The Co-Villains Behind Obesity’s Rise

[Buster's Uncle]

The Co-Villains Behind Obesity’s Rise
By SENDHIL MULLAINATHAN
Published: November 9, 2013
   


Researchers have compared tissue samples from obese mice with those of normal mice to try to determine which behavioral or biological factors might cause humans to gain weight. Here, a 2012 experiment in Leipzig, Germany. Waltraud Grubitzsch/European Pressphoto Agency
 


Why is obesity soaring? The answer seems pretty clear. In 1955, a standard soda at McDonald’s was only seven ounces. Today, a medium is three times as large, and even a child’s-size version is 12 ounces. It’s a widely held view that obesity is a consequence of our behaviors, and that behavioral economics thus plays a central role in understanding it — with markets, preferences and choices taking center stage. As a behavioral economist, I subscribed to that view — until recently, when I began to question my thinking.

For many health problems, of course, behavior plays some role but biology is often a major villain. “Biology” here is my catchall term for the myriad bodily mechanics that are only weakly connected to our choices. A few studies have led me to wonder whether the same is true with obesity. Have I been the proverbial owner of a (behavioral) hammer, looking for (behavioral) nails everywhere? Have I failed to appreciate the role of biology?

A first warning sign comes from looking at other animals. Our pets have been getting fatter along with us. In 2012, some 58.3 percent of cats were, literally, fat cats. That is taken from a survey by the Association for Pet Obesity Prevention. (The very existence of this organization is telling.) Pet obesity, however, can easily be tied to human behavior: a culture that eats more probably feeds its animals more, too.

And yet, a study by a group of biostatisticians in the Proceedings of the Royal Society challenges this interpretation. They collected data from animals raised in captivity: macaques, marmosets, chimpanzees, vervets, lab rats and mice. The data came from labs and centers and spanned several decades. These captive animals are also becoming fatter: weight gain for female lab mice, for example, came out to 11.8 percent a decade from 1982 to 2003.

But this weight gain is harder to explain. Captive animals are fed carefully controlled diets, which the researchers argue have not changed for decades. Animal obesity cannot be explained through eating behavior alone. We must look to some other — biological — driver.

Fittingly, the study is titled “Canaries in the Coal Mine.” Could our inability to explain animal obesity with behavior be a warning sign? Perhaps we are also overlooking biological drivers for human obesity. But what might these culprits be?

A particularly interesting candidate resides in your gut. Your digestive system is actually a complex ecosystem, playing host to hundreds of species of bacteria that do things as diverse as fermenting undigested carbohydrates and providing vitamins. They also regulate how much fat your body stores.

Not everyone, however, has the same gut bacteria. And, interestingly, the composition of this bacteria correlates with obesity. Of course, this relationship could be simple: the obese eat differently, and therefore they have different bacteria.

But a recent study in the journal Science showed that cause and effect could go the other way as well. Researchers harvested bacteria from pairs of twin mice, where one twin was obese and the other was not. Then they transplanted these bacteria into different mice. The mice who received bacteria from the obese twin gained weight, while the others did not. The mice did not eat more: Their metabolism changed so that they put on more weight even with the same caloric input.

What, then, determines your gut bacteria? It could be antibiotics or environmental toxins or how processed your food is. Another possibility is raised by a study in The New England Journal of Medicine  that shows that obesity seems to “spread” across social networks, with people infecting their friends and neighbors. I had always assumed that was because birds of a feather flock together — and that is surely part of the explanation. But because gut bacteria can also spread among people in close proximity, perhaps the obesity epidemic really is, well, an epidemic?

I’m not arguing that behavior does not matter. Biology and behavior often interact; the spread of flu depends on whether we wash our hands. Similarly, the bacteria study found that the “obese gut bacteria” had an impact only when the mice were fed diets heavy in saturated fats.

Perhaps most interestingly, changing biology may even be changing cravings. Some biologists have hypothesized that our gut bacteria actually drive cravings for certain unhealthy foods. A focus on biology doesn’t mean a reduced emphasis on behavior, just a richer understanding of it.

These and other studies raise important possibilities, which deserve more research and attention. At the very least, we should invest as many obesity research dollars in uncovering and understanding these biological channels as we do in understanding behavioral channels. And this is a behavioral economist talking!

After all, this could radically change the way we think about policies to curb obesity. As one newspaper editorial pronounced:

A little town in Sweden has put a local tax on fat men. It is declared that ‘the fat man stands accused by the very fact of his too solid flesh’ (vide “Hamlet”) ‘of gluttony and laziness.’ Millions of fat men throughout the world may rise up and denounce as liars the town councillor who drew up this cruel indictment and those who voted for it, but the gentler way of reproving them would be to point out the tritely recognised danger of generalisation in almost any statement of supposed fact. Not all fat men are lazy and gluttonous. Obesity is in many a congenital habit of body; in others a disease.

That editorial was written in 1923, for the paper known as The Paris Herald. Maybe the writer was on to something.