Scientists explore risk factors for childhood obesity to learn what makes some children gain more weight than others.
Scientists are getting even more insight into early predictors of obesity, according to two new studies in the Journal of the American Medical Association.
The first study shows that infants with heartier appetites grow more quickly from birth through 15 months old, which Cornelia H.M. van Jaarsveld, Ph.D., of University College London, believes may put them at a higher risk for obesity.
A second study finds that low responsiveness to the feeling of being full seems to be one predictor of childhood weight gain in kids with a genetic predisposition to obesity, according to Clare H. Llewellyn, Ph.D., also of University College.
In the first study, researchers looked at data from non-identical, same-sex twins born in the U.K. in 2007. The babies’ weights were measured from the time they were born through the age of 15 months.
The scientists found that babies with higher food responsiveness, or FR (those who ate in response to the smell or sight of food), and lower satiety responsiveness, or SR (those who ate more before feeling full), grew faster than their siblings.
Those with higher FR were about 1.4 pounds heavier than their sibling at six months and approximately 2.1 pounds heavier at 15 months. The data were similar for SR.
“Infants with larger appetites may be at increased risk for rapid weight gain in the current obesogenic environment and might be targeted in strategies to prevent obesity in susceptible individuals,” the authors wrote.
Christopher Ochner, Ph.D., an assistant professor of pediatrics and psychiatry at the Icahn School of Medicine at Mount Sinai in New York City, said the study was interesting because it looked into both genetics and the mothers’ dietary habits during pregnancy.
Unless the authors followed up with these babies to see if they grew up to be overweight or obese, however, he said it’s a leap to say that young children with heartier appetites are at an increased risk for developing obesity.
“It’s an interesting theory, but that’s all it is at this point,” he said, adding that while few clinicians would recommend putting babies on a diet, nearly all of them would likely recommend feeding children a relatively standard amount and not overfeeding them even if they cry or beg for food.
Stephen Cook, M.D., a pediatrician at the Golisano Children’s Hospital at the University of Rochester Medical Center in New York, weighed in as well.
“I’ve had a number of parents describe their infant to me as ‘greedy’ and ‘always seems hungry,’” he said. “I would hope these questions might be used clinically to help parents perceive how their child is eating or feeding.”
Cook said the study’s population may be more homogeneous than the diverse population in the U.S. “I would want to know how parents from different racial and ethnic backgrounds perceive and respond to their infants feeding,” Cook added.
In the second study, researchers wanted to look at the links between a genetic predisposition to obesity, body fat, and satiety responsiveness. They crafted a multi-gene risk score, known as a polygentic risk score (PRS), of 28 obesity-related genes in 2,258 unrelated children. Those with a higher PRS had a greater genetic predisposition to obesity.
According to their data, a higher PRS was linked to lower satiety responsiveness, as well as a higher body mass index (BMI) score and a bigger waist circumference. More children in the top 25 percent of the PRS scale were overweight than in the lowest 25 percent.
The researchers say their conclusions support the notion that common obesity risk genes influence body fat in part by affecting appetite. This may explain how environments and genes interact to determine how much weight a person will gain. People who are less responsive to internal satiety cues, or feelings of fullness, due to their genetic makeup may be more likely to eat more and gain weight.
“Therefore, satiety responsiveness is a potential target for behavioral or pharmacological interventions,” the authors wrote.
However, Ochner said the study doesn’t answer the question of whether lower satiety responsiveness plays a causal role or is just one of many factors that affect obesity risk. Even if it is causal, there’s no telling how large an effect it has.
“It could be just one of a ton of correlates, all of which could be potential explanatory or moderating factors, or just happen to be correlated,” Ochner said. “I don’t want to take anything away from the study—it was probably well done and maybe provides valuable evidence—but causal evidence is required before we start making inferences about how genes cause obesity.”