When those genes no longer fit

If you ask most folks why some of us are obese, they will answer that it’s because overweight people have eaten too much of the wrong foods and not exercised enough. If prompted, they might expand their response by saying that people who come from families with overweight members will usually have more trouble maintaining a healthy weight. It seems to me that just about covers our state-of-the-art understanding of obesity.

You can argue that there is always new information coming out from experiments on genetically altered mice. And, the recently appreciated relationship between sleep deprivation and being overweight sounds interesting. But it still boils down to the simple equation of too much energy in and too little burned.

In 2007, it was discovered that a variant of a gene known as FTO was closely linked to excess weight gain in humans. Individuals with one copy of the gene were on average 3.5 pounds heavier than were those without the gene. Those people with a double copy of the variant gene were 7 pounds heavier and 50% more likely to be obese than was the general population.

It looked like the FTO gene might be one of the answers beyond the simplicity of too much consumption and too little expenditure. But why would the gene suddenly become more prevalent over the last 5 or 6 decades that obesity has become epidemic in America? It seemed unlikely that this shift could occur in such a short time frame.

A recently published study in Proceedings of the National Academy of Sciences (PNAS 2014 [doi: 10.1073/pnas.1411893111]) suggests another more plausible explanation. Using data from the venerable and ongoing Framingham Heart Study, the researchers found that the FTO variant became a risk factor only after World War II. In other words, people with the FTO variant born prior to 1942 weren’t any more likely to be overweight than the rest of the population.

What has changed since the 1940s? Our diet has shifted toward more processed and fried foods. And, our lives and our jobs have become more sedentary. Television crept into our living rooms in the 1950s and into our bedrooms in the 1970s.

The FTO gene variant may have been advantageous to humans in lean times when the heavier of us were more likely to survive long periods of starvation. But now here in the land of fries and soft drinks, the gene has become hazardous to our health. We now look (and are) fat wearing the same genes that seemed to fit us so well a century ago.

We must have sympathy for those of us who have a gene that makes us more vulnerable when food is plentiful, and technology has made it easier to survive with very little energy expenditure. It is tempting to hope that someday scientists will find a way to alter the offending genes to help those cursed to carry them. But this kind of manipulation must be considered cautiously because a natural or man-made catastrophe on a global scale could once again make this gene advantageous.

We must face the fact that it is the environment in which we live – an environment that we have altered and can continue to alter – that is the primary driver of the obesity epidemic. One wonders whether we are experiencing other epidemics analogous to the FTO/obesity story.

Attention-deficit/hyperactivity disorder (ADHD) comes to mind. Some observers feel that a short attention span and impulsivity may have been advantageous when we were hunter-gatherers. The disadvantages of those traits were just a nuisance when having a formal education was merely optional for success. However, we have now trapped those who carry these traits in a one-size-fits-all educational system and sleep deprived them with a combination of electric lights and electronic distractions, to name just a few of the environmental changes that we have imposed.

Maybe it’s not the genes, but the environment that is the issue. The problem is that we haven’t found the genetic variant(s) that might allow us to answer these kinds of questions about ADHD.

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “Coping with a Picky Eater.” E-mail him at [email protected].

If you ask most folks why some of us are obese, they will answer that it’s because overweight people have eaten too much of the wrong foods and not exercised enough. If prompted, they might expand their response by saying that people who come from families with overweight members will usually have more trouble maintaining a healthy weight. It seems to me that just about covers our state-of-the-art understanding of obesity.

You can argue that there is always new information coming out from experiments on genetically altered mice. And, the recently appreciated relationship between sleep deprivation and being overweight sounds interesting. But it still boils down to the simple equation of too much energy in and too little burned.

In 2007, it was discovered that a variant of a gene known as FTO was closely linked to excess weight gain in humans. Individuals with one copy of the gene were on average 3.5 pounds heavier than were those without the gene. Those people with a double copy of the variant gene were 7 pounds heavier and 50% more likely to be obese than was the general population.

It looked like the FTO gene might be one of the answers beyond the simplicity of too much consumption and too little expenditure. But why would the gene suddenly become more prevalent over the last 5 or 6 decades that obesity has become epidemic in America? It seemed unlikely that this shift could occur in such a short time frame.

A recently published study in Proceedings of the National Academy of Sciences (PNAS 2014 [doi: 10.1073/pnas.1411893111]) suggests another more plausible explanation. Using data from the venerable and ongoing Framingham Heart Study, the researchers found that the FTO variant became a risk factor only after World War II. In other words, people with the FTO variant born prior to 1942 weren’t any more likely to be overweight than the rest of the population.

What has changed since the 1940s? Our diet has shifted toward more processed and fried foods. And, our lives and our jobs have become more sedentary. Television crept into our living rooms in the 1950s and into our bedrooms in the 1970s.

The FTO gene variant may have been advantageous to humans in lean times when the heavier of us were more likely to survive long periods of starvation. But now here in the land of fries and soft drinks, the gene has become hazardous to our health. We now look (and are) fat wearing the same genes that seemed to fit us so well a century ago.

We must have sympathy for those of us who have a gene that makes us more vulnerable when food is plentiful, and technology has made it easier to survive with very little energy expenditure. It is tempting to hope that someday scientists will find a way to alter the offending genes to help those cursed to carry them. But this kind of manipulation must be considered cautiously because a natural or man-made catastrophe on a global scale could once again make this gene advantageous.

We must face the fact that it is the environment in which we live – an environment that we have altered and can continue to alter – that is the primary driver of the obesity epidemic. One wonders whether we are experiencing other epidemics analogous to the FTO/obesity story.

Attention-deficit/hyperactivity disorder (ADHD) comes to mind. Some observers feel that a short attention span and impulsivity may have been advantageous when we were hunter-gatherers. The disadvantages of those traits were just a nuisance when having a formal education was merely optional for success. However, we have now trapped those who carry these traits in a one-size-fits-all educational system and sleep deprived them with a combination of electric lights and electronic distractions, to name just a few of the environmental changes that we have imposed.

Maybe it’s not the genes, but the environment that is the issue. The problem is that we haven’t found the genetic variant(s) that might allow us to answer these kinds of questions about ADHD.

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “Coping with a Picky Eater.” E-mail him at [email protected].

If you ask most folks why some of us are obese, they will answer that it’s because overweight people have eaten too much of the wrong foods and not exercised enough. If prompted, they might expand their response by saying that people who come from families with overweight members will usually have more trouble maintaining a healthy weight. It seems to me that just about covers our state-of-the-art understanding of obesity.

You can argue that there is always new information coming out from experiments on genetically altered mice. And, the recently appreciated relationship between sleep deprivation and being overweight sounds interesting. But it still boils down to the simple equation of too much energy in and too little burned.

In 2007, it was discovered that a variant of a gene known as FTO was closely linked to excess weight gain in humans. Individuals with one copy of the gene were on average 3.5 pounds heavier than were those without the gene. Those people with a double copy of the variant gene were 7 pounds heavier and 50% more likely to be obese than was the general population.

It looked like the FTO gene might be one of the answers beyond the simplicity of too much consumption and too little expenditure. But why would the gene suddenly become more prevalent over the last 5 or 6 decades that obesity has become epidemic in America? It seemed unlikely that this shift could occur in such a short time frame.

A recently published study in Proceedings of the National Academy of Sciences (PNAS 2014 [doi: 10.1073/pnas.1411893111]) suggests another more plausible explanation. Using data from the venerable and ongoing Framingham Heart Study, the researchers found that the FTO variant became a risk factor only after World War II. In other words, people with the FTO variant born prior to 1942 weren’t any more likely to be overweight than the rest of the population.

What has changed since the 1940s? Our diet has shifted toward more processed and fried foods. And, our lives and our jobs have become more sedentary. Television crept into our living rooms in the 1950s and into our bedrooms in the 1970s.

The FTO gene variant may have been advantageous to humans in lean times when the heavier of us were more likely to survive long periods of starvation. But now here in the land of fries and soft drinks, the gene has become hazardous to our health. We now look (and are) fat wearing the same genes that seemed to fit us so well a century ago.

We must have sympathy for those of us who have a gene that makes us more vulnerable when food is plentiful, and technology has made it easier to survive with very little energy expenditure. It is tempting to hope that someday scientists will find a way to alter the offending genes to help those cursed to carry them. But this kind of manipulation must be considered cautiously because a natural or man-made catastrophe on a global scale could once again make this gene advantageous.

We must face the fact that it is the environment in which we live – an environment that we have altered and can continue to alter – that is the primary driver of the obesity epidemic. One wonders whether we are experiencing other epidemics analogous to the FTO/obesity story.

Attention-deficit/hyperactivity disorder (ADHD) comes to mind. Some observers feel that a short attention span and impulsivity may have been advantageous when we were hunter-gatherers. The disadvantages of those traits were just a nuisance when having a formal education was merely optional for success. However, we have now trapped those who carry these traits in a one-size-fits-all educational system and sleep deprived them with a combination of electric lights and electronic distractions, to name just a few of the environmental changes that we have imposed.

Maybe it’s not the genes, but the environment that is the issue. The problem is that we haven’t found the genetic variant(s) that might allow us to answer these kinds of questions about ADHD.

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “Coping with a Picky Eater.” E-mail him at [email protected].