Infants with a heartier appetite grew more rapidly up to age 15 months, which may be an increased risk for obesity, in a study of twins by Cornelia H.M. van Jaarsveld, Ph.D., of University College London, England, and colleagues.
Obesity is a major issue in child health and identifying factors that promote or protect against weight gain could help identify targets for obesity intervention and prevention, according to the study background.
The authors used data from nonidentical, same-sex twin pairs born in the United Kingdom in 2007 who differed on questionnaires measuring appetite and satiety, and whose weight was measured from birth up to age 15 months.
Within the twin pairs, children who had higher food responsiveness (FR, eating in response to food smell or sight) and those with lower satiety responsiveness (SR, eating more before feeling full) grew faster than their siblings. Those with higher FR were 654g heavier (about 1.4 pounds) than their sibling at six months and 991g heavier (about 2.1 pounds) at 15 months. Weight differences between siblings with differing SR were 637g (about 1.4 pounds) at age six months and 918g (about 2 pounds) at age 15 months.
“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 conclude.
JAMA Pediatr. Published online February 17, 2014. doi:10.1001/jamapediatrics.2013.4951
A low responsiveness to satiety cues appears to be one of the mechanisms through which children with a genetic predisposition to obesity gain weight, according to a study by Clare H. Llewellyn, Ph.D., of University College London, England, and colleagues.
Obesity-related genes are being identified and discovering the mechanisms through which these genes influence weight can help pinpoint targets for intervention, according to the study background.
To examine associations between genetic predisposition to obesity, adiposity (body fat) and satiety responsiveness, the authors created a polygenic (multiple genes) risk score (PRS) of 28 obesity-related genes among 2,258 unrelated children (average age of just less than 10 years). Higher PRS scores indicated a greater genetic predisposition to obesity.
Higher PRS was associated with lower satiety responsiveness and with larger BMI and waist circumference. More children in the top 25 percent of the PRS were overweight than in the lowest 25 percent.
“In summary, these findings support the hypothesis that common obesity risk genes influence adiposity in part via appetitive mechanisms. This helps explain how environments and genes combine to determine weight gain: individuals who are less responsive to internal satiety cues by virtue of their genetic blueprint may be more likely to eat to excess when confronted by the multiple eating opportunities of the modern obesogenic environment and consequently gain more weight. Therefore, satiety responsiveness is a potential target for behavioral or pharmacological interventions,” the authors conclude.
JAMA Pediatr. Published online February 17, 2014. doi:10.1001/jamapediatrics.2013.4944.
In a related editorial, Daniel W. Belsky, Ph.D., of the Duke University Medical Center, Durham, N.C., writes: “The obesogenic environment does not affect all children equally. … The fact that children confronted with similar environmental circumstances experience disparate outcomes has been attributed to genetic factors. And family-based and molecular genetic methods indicate substantial genetic contributions to obesity etiology. But just what these genetic factors are and just how they contribute to individual differences in response to the obesogenic environment remains, if not entirely a mystery, an enduring puzzle,” Belsky continues.
“Solving this puzzle is a public health priority,” the author comments.
JAMA Pediatr. Published online February 17, 2014. doi:10.1001/jamapediatrics.2013.5291.
Study One: JAMA Pediatr. Published online February 17, 2014. doi:10.1001/jamapediatrics.2013.4951.
Study Two: JAMA Pediatr. Published online February 17, 2014. doi:10.1001/jamapediatrics.2013.4944. The authors made funding disclosures. Please see article for additional information, including other authors, author contributions and affiliations, etc.
Editorial: JAMA Pediatr. Published online February 17, 2014. doi:10.1001/jamapediatrics.2013.5291. The author is support by a grant from the National Institute on Aging. Please see article for additional information, including other authors, author contributions and affiliations, etc.