Bickering about obesity

by Ari LeVaux
    
Mexico is now more obese than the United States, according to the Food and Agriculture Organization of the United Nations. A third of Mexico’s population carries a body mass index of at least 30, obesity’s official threshold. The American Medical Association recently classified obesity as a disease in and of itself, and it’s a well-known gateway to other illnesses like heart disease, high blood pressure and diabetes. Obesity can take years off your life, disproportionately affects the poor, and adds billions of dollars of drag to our health-care system. It’s a problem worth solving.

In the July issue of The Atlantic, David Freedman argues that the most efficient way to solve the obesity crisis, especially among the fast-food-eating poor, is to improve the quality of fast food. This solution, Freedman argues, is threatened by the “Pollanites,” devotees of the local-food, small-farm, minimally processed food paradigm famously articulated by journalist Michael Pollan.

He casts the Pollanites as ineffective hypocrites, who enjoy food that’s just as “obesogenic” – that is, obesity causing – as the average fast-food meal. He cites a Pollanite recipe for corn and bacon as an example. Freedman makes no secret of his fear of fat; he admits to years ago dropping the oil from his oil and vinegar salad dressing.

“(The) science is, in fact, fairly straightforward,” Freedman writes. “Fat carries more than twice as many calories as carbohydrates and proteins per gram, which means just a little fat can turn a serving of food into a calorie bomb.”

This simplified view of fat makes Freedman’s simple fix for obesity seem within reach. Fast-food companies can simply dial down the fat and other obesogens, replace them with palatable substitutes, and cure obesity.

Freedman’s fat science has been addressed in more detail by others, soI won’t go further. Freedman called Tom Philpott at Mother Jones an Atkinite, based on Philpott’s rebuttal, a reference to Richard Atkins and his infamously fat-philic Atkins Diet.

The other obesogens Freedman frets over are sugars and refined carbohydrates, or “problem carbs,” as he calls them. I agree with him here. But at the same time, he should acknowledge that food processing has the effect of making carbohydrates more accessible. In other words, processing, in general, turns non-problem carbs into problem carbs. This is as true with a sack of whole wheat flour from Whole Foods as it is with a tortilla from Taco Bell.

Freedman doesn’t distinguish between good and bad fats the way he differentiates among carbs. Perhaps he doesn’t mention good fats because good fat is hard to find in the fast-food world. There are fats that are less bad, such as non-trans-fats, but few undisputedly good fats, like olive oil, can be purchased at the drive-thru. Or found in the 10,000-plus words of Freedman’s article.

While the debate rages over which nutrients more readily pack on cellulite, it’s important to remember that caloric intake is only half of the equation behind weight gain or loss. Equally important to the calories you consume is the number of calories you burn, which is a function of your metabolism.

The body’s metabolism is in constant flux, depending on factors like activity level, age and weight.

Earlier this month in Science, researchers presented compelling evidence of a gene that controls metabolism. They deleted a certain mouse gene that had been suspected of playing a role in regulating metabolism. The engineered mice that lacked this gene became obese, while eating and exercising the same amount as their control counterparts, who weighed about half as much.

The human genome includes a nearly identical gene, and this gene has been found missing in an obese human. It’s possible that this gene, even when present, might express itself differently, or be regulated differently, in different individuals. Perhaps it is expressed differently with age.

Any veteran of a high-school reunion has noticed what happens to some of their friends when they hit their 30s. They start to puff out, even while purporting to eat and exercise the same as they always have. Until they figure out that their bodies now require less food, the gain continues. It’s possible that an age-related slowdown in metabolism is programmed into our genes, but such a pathway is far from known.

The mouse gene discovery also supports a long speculated relationship between diet, genetics and obesity, called the “thrifty gene” hypothesis. It credits high rates of obesity in certain Native American populations to their genes being “thrifty” with ingested calories, thanks to generations of near-starvation conditions. The Pima Indian tribe of Arizona, for example, has nearly double the obesity rate of Mexico. According to this hypothesis, when carriers of the thrifty gene, or genes, are given the rich food of the modern Western diet, their bodies save every calorie they can, in the form of fat, for a caloric rainy day.

As the evidence mounts for a genetic component of obesity, one that likely interacts with diet, we should be open to the great complexity in which the ultimate causes of obesity are enshrouded. There is also growing evidence that the timing of eating and exercise, with respect to each other, can influence how many calories are burned in a given workout. Exercising during an hours-long fast appears to burn more calories than the same activity in a non-fasted state.

Wherever they lead, the roots of obesity are not as straightforward as Freedman describes. I won’t argue that there isn’t room for improvement in the quality of fast food. But I can’t see how bashing Pollanites, a segment of the population that’s noticeably non-obese, will help. And I can’t see how the obesity problem is likely to be solved by doubling down on the very system that helped create it.