Genetics may play a role in how infants respond to food and subsequent obesity risk, findings from two studies suggest.
In the first study, Clare Lewellyn, PhD, of University College London, and colleagues found that infants with a higher genetic risk score based on previous genome-wide association studies (GWAS) had reduced satiety and higher BMI than those with a lower risk profile.
A second study led by Jane Wardle, PhD, also of University College London, involving newborn sets of twins showed that the twin with higher responsiveness to food and lower satiety gained more weight than the twin who was more easily sated. Both studies were published online in JAMA Pediatrics.
“Identifying factors that promote or protect against weight gain could help identify targets for obesity intervention and prevention in future,” Wardle said in a press release.
She and colleagues analyzed data from dizygotic twin pairs who participated in the Gemini longitudinal study in the United Kingdom. The study included 172 twin pairs who had different scores on satiety responsiveness, and 121 pairs who were discordant for responsiveness to food.
At six months, twins who were more responsive to food were 654 grams heavier, and those with lower satiety were 637 grams heavier than their less hungry and more easily sated siblings, the researchers found. At 15 months, these differences increased to 991 grams and 918 grams, respectively.
In other study, Llewellyn and colleagues conducted a cross-sectional analysis of a cohort of U.K. twins that included 2,258 unrelated children. One child from each twin pair was selected and genotyped for 28 obesity-associated variants that had been identified in previous GWAS to determine a genetic risk score.
Children with higher genetic risk scores had reduced satiety responsiveness and a higher BMI and waist circumference than those with lower scores, they found.
Compared with the lowest quartile, more children in the top 25% were overweight. Furthermore, satiety responsiveness appeared to significantly mediate associations between childrens’ risk score and adiposity (P=0.006).
“This suggests that satiety sensitivity could be targeted for pharmacological and behavioral interventions, to prevent or treat obesity,” Llewellyn said in a press release. “For example, children with lower satiety sensitivity could be taught techniques that might improve their fullness signals when eating, such as slowing their eating speed.”
In an accompanying editorial, Daniel Belsky, PhD, of Duke University, praised the two studies for identifying potential markers that could help target obesity-prevention interventions, but added that more research is necessary.
“Studies are needed that follow up children from early life into adolescence and adulthood to test whether appetite measured in infancy and childhood is predictive of later obesity,” Belsky wrote.
- van Jaarsveld CHM et al “Appetite and growth: a longitudinal sibling analysis.” JAMA Pediatr. 2014; doi: 10.1001/jamapediatrics.2013.4951.
- Llewellyn CH et al “Satiety mechanisms in genetic risk of obesity.” JAMA Pediatr. 2014; doi: 10.1001/jamapediatrics.2013.4944.
- Belsky DW. JAMA Pediatr. 2014; doi: 10.1001/jamapediatrics.2013.5291.