lisdexamfetamine-dimesylate and Obesity

Binge eating disorder (BED) is the most common eating disorder and was newly recognized in 2013 in the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5). BED is frequently associated with obesity and the metabolic syndrome, as well as with other psychiatric diseases, such as mood (49%), anxiety (41%), and substance use (22%) disorders. BED is highly prevalent and carries a high burden of mental and physical illness and disability. However, BED is frequently under-recognized and under-treated.. This paper reviews the main pharmacological treatments for BED and provides an expert opinion based on the available evidence and on the authors' clinical experience with patients affected by BED.. Several medications have proven to be effective for the treatment of BED, including Lisdexamfetamine (LDX), topiramate as well as anti-anxiety and antidepressant medications. To date, LDX is the only FDA approved medication for BED. Consequently, as a general rule, the use of an FDA approved medication should always be preferred. However, when in the presence of concomitant psychiatric conditions such as anxiety or depression, other medications that have proven efficacy in those comorbid conditions can be used and may contextually provide a benefit for BED.

Topics: Antidepressive Agents; Binge-Eating Disorder; Humans; Lisdexamfetamine Dimesylate; Obesity; Topiramate

Binge-eating disorder (BED) and night-eating syndrome (NES) are two forms of disordered eating associated with overweight and obesity. While these disorders also occur in nonobese persons, they seem to be associated with weight gain over time and higher risk of diabetes and other metabolic dysfunction. BED and NES are also associated with higher risk of psychopathology, including mood, anxiety, and sleep problems, than those of similar weight status without disordered eating. Treatments are available, including cognitive behavior therapy (CBT), interpersonal psychotherapy, lisdexamfetamine, and selective serotonin reuptake inhibitors (SSRIs) for BED; and CBT, SSRIs, progressive muscle relaxation, and bright light therapy for NES.

Topics: Antidepressive Agents; Anxiety Disorders; Binge-Eating Disorder; Clinical Trials as Topic; Comorbidity; Feeding Behavior; Female; Humans; Hydrocortisone; Lisdexamfetamine Dimesylate; Male; Metabolic Syndrome; Models, Psychological; Mood Disorders; Night Eating Syndrome; Obesity; Phototherapy; Prevalence; Psychotherapy; Relaxation Therapy; Selective Serotonin Reuptake Inhibitors; Serotonin; Sex Distribution; Sleep Wake Disorders; Stress, Psychological

Binge-eating disorder (BED) is the most common eating disorder and is associated with poor physical and mental health outcomes. Psychological and behavioral interventions have been a mainstay of treatment for BED, but as understanding of this disorder has grown, pharmacologic agents have become promising treatment options for some patients. At this time, only one drug-the stimulant prodrug lisdexamfetamine-is approved for the treatment of BED. Numerous classes of medications including antidepressants, anticonvulsants, and antiobesity drugs have been explored as off-label treatments for BED with variable success. Although not all patients with BED may be suitable candidates for pharmacotherapy, all patients should be considered for and educated about pharmacologic treatment options.

Topics: Adult; Binge-Eating Disorder; Cognitive Behavioral Therapy; Combined Modality Therapy; Humans; Lisdexamfetamine Dimesylate; Obesity; Off-Label Use; Patient Education as Topic; Psychotropic Drugs; Randomized Controlled Trials as Topic; Treatment Outcome

Psychopharmacologic treatment is playing a greater role in the management of patients with eating disorders. In this paper, we review randomized, placebo-controlled trials (RCTs) conducted in anorexia nervosa (AN), bulimia nervosa (BN), binge eating disorder (BED), and other eating disorders over the past 3 years. Fluoxetine remains the only medication approved for an eating disorder, that being BN. RCTs of antipsychotics in AN have had mixed results; the only agent with some evidence of efficacy is olanzapine. One study suggests dronabinol may induce weight gain in AN. Preliminary studies suggest lack of efficacy of alprazolam, dehydroepiandrosterone, or physiologic estrogen replacement in AN; erythromycin in BN; and the opioid antagonist ALKS-33 in BED. In BED with obesity or overweight, bupropion may cause mild weight loss without seizures, and chromium may improve glucose regulation. Also in BED, three RCTs suggest the stimulant prodrug lisdexamfetamine may reduce binge eating episodes, and another RCT suggests intranasal naloxone may decrease time spent binge eating. There remains a disconnection between the size of eating disorders as a public health problem and the lack of pharmacotherapy research of these conditions.

Topics: Administration, Intranasal; Anorexia Nervosa; Anti-Obesity Agents; Antidepressive Agents, Second-Generation; Antipsychotic Agents; Baclofen; Binge-Eating Disorder; Bulimia Nervosa; Bupropion; Central Nervous System Stimulants; Chromium Compounds; Humans; Lisdexamfetamine Dimesylate; Morphinans; Naloxone; Narcotic Antagonists; Obesity; Randomized Controlled Trials as Topic

We examined the effects of lisdexamfetamine (LDX) treatment on ventral prefrontal cortex (VPFC) and striatal brain activation in binge eating disorder (BED). We hypothesized that participants with BED have an abnormal brain response to palatable food cues, and that VPFC and striatal regions would respond to such cues after LDX treatment. Twenty women with moderate to severe BED consented to a 12-week, open-label trial of LDX with fMRI before and after treatment. Twenty obese women without BED served as healthy controls and received one fMRI. LDX was started at 30 mg/d with a target of 70 mg/d at week 12. At baseline, women with BED showed greater activation in ventrolateral prefrontal cortex (VLPFC), striatum, and globus pallidus to food pictures and brain activation to food pictures predicted clinical outcome at 12 weeks. After 12 weeks of LDX treatment, BED women showed significant reductions in globus pallidus activation. Reductions in ventromedial prefrontal cortex (VMPFC) and thalamus activation specifically correlated with binge eating and obsessive-compulsive symptom reductions, respectively. Results suggest that BED is characterized by an abnormally large VPFC-subcortical brain response to palatable foods that LDX treatment helps modify. Moreover, VPFC-subcortical activation at baseline is a potential biomarker of LDX response.

Topics: Adult; Binge-Eating Disorder; Brain; Corpus Striatum; Dopamine Uptake Inhibitors; Female; Humans; Lisdexamfetamine Dimesylate; Middle Aged; Nerve Net; Obesity; Pilot Projects; Prefrontal Cortex; Treatment Outcome