Thinking Beyond Science

The notion that a calorie from one source is just as fattening as a calorie from any other source is a trope broadcast by the food industry as a way to absolve itself of culpability. Coca‑Cola even put out an ad emphasizing this “one simple commonsense fact.” As the chair of Harvard’s nutrition department put it, this “central argument” from industry is that the “overconsumption of calories from carrots would be no different from overconsumption of calories from soda.” If a calorie is just a calorie, why does it matter what kinds of foods we eat? Let’s take the example of carrots versus Coca‑Cola. While it’s true that in a tightly controlled laboratory setting, 240 calories of carrots—ten carrots—would have the same effect on calorie balance as the 240 calories in a bottle of Coke, this comparison falls flat on its face out in the real world.

You could chug down those liquid calories in less than a minute, but eating 240 calories of carrots could take you more than two and a half hours of constant chewing. (It’s been timed.) Not only would your jaw get sore, but 240 calories of carrots is about five cups you might not even be able to fit them all in your stomach. Like all whole plant foods, carrots have fiber, which adds bulk without adding net calories. What’s more, you wouldn’t even absorb all the carrot calories. As anyone who’s eaten corn can tell you, some bits of vegetable matter can pass right through you, flushing out any calories they contain. A calorie may still be a calorie circling your toilet bowl, but it’s not going to end up on your hips.

And the same number on the scale can mean different things on different diets or in different contexts. You could be losing weight but actually gaining body fat if your body sheds water and muscle mass. So it’s not just about calories in versus calories out, eating less, and moving more.

Today, 71 percent of American adults are overweight and 40 percent of men and women appear to have so much body fat that they can be classified as obese, and there’s no end in sight. Earlier reports had suggested the rise in obesity was at least slowing down, but that doesn’t actually appear to be the case. Similarly, we had thought we were turning the corner on childhood obesity after thirty-five years of unrelenting bad news, but the bad news marches on. 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 as few as one in thirty people to now one in three, but it wasn’t a steady rise.

Something seems to have happened around the late 1970s, and not just in the United States. The obesity pandemic took off at about the same time in most high-income countries around the globe in the 1970s and 1980s. The fact that the rapid rise appeared almost concurrently across the industrialized world suggests a common cause.

The food industry blames inactivity. “If all consumers exercised,” said the CEO of PepsiCo, “obesity wouldn’t exist.” Coca‑Cola went a step further and spent $1.5 million to create the Global Energy Balance Network to downplay the role of diet in the obesity epidemic. Leaked internal documents show the company planned on using the front group 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 likely heard of greenwashing, where companies deceptively pretend to be environmentally friendly. Leanwashing is the term used to describe companies that try to position themselves as helping to solve the obesity crisis when, instead, they’re directly contributing to it. For example, Nestlé, the largest food company in the world, has rebranded itself the “world’s leading nutrition, health and wellness company.” Yes, that Nestlé, of Nestlé Nesquik fame, makers of Cookie Crisp cereal and more than one hundred different brands of candy, including Butterfinger, Kit Kat, Goobers, Gobstoppers, Runts, and Nerds. Another of its slogans is “Good Food, Good Life.” Its Raisinets may have some fruit, but the company seems to me more Willy Wonka than wellness. Let’s just say that on its “What is Nestlé doing about obesity?” web page, the “Read about our Nestlé Healthy Kids programme” link gave me 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 (83 percent) chose lack of exercise, while only 34 percent chose excessive calorie consumption. But blaming couch‑potato‑ness has 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 caloric intake far more powerfully affect overall calorie balance.

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

Formal exercise is only a small part of our total daily activity, though. Think how much more physical work people used to do on the job, 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—and therein lies the problem with the theory: The occupational shifts and advent of labor‑saving devices have been gradual and largely predate the dramatic, recent rise in weight gain the world over. Washing machines, vacuum cleaners, and the Model T were all invented before 1910.

And 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 due mostly to lack of exercise may not just be a benign fallacy, as personal theories of causation appear to impact people’s weight. Those who blame insufficient exercise are significantly more likely to be overweight themselves. Put them in a room with chocolate, for instance, and they can be covertly observed consuming more candy compared to those who put the onus of obesity on poor diet. But you can’t know if such attitudes are playing a role in their weight problem until you put it to the test. So researchers randomized people to read a fictitious article implicating inactivity in the rise of obesity and found they indeed went on to eat significantly more sweets than those who instead were given an article 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.”

To date, about one hundred genetic markers have been linked to obesity, but when you put all of them together, they account for less than 3 percent of the difference in body mass index 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 on Earth who carry a full complement of FTO susceptibility genes? It doesn’t really matter, because this only appears to result in a difference in intake of a few hundred extra calories a year, while what it took to lead to the obesity epidemic is more like a few hundred calories a day. FTO is the gene so far known to have the most effect on excessive weight gain, but the chances of accurately predicting obesity risk based on FTO status are only slightly better than flipping a coin.

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 dairy, meat, and junk food). Those eating more healthfully 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 doesn’t 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 more healthfully, but it may cause others to fatalistically throw their hands up in the air and resign themselves to thinking it just runs in their families. 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 only 21 percent more likely to be overweight. So genetics certainly play a role, but this suggests that it’s more the children’s environment than their DNA.

It’s been said: “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 actually all in our genes. That’s because 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 calories we don’t need right away on our bodies 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. Generation after generation, millennia after millennia, those with lesser appetites may have died out, while those who gorged themselves could have selectively lived long enough to pass along a genetic predisposition to eat and store more calories. That may be how we evolved into such voracious, calorie‑conserving machines. Now that we’re no longer in such lean times, though, we’re no longer so lean.

Source : How Not to Diet by Michael Greger

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