CHILDHOOD EATING BEHAVIORS: PREVENTION OF CHILDHOOD OBESITY AND CHRONIC DISEASES
Location: Children Nutrition Research Center (Houston, Tx)
Title: A GENETIC BASIS FOR EATING IN THE ABSENCE OF HUNGER AMONG HISPANIC CHILDREN
| Commuzie, Anthony - SW RESEARCH FOUNDATION |
| Fisher, Jennifer |
| Cole, Shelly - SW RESEARCH FOUNDATION |
| Mehta, Nitesh - BAYLOR COLLEGE MED |
Submitted to: Meeting Abstract
Publication Type: Abstract Only
Publication Acceptance Date: June 20, 2003
Publication Date: October 11, 2003
Citation: Commuzie, A.C., Fisher, J., Butte, N.F., Cole, S.A., Mehta, N.R. 2003. A genetic basis for eating in the absence of hunger among Hispanic children [abstract]. Obesity Research. 11:A77.
Eating in the absence of hunger (EAH) is associated with overweight in young non-Hispanic white girls and produced, in part, by parents’ use of restrictive feeding practices. The genetic and biological basis of this potential obesity promoting behavior is unknown. This research was conducted to evaluate the genetic basis of EAH in Hispanic children and its association with obesity-related hormones. Participants were 167 Hispanic families (representing 454 children) with at least one overweight Hispanic child from 5-19 y and their siblings. EAH was assessed in those children who indicated that they were no longer hungry after consuming an ad libitum meal offering 50% of total daily energy needs (MEAL). EAH was quantified as total energy consumed during a standard period in which children were provided with generous portions 10 palatable foods and other activities. Height and weight were measured. Fasting serum insulin and leptin were measured by radioimmunoassay. Heritability estimates and genetic/environmental correlations between eating and hormonal measures were estimated using Solar. Both EAH (h2= 0.57, h2std error=0.12, p<0.0001) and MEAL intake (h2= 0.70, h2std error=0.12, p<0.0001) showed a strong heritable component. Fasting leptin showed a smaller heritable component (h2= 0.22, h2std error=0.11, p<0.05) of similar magnitude to that of fasting insulin (h2= 0.232h2 std error=0.10, p<0.01). EAH and MEAL intake showed neither genetic or environment correlation. Meal intake showed a positive genetic correlation with insulin levels (r(G)=0.46, r(G) std error=0.21), but not leptin. Alternatively, EAH showed a negative genetic correlation with fasting leptin (r(G)=-0.83, r(G) std error=0.30), but not insulin. These findings provide new evidence that the behavioral phenotype of EAH among overweight Hispanic children and their siblings is under substantial genetic control. Further, the negative genetic correlation with leptin indicates a potential shared underlying genetic influence affecting eating behavior and hormonal regulation.