Food reinforcement, the dopamine D2 receptor genotype, and energy intake in obese and nonobese humans

Abstract

The authors measured food reinforcement, polymorphisms of the dopamine D2 receptor (DRD2) and dopamine transporter (DAT1) genes, and laboratory energy intake in 29 obese and 45 nonobese humans 18-40 years old. Food reinforcement was greater in obese than in nonobese individuals, especially in obese individuals with the TaqI A1 allele. Energy intake was greater for individuals high in food reinforcement and greatest in those high in food reinforcement with the TaqI A1 allele. No effect of the DAT1 genotype was observed. These data show that individual differences in food reinforcement may be important for obesity and that the DRD2 genotype may interact with food reinforcement to influence energy intake.

Figure 1

Differences in motivated responding for snack foods across variable ratio schedules of reinforcement for those who were obese (body mass index > 30) versus nonobese (top graph), for those with versus without the dopamine D₂ receptor (DRD₂) A1 allele (middle graph), and for the combination of obesity and the A1 allele (bottom graph). Mixed-effects regression models showed that obesity (p = .0014) and the A1 allele (p = .027) independently predicted responding for food. An interaction of obesity with the DRD₂ genotype was observed, as obese participants with the A1 allele responded more for food than obese participants without the A1 allele (p < .0001), whereas there were no significant differences in responding for nonobese participants with or without the A1 allele.

Figure 2

Participants’ energy consumption by food reinforcement value and presence or absence of the A1 allele (p = .003). Participants high in food reinforcement with the A1 allele consumed more food than participants high in food reinforcement without the A1 allele (p = .037) and participants low in food reinforcement with (p < .0002) or without the A1 allele (p = .0005).