scholarly journals The effects of lisdexamfetamine dimesylate on eating behaviour and homeostatic, reward and cognitive processes in women with binge-eating symptoms: an experimental medicine study

2022 ◽  
Vol 12 (1) ◽  
Author(s):  
Elizabeth Schneider ◽  
Elizabeth Martin ◽  
Pia Rotshtein ◽  
Kasim L. Qureshi ◽  
Samuel R. Chamberlain ◽  
...  

AbstractLisdexamfetamine dimesylate (LDX) is the only drug currently approved by the FDA for the treatment of Binge-Eating Disorder (BED), but little is known about the behavioural mechanisms that underpin the efficacy of LDX in treating BED. We examined the behavioural and neural effects of an acute dose of LDX (50 mg) in 22 women with binge-eating symptomatology using a randomised, crossover, double-blind, placebo-controlled experimental medicine design. LDX reduced self-reported appetite ratings and intake of both a pasta meal and a palatable cookie snack. LDX also decreased the eating rate of pasta but not of cookies and reduced self-reported liking ratings for pasta at the end of the meal. When viewing food pictures during an fMRI scan, LDX reduced activity bilaterally in the thalamus. LDX enhanced sustained attention and reduced impulsive responding in a continuous performance task but had no effect on emotional bias or working memory. These results suggest the observed effects of LDX on food intake (and by implication the efficacy of LDX in treating BED) may be related to the actions of the drug to enhance satiety, reduce food-related reward responding when full and/or increase cognitive control. Novel pharmacotherapies for BED might be most effective if they have a broad spectrum of effects on appetite, reward and cognition.

2019 ◽  
pp. 1-10 ◽  
Author(s):  
Katie Walsh ◽  
Georges Iskandar ◽  
Sunjeev K. Kamboj ◽  
Ravi K. Das

Abstract Background Maladaptive learning linking environmental food cues to high-palatability food reward plays a central role in overconsumption in obesity and binge eating disorders. The process of memory reconsolidation offers a mechanism to weaken such learning, potentially ameliorating over-eating behaviour. Here we investigated whether putatively interfering with synaptic plasticity using the mammalian target of rapamycin (mTOR) inhibitor, rapamycin, could weaken retrieved chocolate reward memories through blockade of reconsolidation Methods Seventy five healthy volunteers with a tendency to binge eat chocolate were randomised to retrieve chocolate reward memory under 10 mg rapamycin (RET + RAP, active condition), or placebo (RET + PBO), or they received 10 mg rapamycin without subsequent retrieval (NO RET + RAP). Indices of chocolate reward memory strength were assessed one week pre and post manipulation and at one month follow-up. Results Contrary to hypotheses, the RET + RAP group did not show any greater reduction than control groups on indices of motivational salience of chocolate cues, motivation to consume chocolate or liking of chocolate. Mild evidence of improvement in the RET + RAP group was found, but this was limited to reduced chocolate binge episodes and improved healthy food choices. Conclusions We did not find convincing evidence of comprehensive naturalistic chocolate reward memory reconsolidation blockade by rapamycin. The effects on chocolate bingeing and food choices may warrant further investigation. These limited positive findings may be attributable to insufficient interference with mTOR signalling with 10 mg rapamycin, or failure to destabilise chocolate memories during retrieval.


2015 ◽  
Vol 24 (3) ◽  
pp. 223-231 ◽  
Author(s):  
Susan L. McElroy ◽  
James E. Mitchell ◽  
Denise Wilfley ◽  
Maria Gasior ◽  
M. Celeste Ferreira-Cornwell ◽  
...  

2021 ◽  
Vol 9 (1) ◽  
Author(s):  
Başak İnce ◽  
Johanna Schlatter ◽  
Sebastian Max ◽  
Christian Plewnia ◽  
Stephan Zipfel ◽  
...  

Abstract Background An extensive amount of research has underlined the potential role of impulsivity in the development and maintenance of binge eating behaviour. Food-related impulsivity has particularly received attention given its close relationship with overeating and binge eating episodes. Besides the available evidence, our understanding regarding the effectiveness of treatment modalities for binge eating targeting impulsivity and related constructs (e.g., food craving, inhibitory control, and reward sensitivity) is limited. Thus, this systematic review aimed to investigate whether binge eating behaviour is changeable by interventions that are impulsivity-focused and food-related and whether one of these interventions is superior to the others. Method A search on PubMed and PsycINFO was performed for relevant articles published up to September 2020. Studies delivering food-related impulsivity treatment to individuals suffering from binge eating episodes and including a control condition without this treatment were investigated. Following the search, 15 studies meeting the eligibility criteria were analysed. Results Analyses revealed that available impulsivity-focused approaches can be categorised as psychotherapy, pharmacotherapy, computer-assisted cognitive training, and direct neuromodulation interventions. Regarding their effectiveness, it appeared that all of these approaches might be promising to change food-related impulsivity in individuals with binge eating episodes, particularly to decrease binge eating symptoms. However, a superior intervention approach in this early state of evidence could not be determined, although food-related cue exposure, transcranial direct current stimulation, and the combination of several interventions seem fruitful. Conclusion Efforts to treat binge eating behaviour with interventions focusing on food-related impulsivity appear to be promising, particularly concerning binge eating frequency, and also for food craving and inhibitory control. Given limited research and varying methods, it was not possible to conclude whether one impulsivity-focused intervention can be considered superior to others.


2004 ◽  
Vol 19 (2) ◽  
pp. 102-112 ◽  
Author(s):  
Anne L. Howson ◽  
Sue Batth ◽  
Vadim Ilivitsky ◽  
Armand Boisjoli ◽  
Martine Jaworski ◽  
...  

AbstractEvidence from pre-clinical infrahuman investigations, open-label clinical trials, and a single controlled trial found acute nicotine treatment potentiated up to 4 weeks neuroleptic-induced reductions of dyskinetic symptoms characterizing Tourette’s syndrome (TS). Given the attentional disturbances associated with this syndrome, and the improvements in attentional processes reported with nicotine, this randomized, double-blind, placebo-controlled trial examined the acute (4 h) and sustained (2 weeks) effects of a single dose of transdermal nicotine on clinical (i.e., tics), attentional (continuous performance task, event-related potentials, patient and parental reports) and behavioral symptoms in 23 children and adolescents with TS receiving neuroleptic treatment. In the 14 evaluable patients with complete primary efficacy data, nicotine (compared to placebo) failed to alter symptoms at 4 h but counteracted ERP-P300 signs of diminished attention seen 2 weeks following placebo treatment. Secondary efficacy measures, including patient self-reports and parental ratings, found nicotine to reduce complex tics and improve behaviors related to inattention. Additional work with intermittent dosing schedules is required to characterize optimal clinical and cognitive effects with nicotine treatment.


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