IT IS FAIRLY obvious that obesity runs in families.1 Obese children often have obese siblings. Obese children become obese adults.2 Obese adults go on to have obese children. Childhood obesity is associated with a 200 percent to 400 percent increased risk of adult obesity. This is an undeniable fact. The controversy revolves around whether this trend is a genetic or an environmental problem—the classic nature versus nurture debate.
Families share genetic characteristics that may lead to obesity. However, obesity has become rampant only since the 1970s. Our genes could not have changed within such a short time. Genetics can explain much of the inter- individual risk of obesity, but not why entire populations become obese.
Nonetheless, families live in the same environment, eat similar foods at similar times and have similar attitudes. Families often share cars, live in the same physical space and will be exposed to the same chemicals that may cause obesity—so-called chemical obesogens. For these reasons, many consider the current environment the major cause of obesity.
Conventional calorie-based theories of obesity place the blame squarely on this “toxic” environment that encourages eating and discourages physical exertion. Dietary and lifestyle habits have changed considerably since the 1970s including
Any or all of these factors may contribute to the obesogenic environment. Therefore, most modern theories of obesity discount the importance of genetic factors, believing instead that consumption of excess calories leads to obesity. Eating and moving are voluntary behaviors, after all, with little genetic input.
So—exactly how much of a role does genetics play in human obesity?
NATURE VERSUS NURTURE
THE CLASSIC METHOD for determining the relative impact of genetic versus environmental factors is to study adoptive families, thereby removing genetics from the equation. By comparing adoptees to their biological and adoptive parents, the relative contribution of environmental influences can be isolated. Dr. Albert J. Stunkard performed some of the classic genetic studies of obesity.3 Data about biological parents is often incomplete, confidential and not easily accessible by researchers. Fortunately, Denmark has maintained a relatively complete registry of adoptions, with information on both sets of parents.
Studying a sample of 540 Danish adult adoptees, Dr. Stunkard compared them to both their adoptive and biological parents. If environmental factors were most important, then adoptees should resemble their adoptive parents. If genetic factors were most important, the adoptees should resemble their biological parents.
No relationship whatsoever was discovered between the weight of the adoptive parents and the adoptees. Whether adoptive parents were thin or fat made no difference to the eventual weight of the adopted child. The environment provided by the adoptive parents was largely irrelevant.
This finding was a considerable shock. Standard calorie-based theories blame environmental factors and human behaviors for obesity. Environmental cues such as dietary habits, fast food, junk food, candy intake, lack of exercise, number of cars, and lack of playgrounds and organized sports are believed crucial in the development of obesity. But they play virtually no role. In fact, the fattest adoptees had the thinnest adoptive parents.
Comparing adoptees to their biological parents yielded a considerably different result. Here there was a strong, consistent correlation between their weights. The biological parents had very little or nothing to do with raising these children, or teaching them nutritional values or attitudes toward exercise. Yet the tendency toward obesity followed them like ducklings.
When you took a child away from obese parents and placed them into a “thin” household, the child still became obese. What was going on?
Studying identical twins raised apart is another classic strategy to distinguish environmental and genetic factors. Identical twins share identical genetic material, and fraternal twins share 25 percent of their genes. In 1991,
Dr. Stunkard examined sets of fraternal and identical twins in both conditions of being reared apart and reared together.4 Comparison of their weights would determine the effect of the different environments. The results sent a shockwave through the obesity-research community. Approximately 70 percent of the variance in obesity is familial.
Seventy percent.
Seventy percent of your tendency to gain weight is determined by your parentage. Obesity is overwhelmingly inherited.
However, it is immediately clear that inheritance cannot be the sole factor leading to the obesity epidemic. The incidence of obesity has been relatively stable through the decades. Most of the obesity epidemic materialized within a single generation. Our genes have not changed in that time span. How can we explain this seeming contradiction?
THE THRIFTY-GENE HYPOTHESIS
THE FIRST ATTEMPT to explain the genetic basis of obesity was the thrifty-gene hypothesis, which became popular in the 1970s. This hypothesis assumes that all humans are evolutionarily predisposed to gain weight as a survival mechanism.
The argument goes something like this: In Paleolithic times, food was scarce and difficult to obtain. Hunger is one of the most powerful and basic of human instincts. The thrifty gene compels us to eat as much as possible, and this genetic predisposition to gain weight had a survival advantage.
Increasing the body’s food stores (fat) permitted longer survival during times of scarce or no food. Those who tended to burn the calories instead of storing them were selectively wiped out. However, the thrifty gene is ill adapted to the modern all-you-can-eat world, as it causes weight gain and obesity. But we are simply following our genetic urge to gain fat.
Like a decomposing watermelon, this hypothesis seems quite reasonable on the surface. Cut a little deeper, and you find the rotten core. This theory has long ceased to be taken seriously. However, it is still mentioned in the media, and so its flaws bear some examination. The most obvious problem is that survival in the wild depends on not being either underweight or overweight. A fat animal is slower and less agile than its leaner brethren. Predators would preferentially eat the fatter prey over the harder-to-catch, lean prey. By the same token, fat predators would find it much more difficult to catch lean and swift prey. Body fatness does not always provide a survival advantage, but instead can be a significant disadvantage. How many times have you seen a fat zebra or gazelle on the National Geographic channel?
What about fat lions and tigers? The assumption that humans are genetically predisposed to overeat is incorrect. Just as there are hormonal signals of hunger, there are multiple hormones that tell us when we’re full and stop us from overeating. Consider the all-you-can-eat buffet. It is impossible to simply eat and eat without stopping because we get “full.” Continuing to eat may make us become sick and throw up. There is no genetic predisposition to overeating. There is, instead, powerful built-in protection against it.
The thrifty-gene hypothesis assumes chronic food shortages prevented obesity. However, many traditional societies had plentiful food year round. For example, the Tokelau, a remote tribe in the South Pacific, lived on coconut, breadfruit and fish, which were available year round. Regardless, obesity was unknown among them until the onset of industrialization and the Westernization of their traditional diet. Even in modern-day North America, widespread famine has been uncommon since the Great Depression. Yet the growth of obesity has happened only since the 1970s.
In wild animals, morbid obesity is rare, even with an abundance of food, except when it is part of the normal life cycle, as with hibernating animals. Abundant food leads to a rise in the numbers of animals, not an enormous increase in their size. Think about rats or cockroaches. When food is scarce, rat populations are low. When food is plentiful, rat populations explode. There are many more normal-sized rats, not the same number of morbidly obese rats.
There is no survival advantage to carrying a very high body-fat percentage. A male marathon runner may have 5 percent to 11 percent body fat. This amount provides enough energy to survive for more than a month without eating. Certain animals fatten regularly. For instance, bears routinely gain weight before hibernation—and they do so without illness. Humans, though, do not hibernate. There is an important difference between being fat and being obese. Obesity is the state of being fat to the point of having detrimental health consequences. Bears, along with whales, walruses and other fat animals are fat, but not obese, since they suffer no health consequences. They are, in fact, genetically programmed to become fat. We aren’t. In humans, evolution did not favor obesity, but rather, leanness.
The thrifty-gene hypothesis doesn’t explain obesity, but what does? As we will see in Part 3, “A New Model of Obesity,” the root cause of obesity is a complex hormonal imbalance with high blood insulin as its central feature.
The hormonal profile of a baby is influenced by the environment in the mother’s body before birth, setting up a tendency for high insulin levels and associated obesity later in life. The explanation of obesity as a caloric imbalance simply cannot account for this predominantly genetic effect, since eating and exercise are voluntary behaviors. Obesity as a hormonal imbalance more effectively explains this genetic effect.
But inherited factors account for only 70 percent of the tendency to obesity that we observe. The other 30 percent of factors are under our control, but what should we do to make the most of this? Are diet and exercise the answer?