Food is a powerful reinforcer and the reinforcing value of food may be a determinant of food intake. There are individual differences in food reinforcement, as obese find food more reinforcing and consume more food than non-obese. The reinforcing value of food is mediated in part by the dopaminergic system, and research suggests obesity is related to the density of dopamine D2 receptors. In previous research we found smokers with high food reinforcement who had the A1 allele of the dopamine D2 receptor had increased intake of snack foods in an ad libitum eating task. This polymorphism may influence dopaminergic activity by reducing the density of dopamine D2 receptors (DRD2). We have shown a similar pattern of energy intake in pilot research with non-smokers. In addition, these pilot data have shown differences in BMI in relationship to dopamine genotypes and that obesity and dopamine genotypes interact to influence food reinforcement. This application builds upon this research to examine relationships between food reinforcement, obesity, DRD2 genotypes. Three hundred sixteen participants of mixed ethnicity and race, including an equal number of obese and non-obese males and females will be studied. Participants will be genotyped for polymorphisms of the DRD2 genotype, ad lib eating and food reinforcement measured in separate laboratory sessions, and their usual energy intake assessed by repeated 24-hour food recalls. This application provides the opportunity to determine whether 1) the A1 allele of the DRD2 genotype is associated with greater BMI and more obesity; 2) food reinforcement and presence of the A1 allele of the DRD2 genotype interact to predict BMI and obesity; 3) obesity is associated with increases in food reinforcement; 4) obesity and the A1 allele of the DRD2 genotype interact to influence food reinforcement; and 5) ad libitum food consumption and food reinforcement in the laboratory and are related to usual energy intake. This study provides important new information on a behavioral factors that may be related to excess energy consumption, and tests how food reinforcement and the DRD2 genotype may interact in obesity. The findings are relevant to a greater understanding of behavioral and genetic factors related to obesity, as well as providing ideas that may be relevant for treatment interventions for those high in food reinforcement. ? ? ?
| Scheid, Jennifer L; Carr, Katelyn A; Lin, Henry et al. (2014) FTO polymorphisms moderate the association of food reinforcement with energy intake. Physiol Behav 132:51-6 |
| Carr, Katelyn A; Lin, Henry; Fletcher, Kelly D et al. (2014) Food reinforcement, dietary disinhibition and weight gain in nonobese adults. Obesity (Silver Spring) 22:254-9 |
| Carr, Katelyn A; Lin, Henry; Fletcher, Kelly D et al. (2013) Two functional serotonin polymorphisms moderate the effect of food reinforcement on BMI. Behav Neurosci 127:387-99 |
| Lin, Henry; Carr, Katelyn A; Fletcher, Kelly D et al. (2013) Food reinforcement partially mediates the effect of socioeconomic status on body mass index. Obesity (Silver Spring) 21:1307-12 |
| Epstein, Leonard H; Carr, Katelyn A; Lin, Henry et al. (2012) Usual energy intake mediates the relationship between food reinforcement and BMI. Obesity (Silver Spring) 20:1815-9 |
| Epstein, Leonard H; Lin, Henry; Carr, Katelyn A et al. (2012) Food reinforcement and obesity. Psychological moderators. Appetite 58:157-62 |
| Carr, Katelyn A; Daniel, Tinuke Oluyomi; Lin, Henry et al. (2011) Reinforcement pathology and obesity. Curr Drug Abuse Rev 4:190-6 |
| Epstein, Leonard H; Carr, Katelyn A; Lin, Henry et al. (2011) Food reinforcement, energy intake, and macronutrient choice. Am J Clin Nutr 94:12-8 |
| Carr, Katelyn A; Epstein, Leonard H (2011) Relationship between food habituation and reinforcing efficacy of food. Learn Motiv 42:165-172 |
| Epstein, Leonard H; Dearing, Kelly K; Erbe, Richard W (2010) Parent-child concordance of Taq1 A1 allele predicts similarity of parent-child weight loss in behavioral family-based treatment programs. Appetite 55:363-6 |
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