Obesity genes cause rapid growth in children, study finds

June 05, 2012
 
Dr. Daniel Belsky

Dr. Daniel Belsky

A rapid growth spurt in childhood could foretell obesity in adulthood.

 
According to a new study authored by a UNC Gillings School of Global Public Health graduate in the Archives of Pediatric and Adolescent Medicine (a Journal of the American Medical Association Network publication), children who are genetically predisposed to obesity experience a growth spurt in early childhood that leads to obesity later in life.
 
The longitudinal study, which followed 1,032 children for 38 years, shows that children who were genetically predisposed to obesity were less likely to be obese in adulthood if they did not have a growth spurt in childhood.
 
“The so-called obesity genes turned out to be rapid early growth genes,” explained study author Daniel Belsky, PhD. Belsky graduated from the UNC public health school’s Department of Health Policy and Management in May.
 
Obesity is a costly and serious health issue that’s on the rise. Though many researchers know that obesity is a problem, studies like Belsky’s help illuminate how a genetic risk causes an outcome. In this case, the rapid growth in childhood (or, conversely, normal growth) was a predictive factor for obesity.
 
“Our findings affirm the importance of early intervention to address the obesity epidemic,” said Belsky, currently a postdoctoral fellow at the Institute for Genome Sciences and Policy at Duke University. “Our findings also highlight the need for a life course, longitudinal approach to study the genetic etiology of obesity.”
 
Though obesity long has been associated with heritability and genetic risk factors, this is the first study to show that children with high genetic risk scores for obesity had higher body mass indexes (BMIs) between the ages of three and 38. Children with high genetic risk scores were 1.9 times more likely to be chronically obese, as well.
 
Belsky’s subjects were part of the Dunedin Multidisciplinary Health and Development Study, which collects data on children from a variety of socioeconomic and health background born in Dunedin, New Zealand, between April 1972 and March 1973.
 
The genetic risk factors for obesity were linked to 32 known single-nucleotide polymorphisms (SNPs), or genetic markers in DNA structures. These 32 SNPs were associated with obesity in thousands of adults who participated in genome-wide association studies (GWAS). Children with these risk factors were more likely to become obese, regardless of whether or not their parents had normal BMIs.
 

Share

 
 
UNC Gillings School of Global Public Health contact: Linda Kastleman, communications editor, (919) 966-8317 or linda_kastleman@unc.edu.