Why We Get Fat: And What to Do About It (18 page)

Earlier I talked about the twenty-four-hour cycle of storing and burning fat. We gain it during the day, when we’re digesting meals (because of the effects of carbohydrates on insulin); we lose it in the hours until our next meal, and at night, while we’re sleeping. Ideally, the fat we gain during the fat-storage phases is balanced by the fat we lose during the fat-burning phases. What we gain during the day is burned during the night, and it’s insulin that ultimately controls this cycle. As I’ve said, when insulin levels go up, we store fat. When they come down, we mobilize the fat and use it for fuel.

This suggests that anything that makes us secrete more insulin than nature intended, or keeps insulin levels elevated for longer than nature intended, will extend the periods during which we store fat and shorten the periods when we burn it. As we know, the imbalance that results—more fat stored, less burned—can border on infinitesimal, twenty calories a day, and it can lead us to obesity within a couple of decades.
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By extending the periods when we’re storing fat rather than
burning it, insulin indirectly has another effect. Remember, we depend on fatty acids for fuel in the hours after a meal, as blood sugar levels are dropping to their pre-meal level. But the insulin suppresses the flow of fatty acid from the fat cells; it tells the other cells in the body to burn carbohydrates. So, as blood sugar returns to a healthy level, we need a replacement fuel supply.

If insulin remains elevated, the fat isn’t available. Nor is protein, which our cells can also use for fuel if necessary: insulin also works to keep the protein stored away in the muscles. We can’t use the carbohydrates we’ve stored in the liver and muscle tissue, either, because the insulin keeps that supply locked up as well.

As a result, the cells find themselves starved for fuel, and we quite literally feel
their
hunger. Either we eat sooner than we otherwise would have or we eat more when we do eat, or both. As I said earlier, anything that makes us fatter will make us overeat in the process. That’s what insulin does.

Meanwhile, our bodies are getting bigger because we’re putting on fat, and so our fuel requirements are increasing. When we get fatter, we also add muscle to support that fat. (Thanks again in part to insulin, which assures that whatever protein we consume is used for repairing muscle cells and organs and for adding muscle, if necessary.) So, as we fatten, our energy demand increases, and our appetite will increase for this reason as well—particularly our appetite for carbohydrates, because this is the only nutrient our cells will burn for fuel when insulin is elevated. This is a vicious cycle, and it’s precisely what we’d like to avoid. If we’re predisposed to get fat, we’ll be driven to crave precisely those carbohydrate-rich foods that make us fat.

If insulin makes people fat, why does it make only some of us fat? We all secrete insulin, after all, and yet plenty of us are lean and will stay lean for life. This is a question of nature—our genetic predisposition—not nurture or the aspects of diet and/or lifestyle that trigger this nature.

The answer lies in the fact that hormones don’t work in a vacuum, and insulin is no exception. The effect of a hormone on any particular tissue or cell depends on a host of factors, both inside and outside cells—on enzymes, for instance, such as LPL and HSL. This allows hormones to differ in their effect from cell to cell, tissue to tissue, and even at different stages of our development and our lives.

One way to think about insulin in this context is as a hormone that determines how fuels are “partitioned” around the body. After a meal, insulin and the various enzymes it influences, such as LPL, determine what proportion of the different nutrients will be sent to which tissues, how much will be burned, how much will be stored, and how this will change with need and with time. Since I’m concerned here with whether fuels will be used for energy or stored, imagine insulin and these enzymes as determining which way the needle points on what I’m going to call a fuel-partitioning gauge. Imagine it looking like the fuel gauge in your car, but instead of the “F” standing for “full” on the right, it stands
for “fat,” and the “E” on the left doesn’t stand for “empty,” but for “energy.”

If the needle points to the right—toward the “F”—it means that insulin partitions a disproportionate amount of the calories you consume into storage as fat, rather than use for energy by the muscles. In this case, you’ll have a tendency to fatten, and you’ll have less energy available for physical activity, so you’ll also tend to be sedentary. The farther the needle points toward fat storage, the more calories will be stored, the fatter you’ll be. If you don’t want to be sedentary, of course, then you have to eat more to compensate for this loss of calories into fat.
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It’s the morbidly obese people of the world who live on the far end of this side of the gauge.

When the needle points in the other direction—toward the “E”—you’ll be burning as fuel a disproportionate share of the calories you consume. You’ll have plenty of energy for physical activity, but little will be stored as fat. You’ll be lean and active (just as you’re supposed to be), and you’ll eat in moderation. The farther out you go in this direction, the more energy you’ll have for physical activity and the less will be stored—the leaner you’ll be. Emaciated-looking marathoners can be found down here. Their bodies burn calories—they don’t store them—and so these people literally have energy to burn. They have what pre–World War II metabolism researchers would have called a very powerful impulse to be physically active.

What determines the direction in which the needle points? The answer is not quite as simple as how much insulin you secrete, although that’s probably part of it. Given the same food containing the same amount of carbohydrates, some people will
secrete more insulin than others, and those who do are likely to put on more fat and have less energy. Their bodies work to keep blood sugar levels under control, because high blood sugar is toxic, and they’re willing to overstuff their fat cells, if necessary, to do it.

But another important factor is just how sensitive to insulin your cells happen to be and how quickly they become insensitive—the property called “insulin resistance”—in response to the insulin you secrete. This idea of being resistant to insulin is absolutely critical to understanding the reasons we get fat and also many of the diseases associated with it. I’ll return to it frequently.

The more insulin you secrete, the more likely it is that your cells and tissues will become resistant to that insulin. That means it will take more insulin to do the same glucose-disposal job, keeping blood sugar under control. One way to think about it is that your cells make the decision that they don’t want any more glucose than they’re already getting—too much glucose is toxic for cells, too—so they make it harder for insulin to do its job and get the glucose out of the bloodstream.

The problem (or the solution, depending on point of view) is that the pancreas responds by pumping out still more insulin. And the result is a vicious cycle. When a lot of insulin is secreted—in response to easily digestible carbohydrates, say—your cells are likely to resist the effects of that insulin, at least in the short term, particularly your muscle cells, because they’re getting enough glucose already. If these cells become resistant to insulin, more insulin is required to keep blood sugar levels in check, so now you secrete more insulin, which prompts more insulin resistance. And all the while, that insulin is working to make you fatter (to store calories as fat), unless your fat cells are also resistant to it.

So secreting more insulin will move the needle on the fuel-partitioning gauge toward storage. But if you secrete a healthy amount of insulin, and yet your muscle tissue is relatively quick to become resistant to that insulin, you’ll achieve the same thing.
You’ll secrete more insulin in response to the insulin resistance, and you’ll grow fatter.

A third factor is that your cells will respond differently to insulin. Fat cells, muscle cells, liver cells don’t all become resistant to insulin at the same time, to the same extent, or in the same way. Some of these cells will become more or less sensitive to insulin than others, which means the same amount of insulin will have a greater or lesser effect on different tissues. And how these tissues respond will differ as well—from person to person and, as I’ll discuss, over time in the same individual.

The more sensitive a particular tissue is to insulin, the more glucose it will take up when insulin is secreted. If it’s muscle, it will store more glucose as glycogen and burn more for fuel. If it’s fat, it will store more fat and release less. So, if your muscle cells are very sensitive to insulin and your fat cells less so, then the needle of the fuel-partitioning gauge points toward fuel burning. Your muscles will take up a disproportionate share of the glucose from the carbohydrates you consume, and they’ll use it for energy. The result: you’ll be lean and physically active. If your muscles are relatively insensitive to insulin compared with your fat cells, then your fat tissue will be the repository of a disproportionate share of the calories you consume. As a result, you’ll be fat and sedentary.
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Here’s another complication: how your tissues respond to insulin changes will change with time (and in response to your diet, as I’ll discuss shortly). As you get older, you get more insulin-resistant,
but this almost invariably happens to your muscle tissue first and only later, if at all, to your fat tissue. As a general rule, fat cells always stay more sensitive to insulin than muscle cells do. So, even if you’re lean and active when you’re young, with your fuel-partitioning needle pointing toward fuel burning, your muscle cells are likely to become resistant to insulin as you get older. As they do, you’ll respond by secreting more insulin.

This means the needle on the fuel-partitioning gauge will move to the right as you age—more and more calories will be diverted into fat, leaving fewer and fewer available to fuel the rest of the body. As you enter middle age, you’ll find it increasingly difficult to remain lean. You’ll also begin to manifest a multitude of other metabolic disturbances that accompany this insulin resistance and the elevated insulin levels that go hand in hand: your blood pressure goes up, as does your triglyceride level; your HDL cholesterol (aka, the “good cholesterol”) goes down; you become glucose intolerant, which means you have trouble controlling your blood sugar, and so on. And you’ll become increasingly sedentary, a side effect of the energy drain into the fat tissue.

In fact, the conventional wisdom that those of us who fatten as we move into middle age do so because our metabolism slows down, probably has this cause and effect backward. More likely is that our muscles become increasingly resistant to insulin, and this partitions more of the energy we consume into fat, leaving less available for the cells of muscles and organs to use for fuel. These cells now generate less energy, and this is what we mean when we say that our metabolism slows down. Our “metabolic rate” decreases. Once again, what appears to be a cause of fattening—the slowing of our metabolism—is really an effect. You don’t get fat because your metabolism slows; your metabolism slows because you’re getting fat.

Before I discuss the nurture side of this issue, the foods we eat that make things worse and that we can live without, there is one more issue of nature to discuss: why our children are today getting fatter,
and maybe even coming out of the womb fatter, than just twenty or thirty years ago. This is one aspect of the obesity epidemic that’s emerged recently in studies worldwide. Not only are more children obese now than ever before, but most studies report that they’re noticeably fatter at six months, a phenomenon that obviously has nothing to do with their behavior.

Fat children tend to be born of fat parents, in part because of all the ways that our genes control our insulin secretion, the enzymes that respond to insulin, and how and when we become resistant to insulin. But there’s also another factor that represents cause for concern. Children in the womb are supplied with nutrients from the mother (through the placenta and umbilical cord) in proportion to the level of those nutrients in the mother’s blood. This means that the higher the level of the mother’s blood sugar, the more glucose her child gets in her womb.