Dopamine Transporter Gene (DAT1) Associated with Appetite Suppression to Methylphenidate in a Case–Control Study of Binge Eating Disorder

Davis, Caroline; Levitan, Robert D.; Kaplan, Allan S.; Carter, Jacqueline; Reid, Caroline; Curtis, Claire; Patte, Karen A.; Kennedy, James L.

doi:10.1038/sj.npp.1301348

Cited by 62 publications

(49 citation statements)

References 40 publications

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“…[327] compared neural responses to food-reward outcomes in individuals with BN and with anorexia nervosa (AN), and found that individuals with BN had relatively greater activation in the dorsolateral prefrontal cortex, the insular cortex, and the pre-central gyrus. These studies compliment candidate genetic behavior investigations in BN that have reported altered allelic frequencies for the DAT gene [328] and DA receptor genes [329,330] in individuals with bulimia.…”

Section: Reviewsupporting

confidence: 74%

Reward circuitry dysfunction in psychiatric and neurodevelopmental disorders and genetic syndromes: animal models and clinical findings

Dichter

Damiano

Allen

2012

J Neurodevelop Disord

254

207

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This review summarizes evidence of dysregulated reward circuitry function in a range of neurodevelopmental and psychiatric disorders and genetic syndromes. First, the contribution of identifying a core mechanistic process across disparate disorders to disease classification is discussed, followed by a review of the neurobiology of reward circuitry. We next consider preclinical animal models and clinical evidence of reward-pathway dysfunction in a range of disorders, including psychiatric disorders (i.e., substance-use disorders, affective disorders, eating disorders, and obsessive compulsive disorders), neurodevelopmental disorders (i.e., schizophrenia, attention-deficit/hyperactivity disorder, autism spectrum disorders, Tourette’s syndrome, conduct disorder/oppositional defiant disorder), and genetic syndromes (i.e., Fragile X syndrome, Prader–Willi syndrome, Williams syndrome, Angelman syndrome, and Rett syndrome). We also provide brief overviews of effective psychopharmacologic agents that have an effect on the dopamine system in these disorders. This review concludes with methodological considerations for future research designed to more clearly probe reward-circuitry dysfunction, with the ultimate goal of improved intervention strategies.

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Section: Reviewsupporting

confidence: 74%

Reward circuitry dysfunction in psychiatric and neurodevelopmental disorders and genetic syndromes: animal models and clinical findings

Dichter

Damiano

Allen

2012

J Neurodevelop Disord

254

207

View full text Add to dashboard Cite

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“…Supporting Information Table S11 provides a synopsis of six different candidate gene studies in BED, which examined several different polymorphisms. [85][86][87][88][89][90] Two studies examined DSM-IV BED diagnoses in terms of the MC4R polymorphism and found no evidence that individuals with BED were any more likely to carry this polymorphism than non-BED subjects. 85,86 Similarly, Monteleone et al 87 examined the cDNA 385C polymorphism and failed to find evidence that this genetic abnormality is associated with BED, although it did appear to be associated with obesity.…”

Section: Supporting Informationmentioning

confidence: 99%

The validity and clinical utility of binge eating disorder

Wonderlich

Gordon

Mitchell

et al. 2009

Intl J Eating Disorders

234

115

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Objective: This review attempted to examine the validity and clinical utility of the DSM-IV binge eating disorder (BED) diagnosis across a wide range of validating strategies.Method: Various electronic databases (Pub Med, Psych Info) were searched for terms relevant to the diagnosis of BED (e.g., binge eating disorder, binge eating) in order to identify papers. Additionally, published papers were reviewed in order to locate additional manuscripts and papers that were presented at meetings. Results:The validity and utility of BED varied substantially according to the validator chosen. There is reasonable evidence that BED can be differentiated from other existing eating disorders and is associated with significant impairment and clinical levels of eating disorder psychopathology. The relationship of BED to obesity is complex, and in spite of some positive findings, further research examining the predictive power of BED, beyond the simple presence of obesity and associated psychopathology, in relationship to clinically relevant outcomes is needed.Discussion: Binge eating disorder is being considered for inclusion in the DSM-V and various options regarding this decision are reviewed based upon the empirical findings in the paper. V

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“…Pathologic overeating may be related to dysfunction of the dopamine (DA) and norepinephrine systems, as evidenced by genetic and pharmacologic findings and animal models. [20][21][22][23][24][25] Food stimulation generates abnormal DA responses in obese individuals, 26,27 and methylphenidate-mediated inhibition of DA transport leads to greater increases of DA levels within the caudate in obese individuals with BED compared with those without BED. 27 Agents, such as dextroamphetamine, that inhibit reuptake of DA and norepinephrine and elicit release of monoamine neurotransmitters 28 may alter pathologic BE and be feasible treatment options for BED.…”

mentioning

confidence: 99%

Efficacy and Safety of Lisdexamfetamine for Treatment of Adults With Moderate to Severe Binge-Eating Disorder

et al. 2015

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IMPORTANCE Binge-eating disorder (BED), a public health problem associated with psychopathological symptoms and obesity and possibly with metabolic syndrome, lacks approved pharmacotherapies.OBJECTIVE To examine the efficacy and safety of lisdexamfetamine dimesylate, a dextroamphetamine prodrug, to treat moderate to severe BED. DESIGN, SETTING, AND PARTICIPANTSWe performed a randomized, double-blind, parallel-group, forced dose titration, placebo-controlled clinical trial at 30 sites from May 10, 2011, through January 30, 2012. Safety and intention-to-treat analyses included 259 and 255 adults with BED, respectively.INTERVENTIONS Lisdexamfetamine dimesylate at dosages of 30, 50, or 70 mg/d or placebo were provided to study participants (1:1:1:1). Dosages were titrated across 3 weeks and maintained for 8 weeks. We followed up participants for a mean (SD) of 7 (2) days after the last dose. MAIN OUTCOMES AND MEASURESWe assessed the change in binge-eating (BE) behaviors measured as days per week (baseline to week 11) with a mixed-effects model using transformed log (BE days per week) + 1. Secondary measures included BE cessation for 4 weeks. Safety assessments included treatment-emergent adverse events, vital signs, and change in weight. RESULTS At week 11, log-transformed BE days per week decreased with the 50-mg/d (least squares [LS] mean [SE] change, −1.49 [0.066]; P = .008) and 70-mg/d (LS mean [SE] change, −1.57 [0.067]; P < .001) treatment groups but not the 30-mg/d treatment group (LS mean [SE]change, −1.24 [0.067]; P = .88) compared with the placebo group. Nontransformed mean (SD) days per week decreased for placebo and the 30-, 50-, and 70-mg/d treatment groups by −3.3 (2.04), −3.5 (1.95), −4.1 (1.52), and −4.1 (1.57), respectively. The percentage of participants achieving 4-week BE cessation was lower with the placebo group (21.3%) compared with the 50-mg/d (42.2% [P = .01]) and 70-mg/d (50.0% [P < .001]) treatment groups. The incidence of any treatment-emergent adverse events was 58.7% for the placebo group and 84.7% for the combined treatment group. In the treatment groups, 1.5% of participants had serious treatment-emergent adverse effects. Events with a frequency of at least 5% and changes in heart rate were generally consistent with the known safety profile. The mean (SD) change in body weight was −0.1 (3.09), −3.1 (3.64), −4.9 (4.43), −4.9 (3.93), and −4.3 (4.09) kg for the placebo group, the 30-, 50-, and 70-mg/d treatment groups, and the combined treatment groups, respectively (P < .001 for each dose vs placebo group comparison in post hoc analysis). CONCLUSIONS AND RELEVANCEThe 50-and 70-mg/d treatment groups demonstrated efficacy compared with the placebo group in decreased BE days, BE cessation, and global improvement. The safety profile was generally consistent with previous findings in adults with attentiondeficit/hyperactivity disorder. Further investigation of lisdexamfetamine in BED is ongoing. TRIAL REGISTRATION clinicaltrials.gov Identifier: NCT01291173

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Dopamine Transporter Gene (DAT1) Associated with Appetite Suppression to Methylphenidate in a Case–Control Study of Binge Eating Disorder

Cited by 62 publications

References 40 publications

Reward circuitry dysfunction in psychiatric and neurodevelopmental disorders and genetic syndromes: animal models and clinical findings

Reward circuitry dysfunction in psychiatric and neurodevelopmental disorders and genetic syndromes: animal models and clinical findings

The validity and clinical utility of binge eating disorder

Efficacy and Safety of Lisdexamfetamine for Treatment of Adults With Moderate to Severe Binge-Eating Disorder

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