might be.
Tetri, a gastroenterologist and liver specialist at St. Louis University, undertook a 16-week study of such diets in mice and, on May 22, unveiled his findings at Digestive Disease Week 2007, a research conference, in Washington, D.C.
Those data indicate that when offered the rodent equivalent of McDonald’s fast food, mice fare at least as poorly as people do. Fat accumulations nearly doubled the size of the animals’ livers. And within just 2 weeks of beginning their new diets, mice on the fast-food-like fare exhibited signs of incipient diabetes.
“It was a surprise to see how soon this developed—and very disturbing,” Tetri says.
He emphasizes that all animals were free to eat or drink until sated, much as people do in real life. While mice getting a standard rodent diet stayed trim, those offered high-fat chow and a sweetened beverage voluntarily “over-ate to the point of getting sick.”
Moreover, the pattern of fat accumulation in their livers was similar to what occurs in children with fatty liver disease. That, too, Tetri finds disturbing, since a study in Pediatrics last year pointed out that the incidence of this disease is quite high in youngsters—especially those who are obese (SN: 3/3/07, p. 136). And with U.S. children experiencing an obesity epidemic, the share of youngsters with potentially dangerous liver disease could be poised to skyrocket.
What’s rodent fast food?
In the new mouse trial, some animals dined on regular chow, which derives about 11 percent of its calories from protein, 13 percent from fat, and the rest from carbohydrates. Other mice received specially designed diets that provided 43 percent of a day’s calories from fat.
Moreover, even the type of fat the animals in these two groups ate differed. Most fat in the normal diet came from polyunsaturates. To emulate fast food—at least the type cooked up until very recently—30 percent of all of the fat calories came from trans fats. Those are unsaturated fats that have been engineered through partial hydrogenation to render them solid at room temperature.
Animals on the fast-food diet were offered water sweetened with high-fructose corn syrup in an amount designed to daily deliver about 6 grams of sugar per kilogram of bodyweight. “It’s the equivalent of a person drinking about eight cans of soda a day,” Tetri says, “which, in talking to my patients, I’ve found is not all that unusual.”
Finally, sedentary lifestyle aggravates an individual’s risk of developing fatty liver disease, so Tetri’s team discouraged its fast-food diners from pumping iron by removing a wire rack from near the top of their plastic cages. “Those racks act like a jungle gym,” he says. Removing them “is like putting a TV with a remote in the cage.” The animals may run a little, he says, but mostly “they just sit around with nothing to do.”
The most obvious change in animals on the fast-food diet was weight gain, which emerged within the first week of the study. By the trial’s halfway point, the fast-food group weighed an average of 25 percent more than did mice eating normal chow.
Also within a week of the trial’s launching, mice on the fast-food diet exhibited “early evidence of glucose intolerance”—an inability of their bodies to appropriately shepherd sugar from blood into hungry cells. It’s the first sign of what’s known as insulin resistance, a harbinger of type-2 diabetes. Five weeks later, this condition had worsened dramatically, to the point where fasting blood-sugar concentrations were 22 percent higher for the fast-food group compared to mice on a standard diet.
At least as concerning were the rapid elevations in liver aminotransferase enzymes, known by their acronyms ALT and AST. Such increases indicate that liver damage is occurring—and were the symptoms that most disturbed Spurlock’s physicians in the documentary.
Halfway into the mouse trial, ALT levels in the blood of fast-food-fed mice were already twice those of mice eating ordinary chow. AST concentrations rose more slowly.
Tetri’s team also reported that genes that produce inflammatory proteins were activated in animals on a fast-food diet—as were genes that contribute to scar-tissue formation in the liver. The latter is especially disquieting, Tetri notes, since it’s a sign of serious liver damage. Cirrhosis is a potentially lethal buildup of such scar tissue in the liver.
What’s it all mean?
Fatty liver disease “has become incredibly common—and its incidence is going up,” Tetri notes. “We think it’s because of the increased prevalence of obesity and sedentary lifestyle, because they all go up in parallel.”
Since a buildup of excess liver fat can ultimately lead to cirrhosis, fatty liver is essentially toxic in its own right. However, Tetri notes, this condition is also a sign of susceptibility to insulin resistance and high blood pressure.
Which is why a paper in the October 2006 Pediatrics by a team of San Diego researchers led by Jeffrey B. Schwimmer is so disconcerting. To get a feel for how common fatty liver is, physicians reviewed the livers of 742 children who had died of various causes over the decade ending in 2003. They found a sharp age dependence, with the incidence ranging from 0.7 percent in those under 4 years old, to 17 percent in older teens. Overall, the disease afflicted 13 percent of the examined children, with the highest rate—38 percent—in obese youngsters.
At these rates, Schwimmer’s group notes, “Fatty liver is the most common abnormality in children age 2 to 19,” and the majority goes undiagnosed.
Of course, as Spurlock’s personal experiment so graphically illustrated, adults are not immune—nor do they have to be obese to develop the problem. At his heaviest, the 6-foot 2-inch Spurlock still had a pretty normal weight for someone of his height. However, his enormous intake of fat and sugars each day apparently exceeded what his liver could handle.
The question Tetri will begin to investigate in the next few years is whether excessive caloric intake alone—or something more specific—is the source of fast food’s toxicity to the liver. It’s possible, he says, that some ingredient characteristic of fast-food fare, perhaps the fructose that sweetens soft drinks, is especially problematic.
Why single out that sugar? Some preliminary studies suggest that fructose can fool the body’s satiety meter, thereby fostering overeating (SN: 4/2/05, p. 216).
In addition, Tetri notes, a host of studies have linked heavy consumption of this particular sugar to fatty liver disease. One of the more recent of these studies appeared in the May 2005 Hypertension. Indeed, the authors of this rat study concluded that a fructose-enriched diet “can be a suitable model for human nonalcoholic fatty liver disease.”
Even for a carnivore like me, a salad is starting to sound mighty tasty.
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