Why We Get Fat
the science itself makes clear that hormones, enzymes, and growth factors regulate our fat tissue, just as they do everything else in the human body, and that we do not get fat because we overeat; we get fat because the carbohydrates in our diet make us fat.
The science tells us that obesity is ultimately the result of a hormonal imbalance, not a caloric one—specifically, the stimulation of insulin secretion caused by eating easily digestible, carbohydrate-rich foods: refined carbohydrates, including flour and cereal grains, starchy vegetables such as potatoes, and sugars, like sucrose (table sugar) and high-fructose corn syrup. These carbohydrates literally make us fat, and by driving us to accumulate fat, they make us hungrier and they make us sedentary.
So many different belief systems enter into the question of what constitutes a healthy diet that the scientific question—why do we get fat?—has gotten lost along the way. It’s been overshadowed by ethical, moral, and sociological considerations that are valid in themselves and certainly worth discussing but have nothing to do with the science itself and arguably no place in a scientific inquiry.
What sets science and the law apart from religion is that nothing is expected to be taken on faith.
Can it be possible that the obesity epidemic is caused by prosperity, so the richer we get, the fatter we get, and that obesity associates with poverty, so the poorer we are, the more likely we are to be fat?
No wonder obesity is so rarely cured. Eating less—that is, undereating—simply doesn’t work for more than a few months, if that.
Until the 1970s, low-calorie diets were referred to in medical literature as “semi-starvation” diets. After all, what’s expected on these diets is that we eat half or even less of what we’d typically prefer to eat. But we can’t be expected to semi-starve ourselves for more than a few months, let alone indefinitely, which is what such diets implicitly require if we are to maintain whatever weight loss we may initially experience.
But if sedentary behavior makes us fat and physical activity prevents it, shouldn’t the “exercise explosion” and the “new fitness revolution” have launched an epidemic of leanness rather than coinciding with an epidemic of obesity?
If we believe in calories-in/calories-out, and that in turn leads us to conclude that we have to run half-marathons five days a week (in our forties, and more in our fifties, and more in our sixties …) to maintain our weight, it may, once again, be time to question our underlying beliefs.
(If your goal is to lose weight—even if your health and your life depend on it, as they very well may—would you train to run a twenty-six-mile foot race upon being told that you might lose five pounds of fat after a year and half of work?)
Obesity is not a disorder of energy balance or calories-in/calories-out or overeating, and thermodynamics has nothing to do with it. If we can’t understand this, we’ll keep falling back into the conventional thinking about why we get fat, and that’s precisely the trap, the century-old quagmire, that we’re trying to avoid.
Thermodynamics tells us that if we get fatter and heavier, more energy enters our body than leaves it. Overeating means we’re consuming more energy than we’re expending. It says the same thing in a different way. Neither happens to answer the question why. Why do we take in more energy than we expend? Why do we overeat? Why do we get fatter?†
The experts who say that we get fat because we overeat or we get fat as a result of overeating—the vast majority—are making the kind of mistake that would (or at least should) earn a failing grade in a high-school science class.
eating less and/or exercising more is not a viable treatment for obesity or overweight and shouldn’t be considered as such.
the animal doesn’t get fat because it overeats, it overeats because it’s getting fat.
Anything that increases its mass, for whatever reason, will take in more energy than it expends.
The obvious conclusion, suggested first by the neuroanatomist Stephen Ranson, whose Northwestern University laboratory pioneered these experiments in the 1930s, is that the surgery has the direct effect of increasing body fat on these rodents. After the surgery, their fat tissue sucks up calories to make more fat; this leaves insufficient fuel for the rest of the body—what Ranson called “hidden semi-cellular starvation”—and “force[s] the body either to increase its general food intake or to cut down its expenditure, or both.” The only way to prevent these animals from getting obese is to starve them—to inflict what a Johns Hopkins University physiologist in the 1940s called “severe and permanent” food restriction. If these animals are allowed to eat even moderate amounts of food, they end up obese. In other words, they get fat not by overeating but by eating at all.
As animals starve, and the same is true of humans, they consume their muscles for fuel, and that includes, eventually, the heart muscle.
The message of eighty years of research on obese animals is simple and unconditional and worth restating: obesity does not come about because gluttony and sloth make it so; only a change in the regulation of the fat tissue makes a lean animal obese.
We don’t get fat because we overeat; we overeat because we’re getting fat.
Imagine that you’re eating a meal that contains both carbohydrates and fat, which most meals do. As the fat is digested, it’s shipped off directly to the fat cells for storage. Think of it as being set aside temporarily while the body deals with the carbohydrates, which demand more immediate action. As these carbohydrates are digested, they appear in the bloodstream in the form of glucose, which is the “sugar” in “blood sugar.”
Another way to think of this is that your fat cells work as energy buffers. They provide a place to put the calories that you consumed during a meal and don’t use immediately, and then they release the calories back into the circulation as you need them—just as your wallet provides a place to put the money you withdraw from the ATM and then releases it, so to speak, as you need it throughout the day.
LPL is the enzyme that sticks out from the membranes of different cells and then pulls fat out of the bloodstream and into the cells. If the LPL is on the surface of a muscle cell, then it directs the fat into the muscle to be used for fuel. If it’s on a fat cell, then it makes that fat cell fatter.
One way to think about what hormones do is that they instruct the body to do something—grow and develop (growth hormones), reproduce (sex hormones), flee or fight (adrenaline).
One way to think about insulin in this context is as a hormone that determines how fuels are “partitioned” around the body.
The most fattening foods are the ones that have the greatest effect on our blood sugar and insulin levels.
These are the concentrated sources of carbohydrates, and particularly those that we can digest quickly: anything made of refined flour (bread, cereals, and pasta), liquid carbohydrates (beers, fruit juices, and sodas), and starches (potatoes, rice, and corn).
Given an apple and a potato of the same weight, the potato will have a significantly greater effect on blood sugar, which suggests that it should be more fattening. But that doesn’t mean fruit won’t fatten some people.
The point to keep in mind is that you don’t lose fat because you cut calories; you lose fat because you cut out the foods that make you fat—the carbohydrates.
Banting credited Harvey for the diet, but it was Banting’s name that entered the English language (and the Swedish) as a verb meaning “to diet,” and it was Banting who took the heat from the medical community.
They believed it, though, because people they respected believed it, and those people believed it because, well, other people they respected believed it.
Just two hundred years ago, we ate less than a fifth of the sugar we eat today.
So, if carbohydrates make us fat, which they do, and fat or saturated fat causes heart disease, which the authorities tell us they do, then we have a paradox: now the diet that naturally makes us leaner is also the diet that gives us heart disease. Getting leaner now increases our risk of heart disease, whereas it should do the opposite.
Health authorities who insist that saturated fat causes heart disease have tried to escape this paradox—the diet that naturally makes us lean gives us heart disease—by blaming dietary fat for weight problems as well. They’ll argue that fat is the most energy-dense nutrient in the diet, and this makes it fattening. It has nine calories per gram, compared with four for either protein or carbohydrates.
Multiple hormones and enzymes affect our fat accumulation, and insulin happens to be the one hormone that we can consciously control through our dietary choices.
The conventional logic of diets is that people go on them expecting relatively quick returns in weight loss. By this logic, the dieters are not trying to reregulate their fat tissue; they’re only reducing the calories they consume, with the expectation that their fat cells will willingly respond by giving up the calories they’ve sequestered.
You enter into a weight-loss diet with the singular purpose of becoming as lean as you safely can be, and so all other gustatory desires should be put on hold temporarily until that goal is achieved. When you have achieved your goal and the excess fat has been lost, you can decide if you feel the need to incorporate back into your diet some of the foods you’ve been avoiding.
You can eat all you want of protein and fat, so you don’t get hungry and you don’t expend less energy. You might even expend more. The biggest challenge is the craving for carbohydrates.
As I discussed earlier, sugar appears to be addictive in the brain in the same way in which cocaine, nicotine, and heroin are.
Whether the addiction is in the brain or the body or both, the idea that sugar and other easily digestible carbohydrates are addictive also implies that the addiction can be overcome if you make the effort and have sufficient patience.
A common experience is to give up fattening carbohydrates and find that you’re not as hungry as you used to be, that mid-morning snacks are no longer necessary. Intrusive thoughts of food and the urge to satisfy them vanish. But that’s because you’re now burning your fat stores for fuel, which you didn’t do before. Your fat cells are now working properly as short-term energy buffers, not long-term lockups for the calories they’ve sequestered.
There are very good reasons to be physically active, but weight loss, as I discussed earlier, does not appear to be one of them.