Why We Get Fat: And What to Do About It (13 page)

The way Wade explained it to me, the animal doesn’t get fat because it overeats, it overeats because it’s getting fat. The cause and effect are reversed. Both gluttony and sloth are effects of the drive to get fatter. They are caused fundamentally by a defect in the regulation of the animal’s fat tissue. The removal of the ovaries literally makes the rat stockpile body fat; the animal either eats more or expends less energy, or both, to compensate.

To explain why this happens, I’m going to have to get technical for a moment. As it turns out, removing the rats’ ovaries serves the function of removing estrogen, the female sex hormone that is normally secreted by the ovaries. (When estrogen was infused back into the rats postsurgery, they did not eat voraciously, become slothful, or grow obese. They acted like perfectly normal rats.) And one of the things that estrogen does in rats (and humans) is influence an enzyme called lipoprotein lipase—LPL, for short. What LPL does in turn, very simplistically, is to pull fat from the bloodstream into whatever cell happens to “express” this LPL. If the LPL is attached to a fat cell, then it pulls fat from the circulation into the fat cell. The animal (or the person) in which that fat cell resides gets infinitesimally fatter. If the LPL is attached to a a muscle cell, it pulls the fat into the muscle cell, and the muscle cell burns it for fuel.
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When estrogen levels are low (left), the enzyme LPL is “upregulated” on fat cells, and more fat is pulled from the circulation into the cell. When estrogen levels are high (right), LPL activity is suppressed, and the fat cells accumulate less fat
.
(photo credit 9.1)

Estrogen happens to suppress or “inhibit” the activity of LPL on fat cells. The more estrogen around, the less LPL will be pulling fat out of the bloodstream and into the fat cells, and the less fat those cells will accumulate. Get rid of the estrogen (by removing the ovaries) and fat cells blossom with LPL. The LPL
then does what it always does—pull fat into the cells—but now the animal gets far fatter than normal, because now the fat cells have far more LPL doing that job.

The animal has the urge to eat voraciously because it’s now losing calories into its fat cells that are needed elsewhere to run its body. The more calories its fat cells sequester, the more it must eat to compensate. The fat cells, in effect, are hogging calories, and there aren’t enough to go around for other cells. Now a meal that would previously have satisfied the animal no longer does. And because the animal is getting fatter (and heavier), this increases its caloric requirements even further. So the animal is ravenous, and if it can’t satisfy its newfound hunger, it has to settle for expending less energy.

The only way (short of more surgery) to stop these animals from getting fat—dieting has no effect, and we can be confident that trying to force them to exercise would be futile—is to give them their estrogen back. When that is done, they become lean again, and their appetite and energy levels return to normal.

So removing the ovaries from a rat literally makes its fat cells fatten. And this, very likely, is what happens to many women who get fat when they have their ovaries removed or after menopause. They secrete less estrogen, and their fat cells express more LPL.

The story of these ovariectomized rats 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 tells us that if we pay attention to the hormones and enzymes that regulate the fat tissue itself, we can understand precisely why this is so: not only why these rats get fat but why they exhibit the behaviors that we typically associate with fat people.

Another remarkable aspect of the last half-century of discussion about obesity and weight loss is that medical experts have been remarkably uninterested in the fat tissue itself and how our
bodies happen to regulate it. With very few exceptions, they’ve simply ignored the fat tissue because they’ve already concluded that the problem is behavioral and lies in the brain, not in the body. Had we been discussing disorders of growth—why some people grow to be more than seven feet tall and others never make it to four feet—the only subject of discussion would be the hormones and enzymes that regulate growth. And yet, when we’re discussing a disorder in which the defining symptom is the abnormal growth of our fat tissue, the hormones and enzymes that regulate that growth are considered irrelevant.
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When we pay attention to the regulation of our fat tissue, though, we arrive at an explanation for why we get fat and what to do about it that differs radically from the conventional thinking derived from the focus on the balance of energy consumed and expended. We have to conclude, as Wade did for his rats, that those who get fat do so because of the way their fat happens to be regulated and that a conspicuous consequence of this regulation is to cause the eating behavior (gluttony) and the physical inactivity (sloth) that we so readily assume are the actual causes.

I’m going to discuss this idea first as a hypothesis, a way of thinking about why we get fat that could be correct, and then I’m going to explain why it almost assuredly is.
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Before I get to that, though, there are several critical points about fat and the process
of fattening itself that you’ll have to understand. In honor of the laws of thermodynamics that they’re replacing, we’ll call these the laws of adiposity.

Body fat is carefully regulated, if not exquisitely so.

This is true even though some people fatten so easily that it’s virtually impossible to imagine. What I mean by “regulated” is that our bodies, when healthy, are working diligently to maintain a set amount of fat in our fat tissue—not too much and not too little—and that this, in turn, is used to assure a steady supply of fuel to the cells. The implication (our working assumption) is that if someone gets obese it’s because this regulation has been thrown out of whack, not that it’s ceased to exist.

The evidence that fat tissue is carefully regulated, not just a garbage can where we dump whatever calories we don’t burn, is incontrovertible. We can start with all the observations in
chapter 5
about the wheres, whens, and whos of fattening. That men and women fatten differently tells us that sex hormones play a role in regulating body fat (as do Wade’s experiments and what we know about estrogen and LPL). That some parts of our bodies are relatively fat free—the backs of our hands, for example, and our foreheads—and others not so, tells us that local factors play a role in where we fatten. Just as local factors obviously play a role in where we grow hair—in some places, but not in others.

That obesity runs in families (we’re more likely to be fat if our parents were fat) and that the local distribution of fat itself can be a genetic attribute (the steatopygia of certain African tribes) tells us that body fat is regulated, because how else would the genes passed from generation to generation influence our fat and where we put it, if not through the hormones and enzymes and other factors that regulate it?

That the amount of fat (and even the type of fat) animals carry
is carefully regulated also argues for this conclusion. We are, after all, just another species of animal. Animals in the wild may be naturally fat (hippopotami, for instance, and whales). They’ll put on fat seasonally, as insulation in preparation for the cold of winter or as fuel for annual migrations or hibernations. Females will fatten in preparation for giving birth; males will fatten to give them a weight advantage in fights for females. But they
never
get obese, meaning they won’t suffer adverse health consequences from their fat the way humans do. They won’t become diabetic, for instance.

No matter how abundant their food supply, wild animals will maintain a stable weight—not too fat, not too thin—which tells us that their bodies are assuring that the amount of fat in their fat tissue always works to their advantage and never becomes a hindrance to survival. When animals do put on significant fat, that fat is always there for a very good reason.
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The animals will be as healthy with it as without.

Excellent examples of how carefully animals (and so presumably humans, too) regulate their fat accumulation are hibernating rodents—ground squirrels, for example, which double their weight and body fat in just a few weeks of late summer. Dissecting these squirrels at their peak weight, as one researcher described it to me, is like “opening a can of Crisco oil—enormous gobs of fat, all over the place.”

But these squirrels will accumulate this fat regardless of how much they eat, just like Wade’s ovary-less rats. They can be housed in a laboratory and kept to a strict diet from springtime, when they awake from hibernation, through late summer, and they’ll get just as fat as squirrels allowed to eat to their hearts’ content. They’ll
burn the fat through the winter and lose it at the same rate, whether they remain awake in a warm laboratory with food available or go into full hibernation, eating not a bite, and surviving solely off their fat supplies.

The fact is, there’s very little that researchers can do to keep these animals from gaining and losing fat on schedule. Manipulating the food available, short of virtually starving them to death, is not effective. The amount of fat on these rodents at any particular time of the year is regulated entirely by biological factors, not by the food supply itself or the amount of energy required to get that food. And this makes perfect sense. If an animal that requires enormous gobs of fat for its winter fuel were to require excessive amounts of food to accumulate that fat, then one bad summer would have long ago wiped out the entire species.

It may be true that evolution has singled out humans as the sole species on the planet whose bodies do not work to regulate fat stores carefully in response to periods of both feast and famine, that some people will stockpile so much fat merely because food is available in abundance that they become virtually immobile, but accepting this conclusion requires that we ignore virtually everything we know about evolution.

A final argument for the careful regulation of body fat is the fact that everything else in our bodies is meticulously regulated. Why would fat be an exception? When regulation breaks down, as it does in cancer and heart disease, the result is often fatally obvious. When people accumulate excess fat, this tells us that something has gone awry in the careful regulation of their fat tissue. What we need to know is what that defect is and what to do about it.

Obesity can be caused by a regulatory defect so small that it would be undetectable by any technique yet invented.

Remember the twenty-calorie-a-day problem I discussed earlier? If we overeat by just twenty calories each day—adding just 1 percent or less to our typical daily caloric quota, without a compensatory increase in expenditure—that’s enough to transform us from lean in our twenties to obese in our fifties. In the context of the calories-in/calories-out logic, this led to the obvious question: How do any of us remain lean if it requires that we consciously balance the calories we eat to those we expend with an accuracy of better than 1 percent? That seems impossible, and assuredly is.

Well, these same twenty calories a day is all this regulatory system has to misdirect into our fat cells to make us obese. The same arithmetic applies. If, by some unlucky combination of genes and environment, a regulatory error causes our fat cells to store an excess of just 1 percent of the calories that would otherwise be used for fuel, then we are destined to become obese.

If this misappropriation of calories into fat is only slightly larger, someone could end up grotesquely fat. Yet this would still seem like a relatively minor error in regulatory judgment—just a few percentage points, something exceedingly difficult to measure and yet not that hard to imagine.

Whatever makes us both fatter and heavier will also make us overeat.

This was the ultimate lesson of Wade’s rats. It may be counterintuitive, but it
has
to be true for every species, for every person who puts on pounds of fat. It’s arguably the one lesson we (and our health experts) have to learn in order to understand why we get fat and what to do about it.

This law is one fact we can count on from the first law of thermodynamics, the law of energy conservation, which health experts have been so determined to misapply.
Anything
that increases its mass, for whatever reason, will take in more energy
than it expends. So, if a regulatory defect makes us both fatter and heavier, it is guaranteed to make us consume more calories (and so increase our appetite) and/or expend less than would be the case if this regulation was working perfectly.

Here’s where growing children help as a metaphor to understand this cause and effect of getting fat and overeating. I’m going to use two photos of my oldest son to make this point. The photo below, on the left, was taken when he was not quite two years old and weighed thirty-four pounds.