Why We Get Fat: And What to Do About It (16 page)

To understand obesity and why we get fat, we have to understand what Astwood understood and what obesity experts were beginning to accept before the Second World War put a halt to the proceedings. Both gluttony (overeating) and sloth (sedentary behavior) will be the side effects of any regulatory derangement, minor as it may be, that diverts too many calories into fat tissue for storage. Those of us so afflicted might indeed have the urge or the need to see a psychiatrist before too long. It won’t be our emotional disturbances that make us fat, though, but the inexorable fattening (along with the hunger and the taunting and the accusations of gluttony and lack of “willpower”) that makes us disturbed.

It’s time to roll up our sleeves and get to work. What we need to know is what biological factors regulate the amount of fat in our fat tissue. And, specifically, how this is affected by our diets, so we can know what we’re doing wrong and how to change it. Another way to say this is that we need to know what determines nature—why we might be predisposed to get fat or stay lean—and what elements of nurture, of diet and lifestyle, can be altered to affect this predisposition or combat it.

I’m going to be discussing some basic biology and endocrinology, subjects you may understandably find slow going. All I can promise is that if you pay attention you’ll know virtually everything you need to know about why people get fat and what has to be done to combat it.

The science I’ll be talking about was worked out by researchers between the 1920s and the 1980s. At no point was it particularly controversial. Those who did the research agreed that this was how it worked, and they still agree. The problem, though, as I hope I’ve made clear, is that the “authorities” on obesity, even those who weren’t psychologists or psychiatrists, came to believe that they knew what makes people fat—overeating and sedentary behavior. As a result, nothing else on the subject really mattered to them, including the science of how fat tissue is regulated. They either ignored it entirely or actively rejected it because they didn’t like its implications (which I’ll discuss later). Despite their head-in-the-sand attitude, the regulation of our fat tissue does matter. Whether we get fat or stay lean depends on it.

Simple question: Why do we store fat in the first place? What’s the reason? Okay, some of it provides insulation to keep us warm, and some of it provides padding to protect the more fragile structures within, but what about the rest? The fat around the waist, for instance?

The way the experts typically see it is that fat storage works as a kind of long-term savings account—like a retirement account that you can dip into only in dire need. The idea is that your body takes excess calories and stashes them away as fat, and they remain in the fat tissue until you someday find yourself sufficiently underfed (because you’re now dieting or exercising or perhaps stranded on a desert island) that this fat is mobilized. You then use it for fuel.

But it has been known since the 1930s that this conception is not even remotely accurate. As it happens, fat is continuously flowing out of our fat cells and circulating around the body to be used for fuel and, if it’s not used for fuel, returned to the fat cells. This goes on regardless of whether we’ve recently eaten or exercised. In 1948, after this science was worked out in detail, Ernst Wertheimer, a German biochemist who had emigrated to Israel and is considered the father of the field of fat metabolism, put it this way: “Mobilization and deposition of fat go on continuously, without regard to the nutritional state of the animal.”
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Over the course of any twenty-four-hour period, fat from your fat cells will provide a significant portion of the fuel that your cells will burn for energy. The reason nutritionists like to think (and like to tell us) that carbohydrates are somehow the preferred fuel for the body, which is simply wrong, is that your cells will burn carbohydrates before they’ll burn fat. They do so because that’s how the body keeps blood sugar levels in check after a meal. And if you’re eating a carbohydrate-rich diet, as most people do, your cells will have a lot of carbohydrates to burn before they get to the fat.

(photo credit 11.1)

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.” (A carbohydrate called “fructose” is a special case, and I’ll discuss that later.) Cells throughout the body will burn this glucose for fuel and use it to replenish their backup fuel supplies, but they can’t keep up with this rising tide of blood sugar unless they get help doing it.

This is where the hormone insulin comes in. Insulin plays many roles in the human body, but one critical role is to keep blood sugar under control. You’ll start secreting insulin (from the pancreas) even before you start eating—indeed, it’s stimulated
just by thinking about eating. This is a Pavlovian response. It will happen without any conscious thought. In effect, this insulin is preparing your body for the meal you’re about to eat. When you take your first bites, more insulin will be secreted. And as the glucose from the meal begins flooding the circulation, still more is secreted.

The insulin then signals cells throughout the body to increase the rate at which they’re pumping in glucose from the bloodstream. The cells, as I said earlier, will burn some of this glucose for immediate energy and store some for later use. Muscle cells store the glucose in the form of a molecule called “glycogen.” Liver cells store some as glycogen and convert some to fat. And fat cells store it as fat.

As your blood sugar begins to decrease, and insulin levels decrease along with it, more and more of the fat stored during the meal will be released from fat tissue (or at least it should be) to take up the slack. Some of this fat began life as carbohydrates, and some began life as fat in the diet, but it’s indistinguishable once it finds itself stored in the fat cells. The more time passes after a meal, the more fat you will burn and the less glucose. The reason you can sleep through the night without getting up every few hours to raid the refrigerator (or the reason you should be able to) is that fat flowing out of your fat tissue keeps your cells nicely fueled until the morning.

So the correct way to think about fat tissue is that it’s more like a wallet than a savings or retirement account. You’re always putting fat into it, and you’re always taking fat out. You get a tiny bit fatter (more fat goes into our fat cells than comes out) during and after every meal, and then you get a tiny bit leaner again (the opposite occurs) after the meal is digested. And you get leaner still while sleeping. In an ideal world, one in which you’re not getting any fatter, the calories you store as fat immediately after meals during the day are balanced out over time by the calories you burn as fat after digesting those meals and during the night.

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. It’s only when the reserves of fat are reduced to some minimum amount that you start to get hungry again and are motivated to eat. (Just as we all have some minimum amount of cash we like to have in our wallets, and when we get down to that point, we go to the bank machine and restock.) In the early 1960s, the Swiss physiologist Albert Renold, who followed Ernst Wertheimer as the preeminent scientist in the field of fat metabolism, put it this way: our fat tissue, he wrote, is “the major site of active regulation of energy storage and mobilization, one of the primary control mechanisms responsible for the survival of any given organism.”

The fact that fat is flowing into and out of our fat cells all day long, though, doesn’t explain how the cells decide what fat gets to come and go, and what fat has no choice and is locked away inside. This decision is made very simply, based on the
form
of the fat. The fat in our bodies exists in two different forms that serve entirely different purposes. Fat flows in and out of cells in the form of molecules called “fatty acids”; this is also the form we
burn
for fuel. We
store
fat in the form of molecules called “triglycerides,” which are composed of three fatty acids (“tri-”) bound together by a molecule of glycerol (“glyceride”).

The reason for this role distribution is again surprisingly simple: triglycerides are too big to flow through the membranes that surround every fat cell, whereas fatty acids are small enough to slip through cell membranes with relative ease, and so they do. Flowing back and forth, in and out of fat cells all day long, they can be burned for fuel whenever needed. Triglycerides are the form in which fat is fixed inside fat cells, stashed away for future use. For this reason, the triglycerides first have to be constructed inside a fat cell (the technical term is “esterified”) from their component fatty acids, which is what happens.

When a fatty acid flows into a fat cell (or when it’s created in the fat cell from scratch out of glucose), it will be bound up with a glycerol molecule and two other fatty acids, and the result is a triglyceride, a molecule now too big to get out of the fat cell. Now these three fatty acids are stuck in the fat cell until the triglyceride gets disassembled or falls apart, and they can flow out of the cell again and back into the circulation. Anyone who ever bought a piece of furniture only to realize that it’s too big to fit through the door of the room for which it was intended knows the routine. You take the furniture apart (if possible), you walk the pieces through the door, and then you put the item of furniture back together on the other side. And if you move, and you want to take this particular furniture with you to your new home, you repeat the process in the other direction.

As a result, anything that works to promote the flow of fatty acids into your fat cells, where they can be bundled together into triglycerides, works to store fat, to make you fatter. Anything that works to break down those triglycerides into their component fatty acids so the fatty acids can escape from the fat cells works to make you leaner. As I said, it’s pretty simple. And as Edwin Astwood pointed out half a century ago, there are dozens of hormones and enzymes that play a role in these processes, and it’s very easy to imagine how they can be disturbed so that too much fat gets in and not enough gets out.

Fatty acids are small enough to flow through the membrane of the fat cell and so they do. Inside the fat cell, fatty acids are bound up as triglycerides, molecules too large to fit through the cell membrane. This is the form in which we store fat
.
(photo credit 11.2)