Some years ago, I was doing an experiment where I put pigs on treadmills. The goal was to learn how running stressed the bones in the head. One day, a colleague, Dennis Bramble, walked into the lab, watched what was going on, and declared, “You know, that pig can’t hold its head still!”
This was my “eureka!” moment. I’d observed pigs on treadmills for hundreds of hours and had never thought about this. So Dennis and I started talking about how, when these pigs ran, their heads bobbed every which way and how running humans are really adept at stabilizing their heads. We realized that there were special features in the human neck that enable us to keep our heads still. That gives us an evolutionary advantage because it helps us avoid falls and injuries. And this seemed like evidence of natural selection in our ability to run, an important factor in how we became hunters rather than just foragers and got access to richer foods, which fueled the evolution of our big brains.
So I got interested in how we developed these stable heads. I’m a runner myself. It’s always interesting to study one’s passion. By 2004, we’d found enough evidence to publish a paper in Nature where we declared, “Humans were born to run.” We cited the many dozens of adaptations in the human body that had made us into superlative endurance runners, even compared to dogs and horses.
Before bows and arrows and before horses were tamed, we did “persistence hunting” where we ran kudu, wildebeest and zebra into exhaustion. These animals can’t pant when they gallop. They overheat. People would find a big animal and chase it till it collapsed. You need no technology to do this, just the ability to run long distances, which all of us have.
You can see proof of this capability every November when 45,000 people run for many hours through the streets of New York.
One thing that has always baffled me is how we get fat.
Why We Get Fat by Gary Taubes unearths the biological truth around why we’re getting fat. In the process, Taubes dispels many accepted ideas on weight-loss and nutrition.
While it’s easy to believe that we remain lean because we’re virtuous and we get fat because we lack self-control or discipline, the evidence clearly says otherwise. Taubes methodically tackles conventional (and governmental) wisdom and why it is wrong.
This is a biology book, not a diet book. It’s about the science of what’s happening in our body that makes us fat. Let’s explore Taubes argument.
Is this a simple calories-in calories-out problem?
Do low-calorie diets work? In the short-term yes but overall, no.
“The two researchers who may have had the best track record in the world treating obesity in an academic setting are George Blackburn and Bruce Bistrian of Harvard Medical School. In the 1970s, they began treating obese patients with a six-hundred-calorie-a-day diet of only lean meat, fish, and fowl. They treated thousands of patients, said Bistrian. Half of them lost more than forty pounds.”
They concluded, “This is an extraordinarily effective and safe way to get large amounts of weight loss.” Yet, shortly after, Taubes says “Bistrian and Blackburn gave up on the therapy because they didn’t know what to tell their patients to do after the weight was lost. The patients couldn’t be expected to live on six hundred calories a day forever, and if they returned to eating normally, they’d gain all the weight back.”
So, even if you lose weight on a low-calorie diet, you’re stuck with the what now problem.
What if i just exercise more?
What happens when we increase our energy expenditure by upping our physical activity? Taubes says “Considering the ubiquity of the message, the hold it has on our lives, and the elegant simplicity of the notion-burn calories, lose weight, prevent disease-wouldn’t it be nice if it were true?”
Alas, believing doesn’t make it so. While there are many reasons to exercise regularly, losing weight isn’t one of them.
Taubes looks at the evidence and walks us through a chain of reasoning. The evidence says obesity associates with poverty. In most modern parts of the world, the poorer people are, the fatter they are likely to be. Yet, it’s the poor and disadvantaged who sweat out a living with physical labor. This is one of the reasons to doubt the assertion that expending a large amount of energy on a regular basis makes us fat.
Another reason to doubt the calorie-out hypothesis is the obesity epidemic itself. We’ve been getting fatter for the past few decades which suggests that we’re getting more sedentary. Until the 1970s, that is, before the obesity problem, Americans were not believers in the need to spend leisure time sweating.
In addition, it turns out there is very little hard evidence to support the belief that the number of calories we burn has any meaningful impact on how fat we become. The American Heart Association even calls the data supporting this claim “not particularly compelling.”
A study by Paul Williams and Peter Wood collected detailed information on almost 13k runners and then compared the weekly mileage with how much they weighed year-to-year. As you would expect, those who ran the most tended to weigh the least, but, perhaps unexpectedly, all these runners tended to get fatter with each passing year (even those running more than 40miles a week!)
According to Taubes, the belief in exercising more to weigh less is “based ultimately on one observation and one assumption. The observation is that people who are lean tend to be more physically active than those of us who aren’t. This is undisputed. … But this observation tells us nothing about whether runners would be fatter if they didn’t run or if the pursuit of distance running as full-time hobby will turn a fat man or woman into a lean marathoner. We base our belief in the fat-burning properties of exercise on the assumption that we can increase our energy expenditure (calories-out) without being compelled to increase our energy intake (calories-in).”
This assumption is wrong. We ended up buying into this exercise-more-eat-less story because it feels intuitive, correct, and reinforces our beliefs. We didn’t ask for evidence and none has been forthcoming in the intervening years.
Is it a matter of balancing calories?
No. Weight gain is a gradual process. So once you notice your jeans are getting tight, you can make some smart decisions and cut calories and increase physical activity right? “If it were true that our adiposity is determined by calories-in/calories-out, then this is one implication: you only need to overeat, on average, by twenty calories a day to gain fifty extra pounds in 20 years.” Now think of all the food decisions you make in a day and how impossible it would be, without scientific instrumentation, to balance your food.
Wait, what about thermodynamics. The law that says energy can be transformed from one form to another but not created nor destroyed.
“The very notion that we get fat because we consume more calories than we expend would not exist without the misapplied belief that the laws of thermodynamics make it true. When experts write that obesity is a disorder of energy balance—a declaration that can be found in one form or another in much of the technical writing on the subject—it is shorthand for saying that the laws of thermodynamics dictate this to be true. And yet they don’t.
All the first law of thermodynamics says is that “if something gets more or less massive, then more energy or less energy has to enter it than leave it. It says nothing about why this happens. It says nothing about cause and effect. It doesn’t tell us why anything happens.”
Experts think the first law is relevant because it fits neatly with our existing theories about why we get fact—those who consume more calories than they burn will gain weight. Thermodynamics tells us that if we get fatter and heavier, more energy enters our body than leaves it. But the important question, at least from an obesity perspective, is why do we consume more calories than we expend?
One of the other problems with thermodynamics argument is the assumption that the energy we consume and the energy we exert have little influence on each other—that we can change one without impacting the other.
The literature says that animals whose food is suddenly restricted tend to reduce energy expenditure both by being less active and by slowing energy use in cells, thereby limiting weight loss. They also experience hunger so that once the restriction ends, they will eat more than their prior norm until the earlier weight is obtained. (This is the same problem Bistrian and Blackburn encountered earlier).
Another problem with Thermodynamics is that it doesn’t address why men and women fatten differently. This means, at least at some level, bodily functions and possibly genetics play a role.
When we believe, as we do, that people get fat because they overeat, we’re putting the ultimate blame on a weakness of character and leaving biology out of it. This implies that we can generally tell, just by looking at the waistline, which people have strong self-control.
In the early 1970s, George Wade studied the relationship between sex hormones, weight, and appetite by removing the ovaries from rats. The impact was dramatic: the previously skinny rats ate voraciously and became obese. “The rat eats too much, the excess calories find their way to the fat tissue, and the animal becomes obese,” offers Taubes. He continues, “this would confirm our preconception that overeating is responsible for obesity in humans as well. But Wade did a revealing second experiment, removing the ovaries from the rats and putting them on a strict postsurgical diet. Even if these rats were ravenously hungry after the surgery, even if they desperately wanted to be gluttons, they couldn’t satisfy their urge.” The rats still got just as fat, just as quickly. And that is the start of our understanding of why we actually get fat.
The animal doesn’t get fat because it overeats, it overeats because it’s getting fat. The animal is unable to regulate its fat tissue.
A follow-on experiment, where the rats were injected with estrogen after the surgery, resulted in normal behavior. That is, they did not become slothful or obese. Biologically, one of the things that estrogen does is to influence an enzyme called lipoprotein lipase (LPL). When cells want fat they express their interest by “expressing” LPL. If the LPL comes from a fat cell, we get fatter. If the LPL comes from a muscle cell, it gets pulled in and digested as fuel. LPL, according to Williams Textbook of Endocrinology, “is a key factor in partitioning triglycerides (i.e., fat) among different body tissues.”
One of Estrogen’s roles is to inhibit the activity of LPL “expressed” by fat cells. The rats in Wade’s experiments over-ate because they were losing calories into fat cells that were needed in other places. The fatter the rat got, the more it had to eat to feed the non-fat cells. When the body is unregulated, it creates a cycle of getting fatter and fatter.
This, as Taubes says, “reverses our perception of the cause and effect of obesity. It tells us that two behaviors—gluttony and sloth—that seem to be the reasons we get fat can in fact be the effects of getting fat.” It also tells us that influencing LPL (either positively or negatively) has a dramatic effect on how fat we get.
LPL also explains why men and women get fat in different spots and why exercise doesn’t work. In men, LPL, activity is higher in the gut and lower below the waist. In women, LPL is highest below the waist. Bad news though, after menopause, LPL in a woman’s abdomen catches up to the men. As for exercise, while we’re working out LPL activity decreases on our fat cells and increases on muscle cells—so far, so good—because this prompts the release of fat from our fat tissue so that muscles can use this as energy. When we stop exercising, however, the situation reverses. LPL activity on the muscle cells shuts down and LPL activity on fat cells picks up. The fat cells natural tendency is to get back to their previous state.
So what regulates all of this?
Insulin. The LPL on fat cells is regulated by the presence of insulin. The more insulin our body secretes, the more active the LPL becomes on the fat cells, and the more fat that, rather than being consumed as fuel by the muscle cells, gets stored in fat cells. As if designed to ensure we get fatter, insulin also reduces the LPL expressed by the muscle cells (to ensure there is lots of fat floating around for the fat cells). That is, it tells the muscle cells not to burn fat as a fuel.
Insulin also influences an enzyme called hormone-sensitive lipase, or HSL. And this says Taubes, “may be even more critical to how insulin regulates the amount of fat we store. Just as LPL works to make fat cells (and us) fatter, HSL works to make fat cells (and us) leaner. It does so by working inside the fat cells to break down triglycerides into their component fatty acids so that those fatty acids can then escape into the circulation. The more active this HSL, the more fat we liberate and can burn from fuel and the less, obviously, we store. Insulin also suppresses this enzyme HSL and so it prevents triglycerides from being broken down inside the fat cells to a minimum.” This also helps explain why diabetics often get fatter when they take insulin therapy.
Carbohydrates primarily determine the insulin level in the blood. Here quantity and quality are important. Carbs ultimately determine how fat we get. But most people eat carbs so why are some fatter than others? We all naturally secrete a different level of insulin — given the same food people will secrete different levels of insulin. Another factor is how sensitive your cells are to insulin and how quickly they become insensitive. The more insulin you secrete—naturally or with carbohydrate rich foods—the more likely it is that your body becomes insulin resistant. The result is a vicious circle.
Not all foods containing carbs are equally fattening. The most fattening foods are those that have the greatest impact on our insulin and blood sugar levels. These are the easily digestible carbs. Anything made of refined flour (bread, cereals, and pasta), starches (potatoes, rice, and corn), and liquids (beer, pop, fruit juice). “These foods,” says Taubes, “flood the bloodstream quickly with glucose. Blood sugar shoots up; insulin shoots up; We get fatter.”
Here is Taubes in a 70-minute video explaining more.
In Robert Lustig’s view, sugar should be thought of, like cigarettes and alcohol, as something that’s killing us. But can sugar possibly be as bad as Lustig says?
Lustig’s argument is that sugar has unique characteristics, specifically in the way the human body metabolizes the fructose in it, that may make it singularly harmful, at least if consumed in sufficient quantities.
The first symptom doctors are told to look for in diagnosing metabolic syndrome is an expanding waistline. This means that if you’re overweight, there’s a good chance you have metabolic syndrome, and this is why you’re more likely to have a heart attack or become diabetic (or both) than someone who’s not. Although lean individuals, too, can have metabolic syndrome, and they are at greater risk of heart disease and diabetes than lean individuals without it.
Having metabolic syndrome is another way of saying that the cells in your body are actively ignoring the action of the hormone insulin — a condition known technically as being insulin-resistant. Because insulin resistance and metabolic syndrome still get remarkably little attention in the press (certainly compared with cholesterol), let me explain the basics.
You secrete insulin in response to the foods you eat — particularly the carbohydrates — to keep blood sugar in control after a meal. When your cells are resistant to insulin, your body (your pancreas, to be precise) responds to rising blood sugar by pumping out more and more insulin. Eventually the pancreas can no longer keep up with the demand or it gives in to what diabetologists call “pancreatic exhaustion.” Now your blood sugar will rise out of control, and you’ve got diabetes.
Not everyone with insulin resistance becomes diabetic; some continue to secrete enough insulin to overcome their cells’ resistance to the hormone. But having chronically elevated insulin levels has harmful effects of its own — heart disease, for one. A result is higher triglyceride levels and blood pressure, lower levels of HDL cholesterol (the “good cholesterol”), further worsening the insulin resistance — this is metabolic syndrome.
When physicians assess your risk of heart disease these days, they will take into consideration your LDL cholesterol (the bad kind), but also these symptoms of metabolic syndrome. The idea, according to Scott Grundy, a University of Texas Southwestern Medical Center nutritionist and the chairman of the panel that produced the last edition of the National Cholesterol Education Program guidelines, is that heart attacks 50 years ago might have been caused by high cholesterol — particularly high LDL cholesterol — but since then we’ve all gotten fatter and more diabetic, and now it’s metabolic syndrome that’s the more conspicuous problem.
This raises two obvious questions. The first is what sets off metabolic syndrome to begin with, which is another way of asking, What causes the initial insulin resistance?
Sugar scares me too, obviously. I’d like to eat it in moderation. I’d certainly like my two sons to be able to eat it in moderation, to not overconsume it, but I don’t actually know what that means, and I’ve been reporting on this subject and studying it for more than a decade. If sugar just makes us fatter, that’s one thing. We start gaining weight, we eat less of it. But we are also talking about things we can’t see — fatty liver, insulin resistance and all that follows. Officially I’m not supposed to worry because the evidence isn’t conclusive, but I do.