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J Eat Disord. 2019 Jul 11;7:23. doi: 10.1186/s40337-019-0253-3. eCollection 2019.

Understanding the neural mechanisms of lisdexamfetamine dimesylate (LDX) pharmacotherapy in Binge Eating Disorder (BED): a study protocol.

Author information

1
1The Brain Dynamics Centre, Westmead Institute for Medical Research, The University of Sydney, 176 Hawkesbury Road, Westmead, NSW 2145 Australia.
2
2School of Psychology, The University of Sydney, Camperdown, NSW 2050 Australia.
3
3Translational Health Research Institute, School of Medicine, Western Sydney University, Penrith, NSW 2751 Australia.
4
4Adolescent & Young Adult Medicine, Westmead Hospital, Westmead, NSW 2145 Australia.
5
Centre for Research into Adolescents Health, Westmead, NSW 2145 Australia.
6
6Department of Radiology, Westmead Hospital, Westmead, NSW Australia.
7
7The Discipline of Medical Radiation Sciences, Faculty of Health Science, The University of Sydney, Camperdown, NSW Australia.

Abstract

Background:

The efficacy and safety of Lisdexamfetamine dimesylate (LDX) in the treatment of moderate to severe binge eating disorder (BED) has been demonstrated in multiple randomised clinical trials. Despite this, little is known about how LDX acts to improve binge eating symptoms. This study aims to provide a comprehensive understanding of the neural mechanisms by which LDX improves symptoms of BED. We hypothesise that LDX will act by normalising connectivity within neural circuits responsible for reward and impulse control, and that this normalisation will correlate with reduced binge eating episodes.

Methods:

This is an open-label Phase 4 clinical trial of LDX in adults with moderate to severe BED. Enrolment will include 40 adults with moderate to severe BED aged 18-40 years and Body Mass Index (BMI) of 20-45 kg/m2, and 22 healthy controls matched for age, gender and BMI. Clinical interview and validated scales are used to confirm diagnosis and screen for exclusion criteria, which include comorbid anorexia nervosa or bulimia nervosa, use of psychostimulants within the past 6 months, and current use of antipsychotics or noradrenaline reuptake inhibitors. Baseline assessments include clinical symptoms, multimodal neuroimaging, cognitive assessment of reward sensitivity and behavioural inhibition, and an (optional) genetic sample. A subset of these assessments are repeated after eight weeks of treatment with LDX titrated to either 50 or 70 mg. The primary outcome measures are resting-state intrinsic connectivity and the number of binge eating episodes. Analyses will be applied to resting-state fMRI data to characterise pharmacological effects across the functional connectome, and assess correlations with symptom measure changes. Comparison of neural measures between controls and those with BED post-treatment will also be performed to determine whether LDX normalises brain function.

Discussion:

First enrolment was in May 2018, and is ongoing. This study is the first comprehensive investigation of the neurobiological changes that occur with LDX treatment in adults with moderate to severe BED.

Trial registration:

ACTRN12618000623291, Australian and New Zealand Clinical Trials Registry URL: https://www.anzctr.org.au/Trial/Registration/TrialReview.aspx?id=374913&isReview=true. Date of Registration: 20 April 2018.

KEYWORDS:

Binge eating disorder; Clinical trials; Drug therapy; Neuroimaging

Conflict of interest statement

Competing interestsThe authors declare that they have no competing interests.

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