Obesity Hypothesis

In recent years, obesity has come to be an increasingly massive problem. In the past twenty years alone the average BMI for an American has doubled. But what caused this appalling increase in obesity. The thrifty gene hypothesis and the obesogen hypothesis both try to explain how this problem started. These hypothesis’ reveal that our genetic makeup and environmental factors can both cause obesity.

In order to understand the hypothesis’ we must understand the biological process of how we store and burn fat. Let’s begin by defining the process of respiration. Respiration is one of the major ways a cell manufactures energy from food sources. In humans the process of aerobic respiration breaks down a glucose molecule using ATP (an energy source) into a pyruvate molecule. This is also known as glycolysis. This pyruvate then enters the mitochondria where it undergoes the Krebs cycle. In the Krebs cycle, the pyruvate is oxidized in order to produce energy, in this case ATP. The net gain of ATP in cellular respiration is about 34 molecules of ATP. This model helps us to understand how glucose from food is broken down into its components in order to create energy for the body. It explains how glucose uses ATP to become pyruvate which is oxidized to create an overall gain of ATP, but how can we this to losing weight?

When we eat, sugars from our food are either broken down to produce energy or they are stored as fat molecules. If we just sit around all day eating fatty foods, the chance that glucose will be stored as fat are high. This makes sense because doing nothing does not require energy. But when we are running on a treadmill or playing basketball, our bodies use up energy reserves faster than usual. So, if the body does not have carbohydrates to burn off, it decides to start breaking down fat molecules in order to sustain a constant source of energy. Its sort of like a chain reaction. When our bodies are in a state of increased activity, they need more energy to replenish our bodies. So they begin to break down fat molecules into pyruvate which is oxidized to ultimately produce ATP to be used up by our bodies. This is also know as “burning calories.” A calorie is just a unit for measuring and amount of energy. When we burn calories, what we are actually doing is breaking down fat molecules in order to produce ATP. This is how we lose weight. Another way people lose weight besides burning off calories is ingesting less calories. When we eat less calories, we are actually preventing a buildup of more fat molecules. An even better way to induce weight loss is to adopt a strategy in which you increase your exercise duration and go on a low caloric diet. By doing both you are storing less fat molecules as well as burning off more, therefore losing weight. This may be a successful plan for some people, but for others it may not work so well. These unfortunate people have genetic predispositions that prevent them from losing weight.

The thrifty gene hypothesis, proposed by James V. Neel, tries to explain how negative genes that cause people to gain weight, called thrifty genes, could have become favored through natural selection. He elaborates his hypothesis by saying that these thrifty genes were necessary to survive a couple of generations ago because our ancestors lived in a time where food wasn’t always abundant and our bodies were forced to store up on fat in case of a future shortage of food or a famine. Those who emphasized the thrifty gene were more likely to survive than those who didn’t because they simply would not starve to death. But for the current generation, these thrifty genes are detrimental to our health. Nowadays, especially in America, there is never a shortage of food. People eat every day, all day, as much as they wish. Unfortunately for many of them, their thrifty genes are still active causing them to store fat rather than quickly burn it off. This causes a generation of obesity.

There is an alternative to this hypothesis however. Many other scientist believe that environmental factors, such as chemicals form pollution, affect a fetus or an infant’s genetic expression causing them to convert their connective tissues into fat cells. Of course, an excess of fat cells increases the likelihood of obesity in the children. This hypothesis was supported with an experimental study that was done in UC Irvine. The study consisted of exposing female frogs to TBT, a pollutant expected to cause the disorder that leads to obesity. He found out that a tiny dose of it could create grand results. He repeated this study with rats and found the same thing, TBT made them fat.

However, it is still difficult to tell for sure whether either of the hypothesis’s are correct. They are both very different from one another, yet they also have some striking similarities. They both have environmental factors that affected their genotype in order to change their phenotypes. The thrifty gene hypothesis uses natural selection to starve off those without the thrifty gene and the obesogen hypothesis has the chemical TBT that is attributed to causing obesity. In both hypothesis’, environmental factors alter the genotype of person which ultimately alters the phenotype of that person.

Although both hypothesis’ seem to play a role in obesity, it is more difficult to create an experiment to figure out to what extent the thrifty gene hypothesis has on a person. It is difficult to measure “how much” natural selection occurred, whereas you can have concrete statistical data for the obesogen hypotheses and measure how much of an influence it has on obesity. Both hypothesis’ cannot explain its affects on respiration and ATP production, so it is yet again difficult to determine their mathematical influence on weight gain. However, both hypothesis’ are relevant an play important roles in the obesity epidemic.