Genetics has about the same effect on your weight as it does on your height.

Update:  6 new genes suggest obesity is in your head, not your gut - New research suggests that genes that predispose people to obesity act in the brain and that perhaps some people are simply hardwired to overeat.

We are going to take this threat slow and easy because many people object to the idea their weight may be strongly influenced by their genetics.

We now accept genetics as an explanation in many areas of life. I’ve heard a lot of people say they are worried about heart disease because it runs in their family. I’ve also heard a lot of people say they aren’t worried about cancer because it doesn’t run in their family.

But when you say someone is overweight because obesity runs in their family, many people look at you like you are crazy. People are quick to judge someone who is overweight as lazy with no self control. It wasn’t long ago when being sick meant you were possessed by evil spirits. Likewise, there’s still a lot of misunderstanding around the topic of obesity and genetics.

There isn’t an Eat a Donut Gene

Genes generally don’t work by directly causing a specific behavior. The effect of genes is much more subtle than that. So, it’s true that genes don’t make you eat in the sense that there is no gene that says “stop when you pass a donut shop and order three maple bars.” No, there’s no gene like that.

What do genes do? Technically speaking, genes make regulatory factors, signaling molecules, receptors, and enzymes that interact with your brain and influence you to have tendencies for a particular behavior.

That explanation of what genes do is a bit obscure because genetics is a complex topic, so let’s go back to the cousins as an example.

The cousins had a genetic defect that kept their bodies from making leptin. Without leptin, the brains of the cousins thought they were starving and made them very hungry. The result of being hungry is people will create and carry out a plan to find and eat food.

A cruel person could still say the genes didn’t directly force food down the cousins’ throats, but that’s not how genes work. Genes influence. And as we saw in The Power of Starvation Threat, when you are hungry enough, you will eat anything and you’ll do what it takes to get the food you need.

Your Hunger Drive is Like Your Drive to Procreate, but Stronger

 Most people will say that they want to procreate because it’s instinct. It seems clear to them that they want children because it’s a drive, not because of some rational thought like “I am going to ensure my genes survive by having children.” It’s not like that at all.

People seem to accept the drive to procreate with no problem. When you say we have a drive that means it’s genetic. We want to procreate because it’s in our genes. Sex has been made pleasurable precisely so we’ll have children.

Why is it so hard for people to apply the same sort of logic to eating? You eat because you have a strong drive to eat and that drive is implemented in your genes. The strength of the drive depends on a lot of factors, many of which we will be talking about in various threats to come.

Some people have higher sex drives than others and the difference has been found to be genetic. Though some people remain celibate through their entire life, it’s difficult because over time the drive to procreate is often stronger than the mental control needed to stay celibate.

Let’s imagine that, for some reason, someone is born with a very low sex drive. How hard would celibacy be for them? Let’s imagine another person who was born with a very high sex drive. Wouldn’t we expect celibacy to be much harder for this person? Would you be surprised to find out the person with the higher sex drive slipped-up more often than the person with the lower sex drive?

You would be right to say your sex drive is under mental control, but is your sex drive under perfect mental control? Maybe for some people, but over time it certainly isn’t for all people.

Now let’s imagine we put a person with a high sex drive, who is trying to stay celibate, into an environment where they are continually around people they find extremely attractive and who are willing partners. Wouldn’t you expect people to slip-up more in this situation? Some people will still stay celibate, but we would expect fewer people to succeed.

Why would we expect fewer people to stay celibate over time when surrounded by temptation? Because the drive to procreate is pretty strong. That’s why many people serious about celibacy minimize temptation by living in a monastery-like environment. Unfortunately, you can’t create an environment without food. You must eat to survive and food is all around you.

Drives Like Hunger Succeed Because They Operate Over Long Time Periods

One reason biological drives like breathing, sex, thirst and hunger are so successful is because drives operate over time. A drive works 24 hours a day, every day of your life.

You may be consciously motivated not to eat and you can stop yourself from eating for a while. But the drive will be operating over days, weeks, and years. When you finally give in and eat, you’ll likely think it was a loss of willpower when it was really the expression of the basic biological drive to eat.

The same discussion we’ve had about the drive to procreate also applies to the drive to eat. Only the drive to eat is stronger because without the energy provided by food you can’t do anything else.

Complicating weight loss is that you can’t stop eating or you’ll die. Having to eat continually opens you up to the possibility of overeating. And overeating is so easy when you have a strong drive to eat and you are in an environment filled with tempting food. Many of the strategies try to create a more favorable environment where it is easier not to overeat.

The Human Obesity Gene Map

I was surprised to learn that researchers maintain a website (http://obesitygene.pbrc.edu) documenting the Human Obesity Gene Map. The map identifies over 300 genes and regions of human chromosomes linked to obesity in humans. Over 70 specific gene variants are thought to cause a person to become obese. The obesity map keeps growing as researchers make discoveries using new and more powerful technologies.

There are generally three different ways genes impact on weight: by affecting appetite, overall metabolism, and how fat is stored in the body.

The most common effect of your genetic inheritance is to directly impact on how hungry you are, how full you feel, and how much food you eat. Most people still think genetics either cause a metabolic problem or somehow cause more calories to be stored as fat, but that’s not so, the biggest genetic effect is on your appetite. Human obesity is more a problem of how genes influence your brain than it is a metabolic disease.

There seem to be a large number of genes affecting obesity, but most of them have relatively small effects. You may have many small genetic contributions to your weight rather than having one major defect, like the two cousins with their leptin gene defect. This is one reason why obesity is so hard to treat: even if you figure out how to treat one problem that still leaves all the other problems in place.

Why are there so many genes controlling eating behavior and weight regulation? It gets back to survival again. Eating and weight are so crucial to survival that they need to be regulated by multiple and redundant mechanisms. If one pathway fails then another must be ready and willing to take over.

What is the Genetic Heritability of Obesity? As Much as 80%

Studies in twins, adoptees and families show as much as 80% of the variance in your weight can be attributed to genetic factors. What does this mean exactly? The whole idea of heritability is very confusing.

Heritability doesn’t mean some gene(s) is 80% responsible for obesity. What heritability means is that 80% of the variance, the difference in weight between people, is explained by genes. The actual weight for people is explained by a lot more than genetics. The environment is a key if not the most important factor in explaining your weight.

Americans are No Longer the Tallest People in the World

A fascinating example of the interaction between genes and environment is how quickly height has changed in the world. At one time Americans were the tallest people in the world. After World War II, the Dutch were on average four inches shorter than the average American. But Americans stopped growing in height in 1955 and the rest of the world is catching up.

The Dutch are now three inches taller than the average American and have become the tallest people in the world. Why the sudden change? Could their genetics have changed so quickly? Not likely.

What has changed is their environment. The Dutch are now eating better and have better health care, which has increased their average height. Yet height is still a function of genetics too. You won’t grow to be seven feet tall no matter how good your diet is if it isn’t in your genes. Genes and environment work together.

What Accounts for the Height of the Mystery Plant?

As another example of gene-environment interaction, let’s consider a species of plant called the Mystery plant. The Mystery plant is a fake plant name for this example, so please don’t go searching your plant dictionary for it.

Looking in the handy dandy genetic handbook, we read that the heritability of plant height for the Mystery plant is 80%.

For our example, picture a clump of three Mystery plants growing in the desert, next to a rock at the base of a small hill. One plant is 2 feet tall, the second plant 2 feet 2 inches tall, and the third plant is 3 feet tall.

What is the biggest factor determining the height of the plants? Is it genetics? Or is it the environment?

Think about this a bit. A desert lacks what? Water. Even if a plant has the best genetics in the world it can only get so tall without enough water. The amount of water available to the plants in the desert is probably the biggest factor in determining how tall the plants are.

If you found yourself a big wide brimmed hat and a gigantic watering can and watered only one of the plants every day, that plant would probably be taller than any of the other two plants. So, the biggest factor in determining height is the environment, not genetics.

Now, let’s assume nobody has watered the plants and all the plants are getting close to the same amount of water. What explains the difference in height between the plants? The plants aren’t the exact same height. Something must explain the difference variance between the heights of the three plants.

Recall that the heritability of height for the Mystery plant is 80%. That means 80% of the difference between the plant heights is due to genetics and 20% of the variability is due to the environment.

We have our crack team of scientists analyze the three plants and they noticed the tallest plant has a genetic mutation that makes it process water more efficiently than the other plants, so that’s why it is so much taller.

Now, what would happen if those same Mystery plants were planted in my garden where they would get all the water they need? In this new scenario, the first plant is now 5 feet tall (it was 2 feet tall), the second plant is now 4 feet 10 inches tall (it was 2 feet 2 inches tall), and the third plant is now 4 feet tall (it was 3 feet tall). It’s a complete reversal. The tallest plants are not the shortest and the shortest plants are not the tallest. What happened? What explains the differences in plant height this time?

All the plants are taller because there is so much water available. But why is the third plant when grown in my garden now the shortest plant where it was the tallest plant in the desert?

Every mutation has a cost. The genetic mutation that helped the third plant grow taller in the desert now hurts it because it is unnecessarily spending energy on efficiently processing water instead of spending the energy on growing. With so much water available, the efficient water mutation now hurts instead of helps. The other plants don’t have this mutation so they can spend all their energy on growing.

What’s interesting is how the same mutation can help in one environment and hurt in another. Even more interesting is how genetics still wasn’t the biggest explanatory factor for the height of the plants. It was their environment that provided a better explanation. So if you wanted taller plants you would change their environment, not their genetics.

How does inheritance influence weight?

We’ve looked at the big inheritance number where as much as 80% of the variance in weight can be attributed to genetic factors, but what does that mean for how your body works and how you live your everyday life?

To answer that question, John M. de Castro of the Department of Psychology, University of Texas, has done some really amazing research on the many startling ways inheritance influences how much you eat.

 Your food intake is controlled by a wide range of physiological, genetic, psychological, social and cultural influences. Each individual responds to each of these influences differently. How differently you respond to each influence depends, at least in part, on your genetics.

Here’s a list of some of the different ways heredity influences eating:

·        How much you eat.

·        The size of your meals.

·        How often you eat.

·        The amount of food you tend to have in your stomach before and after a meal. Some people tend to eat their meals with their stomach relatively empty, while others with it relatively full. This matters because if you eat when your stomach is relatively full, you eat smaller meals.

·        How hungry you need to be before you start a meal.

·        How much you will eat when hungry.

·        How hungry you will feel after you eat.

·        How many people you eat with. The more people you eat with, the more you will eat.

·        What time of the day you eat. Meals eaten later in the day are associated with higher weight.

·        How much you like the taste of a meal.

·        How much you will eat when you like the taste of a meal.

·        How much you like the taste of fat and sugar.

All these pieces fit together to influence how much you will eat. Each of us is overweight in our own way because each of us will have different internal settings for all these factors.

More Frequent Genetic Variations are Being Discovered All the Time

The genetic defect afflicting the two cousins is extremely rare, but new technologies are finding more and more weight-related genetic variations.

In April of 2006 scientists using a new gene-mapping tool found that one in 10 people carry a common genetic variation that may make it very hard for people to keep their weight down. This one genetic variation impacts one in 10 people. That’s a lot of people. You could have this genetic variation and not even know it.

University of Florida researchers found nearly 6 percent of morbidly obese children and adults have a genetic defect that keeps them feeling like their stomach is running on empty, no matter how much they have eaten. Only 6 percent of the morbidly obese were found to have this gene, but 6 percent is still a lot of people. Research reports like this are coming out all the time now.

In another report, researchers shared their discovery of genes that control where fat is stored on your body. If fat is more likely to be stored around your stomach, then you are more likely to become insulin resistant, which can lead to diabetes and obesity. This isn’t even a genetic defect. These are simply genes controlling how fat is distributed on your body.

Scientists from the Peninsula Medical School, Exeter, and the University of Oxford found people with two copies of a particular gene have a 70% higher risk of being obese than those with no copies. Over 16% of people were found to have both copies of this gene. Are you one of these people? If so, your chances of being overweight just skyrocketed.

Some genetic influences are because of a defect: something is broken. But most of the genetic influences are genetic variations and it’s just how you are.

The Dynamic Duo of Genes and Environment in Depression

We’ve seen how genes and the environment can interact to affect your weight. Another interesting example of the subtle interplay of genes and environment can be found in clinical depression. The connection between genes and the environment is hard to make, so I am including this example to help you build up a better understanding of the interaction between genes and the environment, not because it relates directly to weight.

Researchers found that a variation in a single gene combined with major life stress more than doubles a person’s chance of becoming clinically depressed. Some examples of stressful events are losing a job or the death of a loved one.

Not all people become seriously depressed after experiencing serious stress events. Why not? One difference between the group that became depressed and the group that didn’t could be found in their serotonin transporter genes. Serotonin is a chemical messenger in the brain, but don’t worry too much about what it is, how it affects you is more important.

The gene for the serotonin transporter comes in a short and a long form. Each person carries a copy of the gene from each of their parents, so you have two copies of the gene.

Forty-three percent of those who had two copies of the short form developed depression while only 17 per cent of those with two long copies became depressed. And those with two long copies seem to be protected from stress as they had the same rates of depression regardless of how many major life stress events they experienced.

What does all this mean? There are several important take home messages in this example.

The first take home message is that it’s not just your genes or the environment. It’s your genes and the environment. If you didn’t have the genes that made you susceptible to stressful events then your chances of becoming clinically depressed are a lot less. And if you lived a life without a lot of stressful events, or if you somehow could react more calmly to stressful events, then it wouldn’t matter if you had the genes. It takes both genes and the environment to bring about your reactions to events.

The second take-home message is that genes and the environment are still not destiny. Having both the genes and the stressful events only increased your chances of becoming clinically depressed. Not everyone became clinically depressed. Why not? Good question. Hopefully scientists will be able to answer that some day.