Why are so many of us carrying so much extra baggage? It’s a question that has, ahem, weighed heavily on researchers ever since obesity rates started swelling in the 1980s.
The chunk of the U.S. adult population classified as obese — defined as having a body mass index of 30 or higher — has roughly doubled, to more than 38 percent, in the last three decades. The cause, according to the most consistent research results, is relatively simple: overeating.
Scientists and snake oil salesmen alike have continued to offer alternative explanations for our collective weight gain. Among the more credible contenders: sugar, hormones and even the microbiome, the personal ecosystem each of us hosts. All of these hypotheses have advocates as well as critics. Both sides of each argument can offer evidence in support of their claim. The research community has built a large body of inconclusive, contradictory research. What they haven’t built is consensus.
“It’s the Wild, Wild West of opinion,” says Dariush Mozaffarian, a cardiologist and dean of the Friedman School of Nutrition Science and Policy at Tufts University.
But maybe that body of conflicting, equivocal evidence does tell us something. If there were no particular food — or component of food, or combination of foods, or virus, or habit, or assortment of gut bacteria — wreaking biochemical havoc, inconclusive research would be exactly what we’d expect to see.
All the contradictory studies may be pointing us to the fact that the simplest explanation is also the most likely: Eating more calories, without expending more, leads to weight gain. Kevin Hall, senior investigator with the National Institute of Diabetes and Digestive and Kidney Diseases, points to recent data that show the amount of calories we consume correlates with the amount of weight we gain. Although the amount we actually eat is difficult to measure accurately, says Hall, the per-capita calories available in the U.S. food supply increased 21 percent from 1973 to 2013, more than enough to account for the 16 percent increase in the average adult’s weight.
The obesity epidemic can’t be blamed on sugar, a virus or even genetics. Despite the evidence, however, the hunt for another explanation continues in labs across the country.
Mozaffarian, for example, doesn’t believe simple overeating explains obesity. He cites sleep habits, socioeconomic status and the microbiome as plausible contributors, but he believes the main problem is sugar and starches. At the same time, he acknowledges there’s disagreement among researchers in the field — with one exception.
That exception is soda. Or, more broadly, the entire category of sugar-sweetened beverages (SSBs). In December, the journal Obesity Facts published the latest indictment of SSBs: a review of 30 recent studies involving nearly 250,000 participants from around the world. According to the review, 93 percent of the research showed a link between SSB consumption and obesity, bolstering the field’s consensus.
That agreement only goes so far, however: Different researchers have different theories about why SSBs are a problem. One of the most hotly debated ideas centers on insulin.
The Insulin Hypothesis: Not So Sweet
Researchers supporting what’s called the Insulin Hypothesis believe that sugar-rich beverages, as well as table sugar and refined starches, are driving dysfunction in our endocrine system, which controls metabolism and other crucial functions.
These dietary carbohydrates, according to the Insulin Hypothesis, boost the body’s insulin secretion, which redirects fat to be stored in fat cells rather than used up as energy. The thinking is that high consumption of products such as SSBs leads to high levels of insulin, and that leads to high levels of fat being trapped in fat cells rather than being available as fuel for muscle and liver cells. The result is what some researchers call a state of “internal starvation” for those energy-deprived cells. The fuel is stored, so the body has fewer calories available to spend, but the need for that fuel remains, triggering hunger.
A vicious cycle sets in: An individual eats more to satisfy that increased hunger, but the body hoards the fuel in fat cells instead of spending it, leading to fewer calories burned, but more hunger.
The theory that a high-carb diet leads to higher insulin levels and more fat accumulation than a diet of equal calories but fewer carbs is testable, and Hall tested it. The results, he says, didn’t support the Insulin Hypothesis.
Hall agrees that carbohydrates are metabolized differently compared with fats and proteins, but he says the difference is not significant enough to help with weight loss. If you compare extreme diets of, say, 80 percent versus 5 percent carbohydrates, “it matters a little bit,” he says. But when you compare the kinds of diets people actually eat — which fall somewhere in the middle in terms of carbs — “it matters very little.”
In the real world, people have tried to lose weight with every possible ratio of fat, carbs and protein, but no particular permutation has emerged as a clear winner across the board, which we would expect to see if the Insulin Hypothesis were correct. While some people lose weight by limiting carbs, others don’t, and study after study comparing diets has reached the same conclusion: The best diet is the one that helps you limit calories.
“As long as you reduce energy [by consuming fewer calories], you lose weight. If you could manipulate the macronutrient content [of fats, carbs and proteins] to gain or lose weight significantly, we would have discovered it by now,” says Alice Lichtenstein, a nutrition science and policy professor at Tufts’ Friedman School.
Trying on the Fat Genes
Tools that allow scientists to map the human genome quickly and cheaply have made it much easier to hunt for a connection between genes and obesity. So far, scientists have identified more than 100 DNA differences that appear to be linked to obesity.
Finding the correlation between genetic makeup and obesity is straightforward: Compare a number of genomes, and see where those of overweight people match up. But the job of figuring out what those genes do, and whether they may cause obesity, is much harder.
Scientists are at the early stage, and they have investigated only a small portion of the potential genetic culprits. But “a lot of them seem to be acting in the brain,” says Mark Goodarzi, an endocrinologist at Cedars-Sinai Medical Center. They’re not regulating metabolism or biochemical processes, but appetite and intake.
Goodarzi adds that the obesity epidemic “is not a genetic phenomenon.” Our genes haven’t changed in the last hundred years; only our environment has, and some of us are better equipped than others to navigate it successfully. Still, “nobody is doomed to being obese,” he says. Weight management may be more difficult for those of us dealt certain genetic cards, but the underlying cause of obesity is still eating more calories than an individual expends.
It Doesn't Take Guts
A recent area of interest for obesity researchers is your gut and the bacteria that dwell there. Some research has found intriguing hints of a powerful relationship between this microbiome and your weight. In 2013, scientists transferred human gut bacteria from twins, one obese and one not, into mice. The mouse with the obese twin’s bacteria gained more weight than the other mouse.
But people aren’t mice, says University of Michigan microbiologist Pat Schloss, author of a 2016 meta-analysis of multiple studies investigating the gut bacteria-obesity connection. Lab mice, for example, are bred specifically for sameness and are kept in highly controlled environments. Humans, by contrast, are nothing but chaos, and no two people are alike.
In the 2016 paper, Schloss found that previous studies comparing the microbiomes of thin and obese people each worked with a different dataset and different type of bacteria, making it impossible to draw any firm conclusions. Nothing but chaos. “We’re the third meta-analysis to say the same thing,” says Schloss.
The search for a connection continues, though. Because even if gut bacteria play only a limited role, any potential is worth exploring in the interest of advancing our understanding of obesity. “My sense is that [the microbiome] is a very small factor compared to all the other factors,” says Schloss. “I eat ice cream every night. It tastes good. I don’t blame my bacteria for that.”
The Blame Game
The simplest explanation for obesity — too many calories in and too few calories spent — isn’t as exciting or exotic as some of the unproven ideas out there, which may explain in part why it’s so doggedly ignored. But there’s another reason for its relative unpopularity: Researchers want to avoid blaming and shaming.
“Depending on how you frame that message,” says Hall, “it can read like we’re accusing everyone of becoming gluttons: ‘It should be about individual responsibility, you slothful, fat person!’ ” That’s certainly not Hall’s message.
Think of it more like this: Let’s say you play Serena Williams at tennis. And you lose, because of course you lose. Is it because your tennis game isn’t good enough? At some level, sure. But the real reason is that you’re wildly overmatched, and you have no business being on the court with Serena Williams in the first place. (If Rafael Nadal is reading this, my apologies.)
That’s what’s going on with the food environment. Corporations have entire divisions of highly trained staff whose job is to formulate food people can’t resist — food with “supernormal appetitive properties,” in Hall’s words. They are Serena Williams. You played varsity in high school, maybe.
“Our moral failings, as many as they may be, didn’t increase at the population level,” says Hall. Obesity is the result of overeating, and a key part of it is navigating a food environment in which, again, we’re wildly overmatched.
To be fair, the other causes of obesity currently under investigation are not figments of the researchers’ imaginations. Yes, there is a difference in how your body processes a diet that’s very high in refined carbohydrates. The microbiome does affect how your body absorbs calories. Some people are genetically predisposed to having a tougher time managing their weight. The issue, says Lichtenstein, is the magnitude. These effects are real but small, and swamped by the simple equation no one really likes: Calories in > calories out = weight gain.
So now what? Addressing the environmental factors that encourage overeating is an urgent priority, says Lichtenstein.
“We’re eating in this environment that is stacked against us,” she says. “There’s too much food. It’s ubiquitous. It’s cheap.” And, to make it harder, “all the social mores about where and when to eat have fallen by the wayside.” We eat in the car, we eat in front of the TV, we eat at sporting events. Lichtenstein notes that her students regularly eat in class.
We’re eating everywhere, and we’re eating bigger portions. Sodas are bigger, burgers are bigger, restaurant portions are bigger. Even the McDonald’s quarter-pounder, with the 4-ounce portion size right there in the name, got a boost to 4.25 ounces in 2015.
New York University nutrition professor Marion Nestle believes those numbers tell the story. “I think large portions are a sufficient explanation for weight gain,” she says. “Portion size, calories and weight all went up in parallel from 1980 to 2000.”
Portion size is a particularly insidious problem for people trying to eat less, Hall says. Because most of us don’t weigh our portions every day, “you don’t notice slightly larger portion sizes. … You’re going to start to creep upward,” he says. And when the portions we see out in the world are uniformly large, we normalize that increase, adds Lichtenstein.
Large portions are normal. High-calorie food is normal. Eating everywhere is normal. To fix obesity, we have to fix normal, and it won’t be easy. But it won’t even be possible unless we decide, collectively, that normal — not carbs, not fat, not insulin, not bacteria — is the problem.
