The Obesity Epidemic – Part 1

I’m Dr. Michael Greger and this is Nutrition Facts.

There’s one thing we’ve been thinking about a lot lately, and that’s how to stay healthy in the middle of a global pandemic. Especially since we’ve learned that those with underlying health problems like obesity, hypertension, diabetes, and heart disease are more likely to have serious complications if they contract COVID-19. So what do we do? We try to stay healthy with evidence-based nutrition.

When I sat down to write my book How Not to Diet, I knew I had to answer this question: “What triggered the obesity epidemic?” Was it inactivity—just kids sitting around playing video games? Was it genetic? Was it epigenetic—something turning our fat genes on? Or was it just the food?

In our first story, we examine common explanations for the cause of the obesity epidemic put forward by the food industry and policymakers.

Obesity isn’t new, but the obesity epidemic is. We went from a few corpulent kings and queens, like Henry VIII or Louis VI (known as Louis le Gros, or “Louis the Fat”), to a pandemic of obesity, now considered to be perhaps the most dire and poorly-contained public health threat of our time. About 37 percent of American men are obese, and 41 percent of American women, with no end in sight. Earlier reports had suggested at least the rise in obesity was slowing down, but even that doesn’t appear to be the case. Similarly, we had thought we were turning the corner; finally, on childhood obesity after 35 years of unrelenting bad news; but, the bad news continues. Child and adolescent obesity rates have continued to rise, now into the fourth decade.

Over the last century, obesity appears to have jumped tenfold, from about 1 in 30 to now 1 in 3. But, it wasn’t a steady rise. Something seems to have happened around the late 1970s, and not just here, but around the globe. The obesity pandemic took off at about the same time across the world in most high-income countries in the 1970s and 1980s. The fact that the rapid rise appeared almost concurrently across the industrialized world suggests a common cause. What might that trigger have been?

Any potential driver would have to be global in nature, and coincide with the upswing of the epidemic. So, the change would have had to have started about 40 years ago, and able to spread rapidly around the globe. Let’s see how all the various theories stack up. For example, some have blamed changes in our “built environment”––shifts in city planning that have made our communities less conducive to walking, biking, and grocery shopping. But that doesn’t meet our criteria for a credible cause, because there was no universal, simultaneous change in our neighborhoods within that time frame.

If you do a survey of hundreds of policymakers, most blame the obesity epidemic on “lack of personal motivation.” But, do you see how little sense that makes? Here in the U.S, for example, obesity shot up across the entire population in the late 1970s. Are you telling me that every single sector of the entire population suffered some sort of simultaneous decline in willpower? Each age, sex, and ethnic group, with all their different attitudes and experiences, coincidentally lost their collective capacity for self-control at the same time? More plausible than a global change in the nature of our characters would be some global change in the nature of our lives.

The food industry blames inactivity. “If all consumers exercised,” said the CEO of PepsiCo, “obesity wouldn’t exist.” Coca-Cola went a step further, spending $1.5 million to create the Global Energy Balance Network to downplay the role of diet. Leaked emails show the company planned on using the front to serve as a “weapon” to “change the conversation” about obesity in its “war” with the public health community.

This tactic is so common among food and beverage companies it even has a name: “leanwashing.” You’ve heard of greenwashing, where companies deceptively pretend to be environmentally friendly. Well, leanwashing is the term used to describe companies that try to position themselves as helping to solve the obesity crisis when they’re instead directly contributing to it. Indeed, the largest food company in the world, for example, Nestlé has rebranded itself as the “world’s leading nutrition, health and wellness company.” Yes; that Nestlé, makers of Cookie Crisp and historically more than 100 different brands of candy, including Butterfinger, Kit Kat, Goobers, Gobstoppers, Runts, and Nerds. Another of their slogans is “Good Food, Good Life.” Their Raisinets may have some fruit, but they seem to me more Willy Wonka than wellness. Let’s just say that on their “What is Nestlé doing about obesity?” webpage, their “Read about our Nestlé Healthy Kids programme” link gives you a Page Not Found error.

The constant corporate drumbeat of overemphasis on physical inactivity appears to be working. In response to a Harris poll question, “Which of these do you think are the major reasons why obesity has increased?”, a large majority chose lack of exercise, while only 34 percent chose excess calorie consumption. That’s actually been identified as one of the most common misconceptions about obesity. The scientific community has come to a fairly decisive conclusion that the factors governing calorie intake more powerfully affect overall calorie balance. It’s more our fast food than our slow motion.

There’s even considerable debate in the scientific literature as to whether changes in physical activity have had “any role whatsoever” in the obesity epidemic. The increase in caloric intake per person is more than enough to explain the obesity epidemic in the United States and around the rest of the world, as well. In fact, if anything, the level of physical activity over the last few decades has actually slightly gone up in both Europe and North America. Ironically, this may actually be a result of the extra energy it takes to move around our heavier bodies, making it a consequence of the obesity problem, rather than the cause.

Formal exercise is only a small part of our total daily activity, though. Think about how much more physical work people used to do in the workplace, or on the farm, or even in the home. It’s not just the shift in collar color from blue to white. Increasing automation, computerization, mechanization, motorization, and urbanization have all contributed to increasingly more sedentary lifestyles over the last century. But that’s the problem with the theory. The occupational shifts and advent of labor-saving devices has been gradual, and largely predated the dramatic recent rise in weight gain the world over. Washing machines, vacuum cleaners, and the Model T were all invented before 1910. Indeed, when put to the test using state-of-the-art methods to measure energy in and energy out, it was caloric intake, not physical activity, that predicted weight gain over time.

The common misconception that obesity is mostly due to lack of exercise may not just be a benign fallacy. Personal theories of causation appear to impact people’s weight. Those who blame insufficient exercise are significantly more likely to be overweight. Put them in a room with chocolate, and they can be covertly observed consuming more candy.

Those holding that view may be different in other ways, though. You can’t prove cause-and-effect until you put it to the test. And indeed, people randomized to read an article implicating inactivity went on to eat significantly more sweets than those reading about research that indicted diet. A similar study evidently found that those presented with research blaming genetics subsequently ate significantly more cookies. The paper was entitled “An unintended way in which the fat gene might make you fat.”

In our next story, we discover the “fat gene” accounts for less than 1% of the differences in size between people.

To date, about 100 genetic markers have been linked to obesity. But, put all of them together and overall, they account for less than 3 percent of the difference in BMI between people. The “fat gene” you may have heard about (called FTO, short for “FaT mass and Obesity associated’’) is the gene most strongly linked to obesity, but it explains less than 1 percent of the difference between people––a mere 0.34 percent.

FTO codes for a brain protein that appears to affect your appetite. Are you one of the billion people that carry the FTO susceptibility genes? Who cares, as it only appears to result in a difference in intake of a few hundred extra calories a year. The energy imbalance that led to the obesity epidemic is on the order of hundreds of calories a day. And that’s the gene so far known to have the most effect. The chances of accurately predicting obesity risk based on FTO status is only slightly better than flipping a coin. In other words, no; those genes don’t make you look fat.

When it comes to obesity, the power of your genes is nothing compared to the power of your fork. Even the small influence the FTO gene does have appears to be weaker among those who are physically active, and may be abolished completely in those eating healthier diets. FTO only appears to affect those eating diets higher in saturated fat (predominantly found in meat, dairy, and junk food). Those eating healthier appear to be at no greater risk of weight gain even if they inherited the “fat gene” from both their parents.

Physiologically, FTO gene status does not appear to affect your ability to lose weight. Psychologically, knowing you’re at increased genetic risk for obesity may motivate some people to eat and live healthier, but may cause others to fatalistically throw their hands up in the air and resign themselves to thinking that it just runs in their family. Obesity does tend to run in families, but so do lousy diets.

Comparing the weight of biological versus adopted children can help tease out the contributions of lifestyles versus genetics. Children growing up with two overweight biological parents were found to be 27 percent more likely to be overweight themselves, whereas adopted children placed in a home with two overweight parents were 21 percent more likely to be overweight. So, genetics plays a role, but this suggests that it’s more the children’s environment than their DNA.

One of the most dramatic examples of the power of diet over DNA comes from the Pima Indians. The Pima Indians of Arizona have among the highest rates of obesity and the highest rates of diabetes in the world. This has been ascribed to their relatively fuel-efficient genetic makeup. Their propensity to store calories may have served them well in times of scarcity when they were living off of corn, beans, and squash. But, when the area became “settled”, their source of water, the Gila river, was diverted upstream. Those who survived the ensuing famine had to abandon their traditional diet to living off of government food programs, and chronic disease rates skyrocketed. Same genes, but different diet, different result.

In fact, a natural experiment was set up. The Pima living over the border in Mexico come from the same genetic pool, but were able to maintain more of their traditional lifestyle sticking with their beans, tortillas, and potatoes. Same genes, but seven times less obesity, and about four times less diabetes. Genes may load the gun, but diet pulls the trigger.

More on gene theory today. In our final story on how weight gain is largely a normal response, by normal people, to an abnormal situation.

It’s been said that “Nothing in biology makes sense except in the light of evolution.” The known genetic contribution to obesity may be small, but in a certain sense, you could argue, it’s all in our genes. The excess consumption of available calories may be hardwired into our DNA.

We were born to eat. Throughout most of human history and beyond, we existed in survival mode, in a context of unpredictable scarcity. So, we’ve been programmed with a powerful drive to eat as much as we can, while we can, and just store the rest for later. Food availability could never be taken for granted, so those who ate more in the moment and were best able to store more fat for the future might better survive subsequent shortages to pass along their genes. So, generation after generation, millennia after millennia, those with lesser appetites may have died out, and those who gorged may have selectively lived long enough to pass along their genetic predisposition to eat and store more calories. This may be how we evolved into such voracious calorie-conserving machines. Now that we’re no longer living in such lean times, though, we’re no longer so lean.

What I just described is the “thrifty gene” concept proposed in 1962: the proposal that obesity is the result of a “mismatch” between the modern environment and the environment in which we evolved. It’s like we’re now polar bears in a jungle. All that fur and fat may have given them an edge up in the Arctic, but would be decidedly disadvantageous in the Congo. Similarly, a propensity to pack on the pounds may have been a plus in prehistoric times, but can turn into a liability when our scarcity-sculpted biology is plopped down into the land of plenty. So, it’s not gluttony or sloth. Obesity may simply be a normal response to an abnormal environment.

Much of our physiology is finely tuned to stay within a narrow range of upper and lower limits. If we get too hot, we sweat; if we get too cold, we shiver. Our body has mechanisms to keep us in balance. In contrast, our bodies have had little reason to develop an upper limit to the accumulation of body fat. In the beginning, there may have been evolutionary pressures to keep us lithe and nimble in the face of predation. But, thanks to things like weapons and fire, we haven’t had to outrun as many saber-tooth tigers for about two million years or so. This may have just left our genes with the one-sided selection pressures to binge on every morsel in sight, and stockpile as many calories onto our bodies as possible.

What was once adaptive is now a problem or at least so says the thrifty gene hypothesis that originated more than a half century ago. It provides a simple and elegant explanation for the modern obesity epidemic and was quickly embraced by scientists and lay people alike. Although Neel later distanced himself from the original proposal, despite remaining mostly theoretical, the basic premise remains largely accepted by the scientific community. The implications are profound.

In 2013, the American Medical Association voted to classify obesity as a disease (against the advice of their own Council on Science and Public Health). Not that it necessarily matters what we call it (a rose by any other name would cause just as much diabetes), but disease implies dysfunction. Bariatric drugs and surgery are not correcting some anomaly of human physiology. Our bodies are just doing what they were designed to do in the face of excess calories. Rather than some sort of disorder, weight gain is largely a normal response, by normal people, to an abnormal situation. More than 70 percent of Americans are now overweight—it’s literally normal.

A body gaining weight when excess calories are available for consumption is behaving normally. Efforts to curtail such weight gain with drugs or surgery are not efforts to correct an anomaly in human physiology, but rather to deconstruct and reconstruct its normal operations at the core.

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Thanks for listening to Nutrition Facts. I’m your host, Dr. Michael Greger.