Dieting doesn’t cure obesity. That’s not news, although it was reconfirmed last week in a particularly mediagenic fashion in a study published by National Institutes of Health researchers. The researchers followed contestants from the “The Biggest Loser” television show as these formerly obese contestants proceeded to regain most of the massive amounts of weight they had lost on the show.

As reported in the journal Obesity, these “Biggest Loser” contestants were the victims of “metabolic compensation.” As they tried to keep their weight under control, their bodies remained particularly resistant to expending energy. The findings implied that to maintain their weight loss they would have to remain hungry and calorie-deprived for the rest of their years, and they might still regain the weight they’d lost and then some. For anyone with weight to lose, the message was dismal.

The hoopla the study generated, and the study itself, was missing the answer to an important question. It described what happened to the “Biggest Loser” contestants but not the most important aspect of why: What had made these people fat to begin with? What established the weight they seemed fated to return to? How did the problem get started?

There is a conventional answer to the “why we get fat” question: We eat too much. Researchers typically say that obesity is an “energy balance disorder” — more calories (energy) consumed than expended. And some of us are more genetically predisposed to this overconsumption than others. It sounds simple, but again it’s a description of what happens when people get obese — their bodies stockpile calories, trapping them as fat rather than using them in more constructive ways. But why?


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A theoretical answer, with roots in research from Germany and Austria before World War II, can be found in the pages of many bestselling diet books: Obesity is a hormonal and metabolic disorder triggered by the carbohydrate content of our diets. What we eat induces a hormonal disregulation that works to trap calories in our fat tissue. We don’t get fat because we eat too much; we get fat because the carbohydrates we eat, specifically highly processed grains and sugars, are literally fattening. If this explanation is right, it means the dismal implications of the “Biggest Loser” study are wrong as well. Obesity is not intractable; fixing it requires us to change what we eat, rather than how much.

When authorities argue about how to think about getting fat, the discussions take on the tenor of religious debates. What the experts don’t do is propose definitive studies to resolve the issue. The National Institutes of Health — an active disseminator of the conventional energy imbalance model — doesn’t fund such studies.

Considering the stakes — $150 billion in yearly medical bills related to obesity and a population growing ever fatter — the competing hypotheses are surely worth testing. So let’s do an experiment, with the “Biggest Loser” contestants’ help.


If this explanation is right, it means the dismal implications of the “Biggest Loser” study are wrong as well. Obesity is not intractable.

At the end of the “Biggest Loser” season, when the contestants have lost the most weight, let’s randomly assign them to eat one of three different follow-up diets — a very low-fat diet, a very low-carbohydrate diet and a nicely balanced diet, with all foods (even sugar) in moderation. The researchers will provide the food (no cheating).

The idea will be to see what exactly is required to maintain their weight loss. The subjects will be weighed every day. If they regain weight, the researchers will feed them fewer calories from their assigned diet. If the subjects lose weight, they’ll have to eat more.

After six months or a year — the longer the study, the more definitive the results — the researchers will tabulate how many calories the subjects consumed on the different diets while maintaining their weight loss. They will also record how hungry they got, what their cravings were and, most important, how much energy — how many calories — they expended.


If the conventional obesity wisdom is correct, the subjects will consume and expend equal amounts of calories to maintain their weight loss no matter which group they are in and what is in their diet. And all three groups will have the same issues with hunger and cravings. A calorie is a calorie, in other words.

The hormonal/metabolic hypothesis, however, predicts something dramatically different: The diet with the least carbohydrates will result in the least weight gain, the least hunger, the least metabolic compensation. The subjects assigned to that diet will be able to eat more and they’ll expend more energy while still maintaining their weight loss. Some subjects might see no metabolic compensation at all.

In fact, something similar to this sort of “Biggest Loser” follow-up experiment has already begun. I co-founded a nonprofit that is funding a carefully measured study by pediatric endocrinologist David Ludwig and his colleagues at Boston Children’s Hospital. Its subjects are overweight students and staff at Framingham State University, not “Biggest Loser” contestants, so it’s not as mediagenic as the study published in Obesity.

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But perhaps we could ratchet up the stakes a bit for the Boston study if we asked America’s obesity experts to publicly predict what will happen. We could establish a website and a betting line in Las Vegas. Which obesity hypothesis will win? Carbohydrates, hormones and metabolism? Or energy balance and a calorie is a calorie? Real money should be wagered. The amount the experts are willing to bet will inform us of the strength of their convictions. And the proceeds might help pay for the “Biggest Loser” experiment as well.

For a big reveal, we could compare predictions and results. After all, putting to rest the “why we get fat” question would make for a hell of a reality TV show.

Science writer Gary Taubes is a co-founder of the nonprofit Nutrition Science Initiative. His latest book is “Why We Get Fat and What to Do About It.”

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