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A new study supports the hypothesis that a genetic disposition to being overweight rests in part on an association with a low level of responsiveness to internal satiety cues, which can lead to overeating and weight gain.
A new study supports the hypothesis that a genetic disposition to being overweight rests in part on an association with a low level of responsiveness to internal satiety cues, which can lead to overeating and weight gain. Investigators in England tested this hypothesis in 2258 children aged about 10 years who had undergone genotyping as part of a large early development study in twins. They randomly selected 1 child from each twin pair.
A polygenic risk score (PRS) that assessed the presence of 28 common obesity-related single nucleotide polymorphisms was calculated for each participant, with higher scores indicating a greater genetic predisposition to obesity. Investigators measured participants’ adiposity via body mass index and waist circumference. Almost three-quarters of the children were in the healthy-weight range for their age and sex, with 13% underweight, 10.7% overweight, and 2.3% obese. The Child Eating Behavior Questionnaire assessed satiety responsiveness.
As expected, more children whose PRS scores were in the top 25% were overweight or obese than those with scores in the lowest 25%. In addition, satiety responsiveness significantly mediated the association between PRS and adiposity, with lower levels of satiety responsiveness related to higher PRS scores and overweight or obesity (Llewellyn CH, et al. JAMA Pediatr. 2014;168:338-344).
MS FREEDMAN is a freelance medical editor and writer in New Jersey. DR BURKE, section editor for Journal Club, is chairman of the department of Pediatrics at Saint Agnes Hospital, Baltimore, Maryland. He is a physician contributing editor for Contemporary Pediatrics. The editors have nothing to disclose in regard to affiliations with or financial interests in any organizations that may have an interest in any part of this article.