Children carrying a genetic variant of the FTO gene are prone to eat more calories, with each copy of the variant resulting in approximately 65 more calories being ingested at each meal, a new study shows.
These findings suggest genetic factors affect eating behavior and food preferences in children, which may help develop public health strategies to halt the onset of child’s obesity.
“Early identification of the physiology and behaviors that constitute early risk factors for subsequent weight gain will help inform best practices for intervention and prevention of obesity in children,” Michael Rosenbaum, MD, said in a press release. Rosenbaum is a professor of pediatrics and medicine at Columbia University Irving Medical Center (CUIMC) in New York City, and senior author of the study.
The study “The FTO Gene and Measured Food Intake in 5‐to 10‐Year‐Old Children Without Obesity” was published in the journal Obesity.
A single change in one nucleotide (the building blocks of DNA sequences) in the FTO gene, previously identified as rs9939609, has been linked to obesity. This association is believed to be mainly due to increased caloric intake. However, until now, it was not known whether the increased caloric intake was a consequence of obesity, or whether it existed before the onset of obesity.
CUIMC researchers and collaborators decided to explore the impact of genetic variability of the FTO gene in children’s dietary intake. To do so, they recruited 122 non-obese children, aged 5 to 10, within the New York City metropolitan area. Children with diabetes or eating disorders, with severe food allergies, or on medication, were excluded from the study.
Parents of the children were interviewed in person about the children’s characteristics, height, weight, and body composition. Researchers collected data on these parameters during the children’s first visit to the lab. They also collected psychiatric information and dietary habits of each child, and evaluated families’ histories of body weight and its associated comorbidities.
Researchers also collected saliva samples from each child, which they then used to analyze the number of the genetic variant of the FTO gene they carried and correlated it with their caloric intake.
On a second visit to the lab, the team once again measured the children’s height and weight. The parents were advised not to allow their child to have anything to eat or drink, except for water, after 10 p.m. the previous night.
The children were then given a breakfast consisting of cereals (Cheerios or Kellogg’s Corn Flakes) and whole milk. Portion sizes were adjusted for energy expenditure based on age, height, and weight. Three-and-a-half hours later, during which children were advised to refrain from eating or drinking (except for water), they were given a buffet lunch consisting of 28 food and beverage items, such as sandwiches, chicken nuggets, fruits and vegetables, salty snacks, and desserts.
Researchers told them they could eat as much as they would like, and after the meal was over there was an accounting of what they had eaten and how much.
The team found a significant effect on the child’s genetic pattern and their caloric intake, even after adjusting their body mass index (BMI). Each FTO copy with the obesity-related mutation led to a consumption of approximately more 65 calories per meal.
“Even though 65 calories is not a lot per se, if this pattern generalized to multiple meals per week or day, this increased caloric intake can add up over time and may contribute to gaining excess weight,” said Rosenbaum.
In addition, they found that in non‐African American children the gene version linked to obesity could lead to an additional caloric intake of around 80 calories, further demonstrating that children may exhibit certain behaviors before the onset of obesity.
“The influence of genotype dose on intake adds support to the hypothesis that FTO genotypic associations with body weight are mediated by effects on food intake more so than on energy expenditure,” researchers wrote.
This “research sheds light into possible behavioral phenotypes for childhood obesity before obesity has developed,” said Tanja Kral, PhD, associate professor in the School of Nursing and the Perelman School of Medicine at the University of Pennsylvania. “Once identified, it will enable us to design personalized behavioral interventions that target the individual components of the [obesity manifestation].”
Further research is needed to understand which behaviors may signal the risk of weight gain and whether these children can be identified for early intervention strategies to reduce the risk for developing obesity.
“The ultimate goal is to prevent the at-risk child or the child who has obesity from becoming an adult with obesity,” said Rosenbaum.