Study Suggests Genes Play a Role in Early Life Weight Gain
By Brenda Goodman, MA
WebMD Health News
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Reviewed by Louise Chang, MD
April 8, 2012 -- An international team of researchers says they've found at least two new gene markers that appear to increase the risk for common childhood obesity.
Little is known about the gene markers, which sit on chromosomes 13 and 17. But they are positioned close to and within genes that are thought to be involved in how the gut functions.
What's more, the markers do not appear to be active in obese adults, leading researchers to conclude that they exert their influence within the first years of life.
"We see a clear genetic signature to childhood obesity, showing that there's more than just an environmental component to the disease," says researcher Struan F.A. Grant, PhD, associate director of the Center for Applied Genomics at The Children's Hospital of Philadelphia, at a news conference.
The study is published in the journal Nature Genetics.
The discovery of a genetic component to childhood obesity does not mean a child who inherits these gene markers is fated to be fat.
Instead, the new markers help explain why obesity runs in families. They may also help explain why some kids, given the roughly the same diets and patterns of physical activity as their peers, may pack on pounds while others stay relatively slim.
"If we can understand how inherited risk factors change susceptibility to obesity -- what's different about the biology of people who are resistant to obesity vs. those who are susceptible -- we would get clues for new therapies or interventions that could be safer and more effective than what is currently available," says researcher Joel Hirschhorn, MD, PhD, director of the Center for Basic and Translational Obesity Research at Children's Hospital Boston, in an email.
"It's very, very exciting," says Nancy Copperman, MS, RD, director of public health initiatives for the North Shore-LIJ Health System in Great Neck, N.Y.
Tracking Genes Linked to Childhood Obesity
For the study, researchers took a new look at genetic information collected from more than 5,500 obese children and 8,300 normal-weight kids in the U.S., Canada, Europe, and Australia.
Advanced gene mapping techniques pinpointed seven markers that were more common in the obese children than in the lean kids. Those risk areas had also previously been linked to adult obesity.
In addition, they identified two new risk areas that appeared to be unique to childhood obesity. One area was near a gene on chromosome 13. The other was within a gene on chromosome 17. In addition, they found a degree of evidence to support the possible role of two other gene markers.
Assuming the genes act on their own, researchers say inheriting the marker near the gene on chromosome 13 would increase a child's odds of becoming obese by 22%. A child with the other marker would have a 14% increased risk of obesity.
Researchers Suspect a Role in Gut Function
At least three newly identified genes seem to work in the digestive system.
The protein compound made by one of the genes, for example, is known to turn off the body's defenses against H. pylori bacteria, which are a cause of stomach ulcers. H. pylori infection, researchers note, is more common in obese people.
In a news conference, Karen Winer, MD, a medical officer at the Eunice Kennedy Shriver National Institute of Child Health & Human Development (NICHD), called the study "groundbreaking work" because it involved the largest collection of genetic material ever compiled to investigate common childhood obesity. The NICHD funded the study.
Previous gene studies had focused on extreme childhood obesity, which is usually associated with defects in a single determining gene, like the inherited Prader-Willi syndrome.
"Common obesity is a very complex disease -- not only genetic or environmental (high-fat diet, inactive lifestyle) -- but an interaction between these two factors," says William S. Garver, PhD, an assistant professor in the department of biochemistry and molecular biology at the University of New Mexico Health Sciences Center in Albuquerque.
Garver studies genes related to obesity, but he was not involved in the research.
"It is likely that most common obesity genes interact with an environmental factor or other 'modifying genes' to promote weight gain," he says in an email to WebMD.
There's still a lot to be learned about the genetic components of childhood obesity. Taken together, Grant says all the markers known to be associated with the condition probably still only account for 5% to 10% of a person's genetic risk.
SOURCES: Bradfield, J. Nature Genetics, April 8, 2012. News release, Nature Genetics. Karen Winer, MD, a medical officer in the Endocrinology, Nutrition and Growth Branch, Eunice Kennedy Shriver National Institute of Child Health & Human Development, National Institutes of Health, Bethesda, Md. Struan F.A. Grant, PhD, associate director, The Center for Applied Genomics, The Children's Hospital of Philadelphia, Pennsylvania. Joel Hirschhorn, MD, PhD, director, center for basic and translational obesity research, Children's Hospital Boston, Massachusetts. Nancy Copperman, MS, RD, director of public health initiatives, North Shore-LIJ Health System, Great Neck, N.Y. William S. Garver, PhD, assistant professor, department of biochemistry and molecular biology, The University of New Mexico Health Science Center, Albuquerque, N.M.
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