Translating taste genetics to adiposity: Sensation, preference and intake of high-fat sweet foods

Date of Completion

January 2007


Biology, Genetics|Health Sciences, Nutrition




There is a well-established chain from oral sensory phenotype to food intake that is mediated via sensory differences from, and preferences for food. Here, four interdisciplinary studies extend current understanding with regard to high fat sweet foods, by including recent advances in taste receptor genotype, emerging phenotypical markers, and links between fat/sweet preferences and central adiposity. Novel statistical approaches, including heterogenous slope regression, hierarchical regression, response surface modeling and structural equation modeling, were applied to secondary data. Major findings include: Study 1—In 198 adults, SNPs in the TAS2R38 gene explained some phenotypic variation, but behavioral methods were still needed to fully characterize oral sensory differences. Study 2—When 79 young adults with low dietary restraint were given a series of fat-sugar mixtures, phenotypic differences resulted in individuals requiring 1.5 or 2-fold differences in the concentration needed to achieve the same level of creaminess or sweetness. Study 3—In the same subjects as study 2, phenotypic groups were created and response surface modeling identified concentrations required for optimal liking. Phenotype separated groups who liked high levels of fat and sugar from those who did not, suggesting phenotype may be predispose individuals to future obesity risk via preference for energy dense foods. Study 4—In a sample of 110 middle-aged women who were diverse in bodyweight, structural equation modeling showed phenotype associated with adiposity via preference for and reported intake of high-fat foods. Additionally, surveyed fat/sweet preference was a better predictor of central adiposity than age or reported fat intake, suggesting preference may capture habitual intake. Collectively, these studies provide new insight to the role oral sensory phenotype plays in obesity risk via preference for high-fat sweet foods. ^