Table 1 Studies that reported a hyperdopaminergic state in binge eating

Wang et al. 48

Case–control

Compare the brain dopamine responses to food stimuli between binge eaters and non-binge eaters

10 BED patients (8 female, 2 male; age: 38.5 ± 13.3; BMI: 43.4 ± 13.5)

8 obese controls (five female, 3 male; age: 41.8 ± 8.9; BMI: 36.5 ± 9.4)

Exclusion: history of medical treatment for weight control, alcohol or drug abuse, neurological or psychiatric disorder, cardiovascular disease, diabetes, head trauma

PET and [11C]raclopride

PET scanning was conducted in different conditions: placebo and methylphenidate under food intervention (view, smell, taste) or neutral intervention (pictures, toys, and clothing items)

Binge eaters had significantly more dopamine release than non-binge eater in caudate after methylphenidate under food intervention. However, the differences in putamen or in ventral striatum were not significant

The increases of dopamine release across all subjects in caudate were correlated with binge eating severity

Nasser et al. 78

Cross-sectional

Assess dopamine response to oral food stimulation using electroretinographic

Correlate dopamine response under placebo, methylphenidate and food stimuli with Binge Eating Scale and the Three Factor Eating Questionnaire

9 healthy, eating disorder-free adults (5 female, 4 male; age: 39 ± 10; BMI: 32 ± 5)

Exclusion: diabetes, thyroid or renal disease, neurological disorders, Tourette’s syndrome, schizophrenia, bipolar disease, current major or situational depression, current or history of anorexia nervosa or bulimia nervosa, current use of any prescription medication, pregnancy, use of tobacco products or recreational drugs

Dopamine responses were assessed under four conditions: placebo (water), 10 mg methylpheidate, 20 mg methylphenidate, food stimulus

A significant increase in b-wave amplitude in response to the 20 mg methylphenidate dose and food stimuli

Significant correlations between b-wave amplitude under the food stimulus condition and the Binge Eating Scale score

Davis et al. 58

Case–control

Compared five polymorphisms known to influence the function of the striatal dopamine D2 receptor between BED and controls

The five polymorphisms: rs1800497[Taq1A], rs1799732 [− 141C ins/del], rs6277 [C957T], rs2283265, and rs12364283

79 BED obese adults (67 female; 12 male; age: 34.8 ± 6.5; BMI: 38.6 ± 7.2)

151 obese adults (104 female; 47 male; age: 35.6 ± 7.2; BMI: 38.7 ± 7.1)

Exclusion: a current diagnosis of any psychotic disorder, substance abuse, alcoholism, or a serious medical/physical illness such as cancer

Non-enzymatic, high salt procedure was used to extract DNA from the whole blood

Compared to weight-matched controls, BED was significantly related to the rs1800497 and rs6277 genotypes that reflect enhanced striatal dopamine neurotransmission

BED is distinguished by a greater density of D2 receptors and higher D2 binding potential compared to the obese controls

The multi-locus D2 genetic profile observed in BED participants suggests enhanced dopamine signaling, and thereby increased striatal reactivity, compared to obese adults without binge eating

Davis et al. 59

Cross-sectional

Examine the associations between a multilocus genetic profile score and binge eating

Multilocus genetic profile: Taq1A C/T, C957T, − 141 Ins/Del, DAT1, Val158Met

120 adults (82 female, 38 male), 24% of participants met the diagnostic criteria for BED

Exclusion: a current diagnosis of any psychotic disorder, substance abuse, or a serious medical/physical illness such as cancer or heart disease

Non-enzymatic, high salt procedure was used to extract DNA from the whole blood

Binge eating questionnaire

Higher multilocus genetic profile score (enhanced ventral striatum striatal dopamine-signaling) was associated with more bingeing

Donofry et al. 65

Cross-sectional

Test whether the COMT met allele increased risk for, and severity of, eating disorder symptomatology in community volunteers

1003 community-based Caucasian adults (female: 51.2%; age: 44.6 ± 6.8; BMI: 27.0 ± 5.4)

Exclusion: a clinical history of neurologic illness, cardiovascular disease, cancer treatment within the previous year, schizophrenia, or other psychoses

DNA was isolated from white blood cells using the PureGene kit

COMT val/met SNP was genotyped using florescence polarization

Eating disorders inventory

Individuals carrying the met allele of the COMT val158met were 87% more likely than individuals with the val/val genotype to report symptoms on the Bulimia subscale

It is possible that met allele carriers have greater difficulty exerting top-down control of behavior driven by midbrain dopamine activation

Gervasini et al. 62

Case–control

Determine dopamine Receptor D4 gene on general psychopathological symptoms in eating disorder patients

74 female with BN (age: 20.9 ± 8.1; BMI: 24.6 ± 6.9)

199 female with AN

Exclusion: dementia, mental retardation, schizophrenia, Turner's syndrome, other neurological disorders and underlying endocrine pathologies

Genomic DNA purification was performed with a Qiagen blood midi kit

Symptom Checklist 90 Revised

General psychopathological features such as somatization, obsessive–compulsive, anxiety, phobic anxiety, and paranoid ideation were significantly higher in BN women who carried haplotype DRD4*2 (non7R-L-C–C)

DRD4 haplotypes may contribute to individual variance in personality features that predispose to disordered eating

Gonzalez et al. 60

Cross-sectional

Analyze the association between three common polymorphisms in the dopaminergic pathways with eating disorder symptoms in patients with BN or BED

Three polymorphisms: DAT1 VNTR 10R/9R, DRD2 A2/A1 and DRD3 Ser9Gly

80 female with BN (BMI: 25.6 ± 8.9)

34 female with BED (BMI: 35.4 ± 11.5)

Exclusion: neurological disorders (such as mental retardation, dementia or Turner syndrome) and underlying endocrine pathologies

Genomic DNA was isolated from whole blood samples using a standard phenol–chloroform extraction method

Eating Disorders Inventory Test-2 (EDI-2)

Revised Symptom Checklist 90 questionnaire

BED patients with the Ser9Gly variant showed higher EDI-2 scores than Ser9Ser carriers

No associations were found for the BN group

Suarez-Ortiz et al. 83

Animal study

Determine the effect of D2 receptor antagonist on binge eating

Female Sprague Dawley rats

Binge eating rats were induced by intermittent access to a sucrose solution

Rats were divided into three groups: no access (control, n = 14), 2-h daily access (intermittent, n = 16), and 24-h daily access (ad libitum, n = 13) during 28 days

Rats in the intermittent access group were randomly assigned to receive injections of vehicle or raclopride (n = 8)

Raclopride tartrate salt (Sigma Chemical Co., Toluca, Mexico) was dissolved in 0.9% saline solution, and was injected into nucleus accumbens

Blockade of dopamine D2 receptors in the nucleus accumbens prevented the effects of the intermittent access to the sucrose solution on meal frequency and duration

Blockade of dopamine D2 receptors specifically decreased the sucrose solution intake

Mineo et al. 75

Animal study

Test whether dopamine manipulation using 6-hydroxydopamine (6-OHDA) and L-dopa will influence binge-like eating behavior

Male Wistar rats (n = 45)

Sham-operated + saline (Sham; n = 15), parkinsonian 6-OHDA + saline (6-OHDA; n = 15), and 6-OHDA + L-dopa (L-dopa; n = 15) rats were randomly allotted into three groups: control group (standard chow), low restriction group, and high restriction group

L-dopa, 6–12 mg/kg plus 12 mg/kg of benserazide intraperitoneally once a day for 7 weeks

Sham-operated animals with intact nucleus accumbens core plasticity reliably developed food-addiction–like behavior when exposed to intermittent access to a highly palatable food

6-OHDA–lesioned animals displayed no increasing interest about the chocolate, but the unresponsiveness was rescued by L-dopa

Food-addiction–like behavior relies on an intact ventral striatum core