Date of Award


Degree Type


Degree Name

Doctor of Philosophy (PhD)

Graduate Group


First Advisor

Charlene W. Compher

Second Advisor

Danielle R. Reed



Paule Valery Joseph

Charlene Compher, PhD, RD

Background: Many illnesses of modern society are due to poor food choices. Excess consumption of sugars has been associated with obesity and diabetes. Children, due to their basic biology, are more vulnerable than adults to overeat foods rich in sugars. Little research has focused on whether there are individual differences among children in their sensitivity to sweet taste and if so the biological correlates of such differences.

Aims: The goal of this study was to determine whether variations in children’s sucrose detection thresholds relate to their age and sex, taste genotype, added sugar or caloric intake, temperament or food neophobia and adiposity.

Methods: Sucrose detection thresholds in children age 7-14 years were tested individually using a validated two-alternative, forced-choice, paired-comparison tracking method. Genetic variants of taste receptor genes were assayed: TAS1R2, TAS1R3 and GNAT3 (sweet taste receptor genes; one variant each) and the bitter receptor gene TAS2R38 (three variants). Children (n=216) were measured for body weight and height. A subset of 96 children was measured for percent body fat, waist to height ratio and added sugar and kcal intake.

Results: Mean sucrose threshold was 12.0 (SD 12.9), 0.23 to 153.8 mM. Girls were more sensitive than boys [t(214) = 2.0, p=0.047] and older children more sensitive than younger children [r(214) = -0.16, p = 0.016]. Variants in the bitter but not the sweet taste receptor genes were related to sucrose threshold and sugar intake; children with two bitter-sensitive alleles could detect sucrose at lower concentrations [F(2,165) = 4.55, p = 0.012; rs1726866]. Children with these variants also reported eating more added sugar (%kcals; [F(2, 62) = 3.64, p = 0.032]) than did children with less sensitive alleles. Sucrose detection thresholds predicted central adiposity [F(2, 59) = 6.1, p = 0.016), but not percent body fat [F(2, 58) = 1.4, p = 0.238]) when adjusted for added sugar intake, temperament, age, sex and negative reaction to foods.

Conclusions: Differences in sweet taste sensitivity may affect childhood dietary sugar intake with long-term health consequences, including obesity. There may be a more complex interplay between the bitter and sweet taste systems during development than previously appreciated. Understanding taste related parameters as well as other dimensions that may affect food consumption might help in developing weight management to minimize childhood obesity risk.