title: Reward sensitivity and the D2 dopamine receptor gene: A case-control study of binge eating disorder.
abstract: OBJECTIVE
  The sensitivity of dopamine reward pathways has been implicated in the risk for various psychiatric disorders including compulsive overeating. The evidence is divided, however, about the direction of causal association. One argument is that a Reward Deficiency Syndrome is the risk factor, while others contend that hyper-sensitivity to reward enhances the motivation for pleasurable activities like eating. Unfortunately, little human research has bridged the gap between psychological and neurobiological approaches to brain reward functioning and disorder. The present study addressed this issue by implementing psychological and biological markers of reward sensitivity in the assessment protocol.
  
  
  METHODS
  Adults with binge eating disorder (BED) were compared to samples of normal-weight and obese controls on two personality measures of reward sensitivity and were genotyped for six markers of the DRD2 dopamine receptor gene.
  
  
  RESULTS
  Genotype x Group ANOVAs revealed significant main effects and an interaction on the personality measures for Taq1A. BED and obese subjects reported greater reward sensitivity than normal-weight controls, but only among those carrying the A1 allele. We also found that normal-weight controls with at least one copy of the T allele of the C957T marker had significantly lower reward sensitivity scores than any of the other groups who did not differ from each other.
  
  
  CONCLUSIONS
  Given evidence linking the A1 allele with reduced receptor density, an inverse relationship was expected between psychological measures of reward sensitivity and presence of the A1 allele. One explanation for our findings could be that the BED and obese participants possess another genetic variant that interacts with the A1 allele to produce higher dopamine activity. These findings have implications for future studies of the molecular genetics of BED and obesity, and for behavioural and pharmacologic therapies targeting these conditions.
authors.affiliation: Kinesiology & Health Sciences, York University, Toronto, Canada. cdavis@yorku.ca
authors.forename: Caroline
authors.initials: C
authors.lastname: Davis
authors.forename: Robert D
authors.initials: RD
authors.lastname: Levitan
authors.forename: Allan S
authors.initials: AS
authors.lastname: Kaplan
authors.forename: Jacqueline
authors.initials: J
authors.lastname: Carter
authors.forename: Caroline
authors.initials: C
authors.lastname: Reid
authors.forename: Claire
authors.initials: C
authors.lastname: Curtis
authors.forename: Karen
authors.initials: K
authors.lastname: Patte
authors.forename: Rudi
authors.initials: R
authors.lastname: Hwang
authors.forename: James L
authors.initials: JL
authors.lastname: Kennedy
mesh_terms: D000328:Adult; D000704:Analysis of Variance; D052018:Bulimia Nervosa / Q000235:genetics* / Q000523:psychology*; D016022:Case-Control Studies; D005260:Female; D005787:Gene Frequency; D020022:Genetic Predisposition to Disease; D005838:Genotype; D006801:Humans; D015810:Linkage Disequilibrium / Q000502:physiology; D008297:Male; D008875:Middle Aged; D020641:Polymorphism, Single Nucleotide; D017448:Receptors, Dopamine D2 / Q000235:genetics*; D012201:Reward; D044465:White People / Q000235:genetics
chemical_list: D017448:Receptors, Dopamine D2