For the first time, scientists have isolated mutations at two gene locations that seem to predispose children to becoming obese.
"We see a clear genetic signature to childhood obesity, showing that there is more than just an environmental component to this disease," Struan Grant, senior author of the research, said at an April 5 press conference.
Although known genes have been linked to adult obesity and also to extreme forms of childhood obesity, the newly identified genes confer only a modest risk of developing common childhood obesity. But they are "very common in the population," Grant added in a telephone interview.
Grant is associate director of the Center for Applied Genomics at the Children's Hospital of Philadelphia Research Institute. His research was published online April 8 in Nature Genetics.
Obesity has become a public health crisis of global proportions, affecting not only adults but also, increasingly, children.
"In the U.S., the prevalence of childhood obesity has tripled in recent decades and related health care costs have quadrupled," said Dr. Karen Winer, a program officer in the endocrinology, nutrition and growth branch of the Eunice Kennedy Shriver U.S. National Institute of Child Health and Human Development, which funded the study.
Clear environmental factors such as changing nutrition and reduced physical exercise have played a role in the childhood obesity crisis, but no genes had, until now, been identified.
The authors of this study pooled results from 14 genome-wide association studies conducted in the United States, Canada, Australia and Europe, involving a total of 5,530 children who were obese and 8,318 non-obese kids ("controls"), all of European descent.
This is the largest collection of DNA related to childhood obesity in the world, Winer said.
Obesity was defined as being above the 95th percentile in body mass index (a measurement that takes into account height and weight) while the healthy controls were all in the leaner half of the population.
When data was combined, two genes stood out: OLFM4 and HOXB5. The genes also showed signals in groups of extremely obese children.
And the genes were identifiable but weaker in adults, indicating that "these variants are conferring their risk early on in life and are really impactful in the first years of life," Grant said at the press conference.
Scientific literature to date indicates that the genes may be operating in the gut.
"We would look probably in that tissue area to see how it was conferring risk," Grant said at the press conference.
It's possible, for instance, that the genes may interact with food, he said.
Eric Schadt, chairman of the department of genetics and genomic sciences at Mount Sinai School of Medicine in New York City, said: "Absolutely, this is a disease that has genetic components and very strong environmental components and likely very strong genetic-by-environmental components. It's very, very complicated. We're only scratching the surface of genetic determinations of childhood obesity."
Once scientists learn more about the genes and how they work, they may lead to new treatments, added Schadt, who was not involved with the study.
SOURCES:
Eric Schadt, Ph.D., professor and chairman, department of genetics and genomic sciences, Mount Sinai School of Medicine, New York City; April 5, 2012, press conference with Struan F.A. Grant, Ph.D., associate director, Center for Applied Genomics, Children's Hospital of Philadelphia Research Institute and Karen Winer, M.D., program officer, endocrinology, nutrition and growth branch, Eunice Kennedy Shriver U.S. National Institute of Child Health and Human Development; April 8, 2012, Nature Genetics, online
"We see a clear genetic signature to childhood obesity, showing that there is more than just an environmental component to this disease," Struan Grant, senior author of the research, said at an April 5 press conference.
Although known genes have been linked to adult obesity and also to extreme forms of childhood obesity, the newly identified genes confer only a modest risk of developing common childhood obesity. But they are "very common in the population," Grant added in a telephone interview.
Grant is associate director of the Center for Applied Genomics at the Children's Hospital of Philadelphia Research Institute. His research was published online April 8 in Nature Genetics.
Obesity has become a public health crisis of global proportions, affecting not only adults but also, increasingly, children.
"In the U.S., the prevalence of childhood obesity has tripled in recent decades and related health care costs have quadrupled," said Dr. Karen Winer, a program officer in the endocrinology, nutrition and growth branch of the Eunice Kennedy Shriver U.S. National Institute of Child Health and Human Development, which funded the study.
Clear environmental factors such as changing nutrition and reduced physical exercise have played a role in the childhood obesity crisis, but no genes had, until now, been identified.
The authors of this study pooled results from 14 genome-wide association studies conducted in the United States, Canada, Australia and Europe, involving a total of 5,530 children who were obese and 8,318 non-obese kids ("controls"), all of European descent.
This is the largest collection of DNA related to childhood obesity in the world, Winer said.
Obesity was defined as being above the 95th percentile in body mass index (a measurement that takes into account height and weight) while the healthy controls were all in the leaner half of the population.
When data was combined, two genes stood out: OLFM4 and HOXB5. The genes also showed signals in groups of extremely obese children.
And the genes were identifiable but weaker in adults, indicating that "these variants are conferring their risk early on in life and are really impactful in the first years of life," Grant said at the press conference.
Scientific literature to date indicates that the genes may be operating in the gut.
"We would look probably in that tissue area to see how it was conferring risk," Grant said at the press conference.
It's possible, for instance, that the genes may interact with food, he said.
Eric Schadt, chairman of the department of genetics and genomic sciences at Mount Sinai School of Medicine in New York City, said: "Absolutely, this is a disease that has genetic components and very strong environmental components and likely very strong genetic-by-environmental components. It's very, very complicated. We're only scratching the surface of genetic determinations of childhood obesity."
Once scientists learn more about the genes and how they work, they may lead to new treatments, added Schadt, who was not involved with the study.
SOURCES:
Eric Schadt, Ph.D., professor and chairman, department of genetics and genomic sciences, Mount Sinai School of Medicine, New York City; April 5, 2012, press conference with Struan F.A. Grant, Ph.D., associate director, Center for Applied Genomics, Children's Hospital of Philadelphia Research Institute and Karen Winer, M.D., program officer, endocrinology, nutrition and growth branch, Eunice Kennedy Shriver U.S. National Institute of Child Health and Human Development; April 8, 2012, Nature Genetics, online
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