Why We Get Fat: And What to Do About It (10 page)

Steatopygia, the prominent fat deposits of the buttocks on this African woman, is a genetic trait, not the product of overeating or sedentary behavior
.
(photo credit 5.1)

It’s been known since the 1930s that obesity has a large genetic component. If your parents are fat, it’s far more likely you will be fat than someone whose parents are lean. Another way to say this is that body types run in families. Similarities in body types between parents and children and between siblings, as Hilde Bruch said, are often “as striking as facial resemblance.” This certainly isn’t always the case, just as parents and children don’t always look alike. But it’s common enough that we all know families in which fathers and sons, mothers and daughters have, in effect, the same bodies. With identical twins, it’s not just the faces that look alike; the bodies do as well.

Here are photos of two pairs of identical twins. The first are lean; the second are obese.

In the calories-in/calories-out model, overeating might conceivably tell us why the first pair of twins are slender and the second are not. The pair on the left ate in moderation, balancing calories-in to calories-out with the exquisite accuracy we now know is required; the second pair didn’t—they overate. But what about the vertical relationships in the photos? Why do the lean twins have identical bodies? And why do the obese twins? Why is their accumulation of fat so nearly identical? Are we to assume that they just overate, more or less, by exactly the same number of calories over the course of their lives because their genes determined precisely the size of the portions they ate at every meal and precisely how sedentary they chose to be—how many hours they sat on the couch rather than getting up and gardening or walking?

Two pairs of identical twins: one lean, one obese. Did their genes influence how much they ate and exercised or the amount and distribution of their body fat?
(photo credit 5.2)

Breeders of livestock have always been implicitly aware of the genetic, constitutional component of fatness. Those engaged in the art and science of animal husbandry have spent many decades breeding cattle, pigs, and sheep to be more fatty or less fatty, just as they breed dairy cattle to increase milk production or dogs for hunting or herding ability. It strains the imagination to believe these livestock breeders are merely manipulating genetic traits that determine the will to eat in moderation and the urge to exercise.

The cow on the top is an Abderdeen Angus, which is bred for the high fat content of its meat. On the bottom is a Jersey cow. It’s a lean breed; we can see its ribs protruding through its skin. Jersey cattle are dairy cows, milk producers, which is why the udders on this particular cow are swollen appropriately.

Now, are we to assume, once again, that these Aberdeen Angus cattle are loaded down with what’s known in the business as “marbling,” or “intramuscular” fat, because they graze longer or more efficiently than the lean Jersey cattle? That the genes of the Aberdeen Angus program them to take bigger bites and so get more calories per hour grazed? Maybe the Jersey cattle get a little more exercise. When the Aberdeen Angus are grazing or sleeping, perhaps the Jersey cattle are loping across the fields, emulating their ancient ancestors who had to run to avoid predators. This sounds absurd, of course, but anything is possible.

The full udders on the Jersey cow and the intramuscular fat on the Aberdeen Angus suggest another possibility. After all, what we want in dairy cattle are animals that convert the maximal amount of energy they consume into milk. This is their utility. We don’t want them wasting energy building up fat. With the Aberdeen Angus we want an animal that efficiently converts fuel into meat into protein and fat in the muscles. That’s where the energy is directed and where it accumulates.

The stocky cow on the top
(photo credit 5.3)
is an Aberdeen Angus; the lean cow on the bottom
(photo credit 5.4)
is a Jersey cow. Their genes probably determine how they partition the calories they consume—into fat, muscle, or milk—not their eating or exercise behavior
.

Hence, a likely explanation is that the genes that determine the relative adiposity of these two breeds have little or nothing to do with their appetite or physical activity but, rather, with how they
partition
energy—whether they turn it into protein and fat
in the muscles or into milk. The genes don’t determine how many calories these animals consume, but what they do with those calories.

Another conspicuous piece of evidence arguing against calories-in/calories-out is that men and women fatten differently. Men typically store fat above the waist—the beer belly—and women below the waist. Women put on fat in puberty, particularly in breasts, hips, butt, and thighs, and men lose fat during puberty and gain muscle.

When boys become men, they become taller, more muscular, and leaner. Girls enter puberty with very slightly more body fat than boys (6 percent more, on average), but by the time puberty is over, they have 50 percent more. “The energy conception can certainly not be applied to this realm,” as the German physician Erich Grafe said about this distribution of fat and how it differs by sex in his 1933 textbook
Metabolic Diseases and Their Treatment
. In other words, when a girl enters puberty as slender as a boy and leaves it with the shapely figure of a woman, it’s not because of overeating or inactivity, even though it’s mostly the fat she’s acquired that gives her that womanly shape and she had to eat more calories than she expended to accommodate that fat.

Still more evidence against the conventional wisdom is provided by a very rare disorder known technically as progressive “lipodystrophy.” (“Lipo” means “fat”; a “lipodystrophy” is a disorder of fat accumulation.)

By the mid-1950s, some two hundred cases of this disorder had been reported, the great majority in women. It’s characterized by the complete loss of subcutaneous fat (the fat immediately beneath the skin) in the upper body, and an excess of fat below the waist. The disorder is called “progressive” because the loss of fat from the upper body progresses with time. It begins with the face and then moves slowly downward to neck, then shoulders, arms, and trunk. The photo is of a case reported first in 1913.

A case of the rare disorder known as “progressive lipodystrophy.” At age twenty-four, this woman would be considered obese by today’s definition, yet virtually all her body fat was located from her waist down
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(photo credit 5.5)

This young woman began losing the fat from her face when she was ten years old; the fat loss stopped at her waist when she was thirteen. Two years later, she began fattening below the waist. The photo was taken when she was twenty-four; she was five feet four and weighed 185 pounds. By today’s standards, she would be considered clinically obese—with a body mass index of almost 32.
^*
But effectively
all
of her body fat was located below her waist. She was as fat as a sumo wrestler from the waist down, as lean as any of the front-runners of an Olympic marathon above it.

So what does this have to do with calories-in/calories-out? If we believe that we get fat because we overeat and we get lean by undereating, are we to assume that these women lost fat on their upper bodies because they underate? And gained fat on their lower bodies because they overate?

This is obviously a ridiculous suggestion. But why is it that when fat loss and fat gain are localized like this—when the obesity or the extreme leanness covers only half the body, or only a
part and not all—they clearly have nothing to do with how much the person ate or exercised; yet when the whole body becomes obese or lean, the difference between calories consumed and expended supposedly explains it?

If this young lady had a few more pounds of fat on her upper body, just enough to soften her features, round out her curves, and if she were to see a doctor today, she would be diagnosed as obese and promptly told to eat less and exercise more. And this would seem perfectly reasonable. But can a valid explanation for obesity and its causes really depend on a few pounds of fat—the difference between sense and nonsense? With these extra pounds, her condition would be blamed on overeating, on the difference between the calories she consumed and expended. Without those extra pounds, with the full lipodystrophy revealed, this explanation becomes nonsensical.

There’s a modern example of a lipodystrophy that’s not nearly so uncommon—HIV-related lipodystrophy, apparently caused by the anti-retroviral drugs that people infected with HIV take to subdue the virus and keep full-blown AIDS at bay.

Before and after photos of a man who developed HIV-related lipodystrophy after beginning anti-retroviral therapy
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(photo credit 5.6)

These people, too, lose the subcutaneous fat in the face, as well as arms, legs, and buttocks, and they also put on fat elsewhere; the gain and loss of fat often happen at different times. They get double chins and a distinctive fat formation on the upper back known as a “buffalo” or “camel hump.” Their breasts enlarge, even in men, and they often get a potbelly that looks indistinguishable from the kind we might otherwise attribute to drinking too much beer, as in the case on the previous page. The photo on the left was taken before this patient began anti-retroviral therapy for his HIV; the photo on the right was taken four months afterward.