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Is obesity caused by a genetics? And what kind of genes are associated with obesity?

-A curious adult from India

Genes don’t usually cause obesity. But they can sometimes make it harder for some people to keep a healthy weight.

Some genes can affect obesity by influencing what decisions we make. If you have a set of genes that makes you crave sugar more than your friend, you may struggle with your weight more than he does. Or if your genes make you hate exercise, you might be more likely to end up heavier than you’d like to be. 

Other genes that can affect obesity control how our bodies use and store energy from food. Maybe your genes give your body a fast metabolism so your body doesn’t like to keep a lot of fat or muscle on your body. This means you quickly lose fat making you less likely to have weight issues.

What Factors Cause Obesity?

Genes can make us more likely to be obese for these reasons. But there are other factors that also play a big role in making us obese. These include things like how much food is available and how often you get off the couch.

These “environmental factors” have changed quickly over a generation. The sizes of our meals keep growing. We also spend more time sitting watching TV or using a computer. 

Public health experts think these factors are more important than the genetic ones for obesity. Which makes perfect sense.

Obesity has only become a problem in the last few decades. Genetics takes way longer than that to change. But as I said before, genes do make some people more likely to overeat.

And there are some rare cases where genes play a much stronger role. One of these is a genetic disease called Prader-Willi syndrome.

These folks have severe weight gain along with other symptoms. The effects are so strong that little can be done to keep their weight down.

But they are the exception. For the most part, the rest of us are more or less likely to be obese because of what we do and how much we eat. 

Why Does Obesity Happen?

If being obese is unhealthy, why are our bodies able to get overweight in the first place? Why doesn’t our body choose to not take in more food once it has enough? One of the leading theories called the “thrifty gene hypothesis” tries to answer this.

Long ago, before we were farmers, food was hard to come by during some parts of the year. Long winters and/or droughts meant that people had to be ready to starve some of the time.

Back then it helped to put on a lot of weight when there was lots of food around. You could then burn that fat off during the hard times. This is kind of like what squirrels and bears do today.

The “thrifty gene hypothesis” says that we have genes to put on fat in the good times because of this advantage. But nowadays, we always have access to food.

We evolved to thrive in one environment but now things have changed. We now have access to food almost everywhere, anytime. These genes are now a disadvantage if they keep us overweight year-round.

Some people have had more trouble getting food in the past than others. Some of these populations are now more likely than other people to be overweight. Scientists say that the “thrifty gene hypothesis” explains their higher rates of obesity.

For example, the Pima people in the deserts of Arizona have one of the highest rates of type 2 diabetes. The Pima people used to eat a light diet of vegetables like beans and squash. 

But 100 years ago, this all changed when their river was diverted. They had to switch to a modern diet. Since then, obesity in the Pima people has become a serious problem.

Are There “Obesity Genes” in Humans?

Geneticists are studying the Pima people and other groups to find genes that add to the risk of obesity. However, this research is harder than it might sound.

If two obese parents have an obese child, is this because of genetics? Or is it because the child picks up the eating habits of the parents?

How should we define whether someone is obese or not? Should we control the diets of people in these studies?

Despite these problems, there are a few genes that are correlated with high body mass index (BMI). However, they add very little to obesity risk. This means that if you knew that someone had a mutation in these genes, it won’t really predict very well if that person is actually obese.

Geneticists think that there are “obesity genes” that interact with others to add to obesity risk. Some of these genes might do nothing on their own. This makes it even harder to find them. Geneticists are still studying our genes to learn more about obesity. 

Are There “Obesity Genes” in Other Animals?

In lab animals such as mice, each gene can be modified in an experiment to study what they do. A gene called ob is a famous example.

Mice with mutations of the ob gene cannot make a hormone called leptin. Leptin signals to the mouse’s brain that it is full and should stop eating. Mice with copies of ob that don’t work properly can weigh up to three times as much as a healthy mouse! 

Since humans are genetically very similar to mice, scientists looked at the human version of the ob gene, called LEP. LEP is also responsible for producing leptin.

People without a working copy of LEP find it hard to stop eating. However, these mutations in LEP have been seen in fewer than ten people. So a gene like LEP can’t be responsible for obesity for most people.

In summary, genetics isn’t enough to cause obesity alone. There are a few exceptions but they are rare.

But this doesn’t mean genes don’t contribute at all. There are definitely genes that make it harder for some people to lose weight than others.

Our genes encode our ability to become obese and how easy it is for us to be obese. But whether or not someone is obese is actually mostly up to how much they decide to eat and exercise. 

By Alex Han, Stanford University


Some would be able to resist this chocolate lava cake better than others! (Flickr)


Changes in what we do have probably had a bigger impact on the obesity problem than our genes. (Flickr)


Mice without a working version of the ob gene become very obese like the one on the left. (Wikimedia Commons)