Tag: BED: Binge Eating Disorder

What is Lisdexamfetamine?

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Introduction

Lisdexamfetamine, sold under the brand names Vyvanse and Elvanse among others, is a stimulant medication that is used to treat attention deficit hyperactivity disorder (ADHD) in children and adults and for moderate-to-severe binge eating disorder in adults. Lisdexamfetamine is taken by mouth. Its effects generally begin within two hours and last for up to 14 hours.

Common side effects of lisdexamfetamine include loss of appetite, anxiety, diarrhoea, trouble sleeping, irritability, and nausea. Rare but serious side effects include mania, sudden cardiac death in those with underlying heart problems, and psychosis. It has a high potential for substance abuse. Serotonin syndrome may occur if used with certain other medications. Its use during pregnancy may result in harm to the baby and use during breastfeeding is not recommended by the manufacturer.

Lisdexamfetamine is an inactive prodrug that works after being converted by the body into dextroamphetamine, a central nervous system (CNS) stimulant. Chemically, lisdexamfetamine is composed of the amino acid L-lysine, attached to dextroamphetamine.

Lisdexamfetamine was approved for medical use in the United States in 2007, and in the European Union in 2012. In 2022, it was the 69th most commonly prescribed medication in the United States, with more than 9 million prescriptions. It is a Class B controlled substance in the United Kingdom, a Schedule 8 controlled drug in Australia, and a Schedule II controlled substance in the United States.

Brief History

Lisdexamfetamine was developed by New River Pharmaceuticals, who were bought by Takeda Pharmaceuticals through its acquisition of Shire Pharmaceuticals, shortly before it began being marketed. It was developed to create a longer-lasting and less-easily abused version of dextroamphetamine, as the requirement of conversion into dextroamphetamine via enzymes in the red blood cells delays its onset of action, regardless of the route of administration.

In February 2007, the US Food and Drug Administration (FDA) approved lisdexamfetamine for the treatment of ADHD. In August 2009, Health Canada approved the marketing of lisdexamfetamine for prescription use.

In January 2015, lisdexamfetamine was approved by the FDA for the treatment of binge eating disorder in adults.

The FDA gave tentative approval to generic formulations of lisdexamfetamine in 2015. The expiration date for patent protection of lisdexamfetamine in the US was 24 February 2023. The Canadian patent expired 20 years from the filing date of 01 June 2004.

Production quotas for 2016 in the United States were 29,750 kg.

Uses

Medical

Lisdexamfetamine is used primarily as a treatment for attention deficit hyperactivity disorder (ADHD) and binge eating disorder; it has similar off-label uses as those of other pharmaceutical amphetamines such as narcolepsy. Individuals over the age of 65 were not commonly tested in clinical trials of lisdexamfetamine for ADHD. According to a 2019 systematic review, lisdexamfetamine was the most effective treatment for adult ADHD.

ADHD

Long-term amphetamine exposure at sufficiently high doses in some animal species is known to produce abnormal dopamine system development or nerve damage, but, in humans with ADHD, long-term use of pharmaceutical amphetamines at therapeutic doses appears to improve brain development and nerve growth. Reviews of magnetic resonance imaging (MRI) studies suggest that long-term treatment with amphetamine decreases abnormalities in brain structure and function found in subjects with ADHD, and improves function in several parts of the brain, such as the right caudate nucleus of the basal ganglia.

Reviews of clinical stimulant research have established the safety and effectiveness of long-term continuous amphetamine use for the treatment of ADHD. Randomised controlled trials of continuous stimulant therapy for the treatment of ADHD spanning 2 years have demonstrated treatment effectiveness and safety. Two reviews have indicated that long-term continuous stimulant therapy for ADHD is effective for reducing the core symptoms of ADHD (i.e. hyperactivity, inattention, and impulsivity), enhancing quality of life and academic achievement, and producing improvements in a large number of functional outcomes across 9 categories of outcomes related to academics, antisocial behaviour, driving, non-medicinal drug use, obesity, occupation, self-esteem, service use (i.e. academic, occupational, health, financial, and legal services), and social function. Additionally, a 2024 meta-analytic systematic review reported moderate improvements in quality of life when amphetamine treatment is used for ADHD. One review highlighted a nine-month randomised controlled trial of amphetamine treatment for ADHD in children that found an average increase of 4.5 IQ points, continued increases in attention, and continued decreases in disruptive behaviours and hyperactivity. Another review indicated that, based upon the longest follow-up studies conducted to date, lifetime stimulant therapy that begins during childhood is continuously effective for controlling ADHD symptoms and reduces the risk of developing a substance use disorder as an adult. A 2025 meta-analytic systematic review of 113 randomized controlled trials demonstrated that stimulant medications significantly improved core ADHD symptoms in adults over a three-month period, with good acceptability compared to other pharmacological and non-pharmacological treatments.

Models of ADHD suggest that it is associated with functional impairments in some of the brain’s neurotransmitter systems; these functional impairments involve impaired dopamine neurotransmission in the mesocorticolimbic projection and norepinephrine neurotransmission in the noradrenergic projections from the locus coeruleus to the prefrontal cortex. Stimulants like methylphenidate and amphetamine are effective in treating ADHD because they increase neurotransmitter activity in these systems. Approximately 80% of those who use these stimulants see improvements in ADHD symptoms. Children with ADHD who use stimulant medications generally have better relationships with peers and family members, perform better in school, are less distractible and impulsive, and have longer attention spans. The Cochrane reviews on the treatment of ADHD in children, adolescents, and adults with pharmaceutical amphetamines stated that short-term studies have demonstrated that these drugs decrease the severity of symptoms, but they have higher discontinuation rates than non-stimulant medications due to their adverse side effects. A Cochrane review on the treatment of ADHD in children with tic disorders such as Tourette syndrome indicated that stimulants in general do not make tics worse, but high doses of dextroamphetamine could exacerbate tics in some individuals.

Binge Eating Disorder

Binge eating disorder (BED) is characterised by recurrent and persistent episodes of compulsive binge eating. These episodes are often accompanied by marked distress and a feeling of loss of control over eating. The pathophysiology of BED is not fully understood, but it is believed to involve dysfunctional dopaminergic reward circuitry along the cortico-striatal-thalamic-cortical loop. As of July 2024, lisdexamfetamine is the only USFDA- and TGA-approved pharmacotherapy for BED. Evidence suggests that lisdexamfetamine’s treatment efficacy in BED is underpinned at least in part by a psychopathological overlap between BED and ADHD, with the latter conceptualised as a cognitive control disorder that also benefits from treatment with lisdexamfetamine.

Lisdexamfetamine’s therapeutic effects for BED primarily involve direct action in the central nervous system after conversion to its pharmacologically active metabolite, dextroamphetamine. Centrally, dextroamphetamine increases neurotransmitter activity of dopamine and norepinephrine in prefrontal cortical regions that regulate cognitive control of behaviour. Similar to its therapeutic effect in ADHD, dextroamphetamine enhances cognitive control and may reduce impulsivity in patients with BED by enhancing the cognitive processes responsible for overriding prepotent feeding responses that precede binge eating episodes. In addition, dextroamphetamine’s actions outside of the central nervous system may also contribute to its treatment effects in BED. Peripherally, dextroamphetamine triggers lipolysis through noradrenergic signalling in adipose fat cells, leading to the release of triglycerides into blood plasma to be utilized as a fuel substrate. Dextroamphetamine also activates TAAR1 in peripheral organs along the gastrointestinal tract that are involved in the regulation of food intake and body weight. Together, these actions confer an anorexigenic effect that promotes satiety in response to feeding and may decrease binge eating as a secondary effect. While lisdexamfetamine’s anorexigenic effects contribute to its efficacy in BED, evidence indicates that the enhancement of cognitive control is necessary and sufficient for addressing the disorder’s underlying psychopathology. This view is supported by the failure of anti-obesity medications and other appetite suppressants to significantly reduce BED symptom severity, despite their capacity to induce weight loss.

Medical reviews of randomised controlled trials have demonstrated that lisdexamfetamine, at doses between 50–70 mg, is safe and effective for the treatment of moderate-to-severe BED in adults. These reviews suggest that lisdexamfetamine is persistently effective at treating BED and is associated with significant reductions in the number of binge eating days and binge eating episodes per week. Furthermore, a meta-analytic systematic review highlighted an open-label, 12-month extension safety and tolerability study that reported lisdexamfetamine remained effective at reducing the number of binge eating days for the duration of the study. In addition, both a review and a meta-analytic systematic review found lisdexamfetamine to be superior to placebo in several secondary outcome measures, including persistent binge eating cessation, reduction of obsessive-compulsive related binge eating symptoms, reduction of body-weight, and reduction of triglycerides. Lisdexamfetamine, like all pharmaceutical amphetamines, has direct appetite suppressant effects that may be therapeutically useful in both BED and its comorbidities. Based on reviews of neuroimaging studies involving BED-diagnosed participants, therapeutic neuroplasticity in dopaminergic and noradrenergic pathways from long-term use of lisdexamfetamine may be implicated in lasting improvements in the regulation of eating behaviours that are observed.

Narcolepsy

Narcolepsy is a chronic sleep-wake disorder that is associated with excessive daytime sleepiness, cataplexy, and sleep paralysis. Patients with narcolepsy are diagnosed as either type 1 or type 2, with only the former presenting cataplexy symptoms. Type 1 narcolepsy results from the loss of approximately 70,000 orexin-releasing neurons in the lateral hypothalamus, leading to significantly reduced cerebrospinal orexin levels; this reduction is a diagnostic biomarker for type 1 narcolepsy. Lateral hypothalamic orexin neurons innervate every component of the ascending reticular activating system (ARAS), which includes noradrenergic, dopaminergic, histaminergic, and serotonergic nuclei that promote wakefulness.

Amphetamine’s therapeutic mode of action in narcolepsy primarily involves increasing monoamine neurotransmitter activity in the ARAS. This includes noradrenergic neurons in the locus coeruleus, dopaminergic neurons in the ventral tegmental area, histaminergic neurons in the tuberomammillary nucleus, and serotonergic neurons in the dorsal raphe nucleus. Dextroamphetamine, the more dopaminergic enantiomer of amphetamine, is particularly effective at promoting wakefulness because dopamine release has the greatest influence on cortical activation and cognitive arousal, relative to other monoamines. In contrast, levoamphetamine may have a greater effect on cataplexy, a symptom more sensitive to the effects of norepinephrine and serotonin. Noradrenergic and serotonergic nuclei in the ARAS are involved in the regulation of the REM sleep cycle and function as “REM-off” cells, with amphetamine’s effect on norepinephrine and serotonin contributing to the suppression of REM sleep and a possible reduction of cataplexy at high doses.

The American Academy of Sleep Medicine (AASM) 2021 clinical practice guideline conditionally recommends dextroamphetamine for the treatment of both type 1 and type 2 narcolepsy. Treatment with pharmaceutical amphetamines is generally less preferred relative to other stimulants (e.g. modafinil) and is considered a third-line treatment option. Medical reviews indicate that amphetamine is safe and effective for the treatment of narcolepsy. Amphetamine appears to be most effective at improving symptoms associated with hypersomnolence, with three reviews finding clinically significant reductions in daytime sleepiness in patients with narcolepsy. Additionally, these reviews suggest that amphetamine may dose-dependently improve cataplexy symptoms. However, the quality of evidence for these findings is low and is consequently reflected in the AASM’s conditional recommendation for dextroamphetamine as a treatment option for narcolepsy.

Enhancing Performance

Cognitive Performance

In 2015, a systematic review and a meta-analysis of high quality clinical trials found that, when used at low (therapeutic) doses, amphetamine produces modest yet unambiguous improvements in cognition, including working memory, long-term episodic memory, inhibitory control, and some aspects of attention, in normal healthy adults; these cognition-enhancing effects of amphetamine are known to be partially mediated through the indirect activation of both dopamine D1 receptor and α2-adrenergic receptor in the prefrontal cortex. A systematic review from 2014 found that low doses of amphetamine also improve memory consolidation, in turn leading to improved recall of information. Therapeutic doses of amphetamine also enhance cortical network efficiency, an effect which mediates improvements in working memory in all individuals. Amphetamine and other ADHD stimulants also improve task saliency (motivation to perform a task) and increase arousal (wakefulness), in turn promoting goal-directed behavior. Stimulants such as amphetamine can improve performance on difficult and boring tasks and are used by some students as a study and test-taking aid. Based upon studies of self-reported illicit stimulant use, 5–35% of college students use diverted ADHD stimulants, which are primarily used for enhancement of academic performance rather than as recreational drugs. However, high amphetamine doses that are above the therapeutic range can interfere with working memory and other aspects of cognitive control.

Physical Performance

Amphetamine is used by some athletes for its psychological and athletic performance-enhancing effects, such as increased endurance and alertness; however, non-medical amphetamine use is prohibited at sporting events that are regulated by collegiate, national, and international anti-doping agencies. In healthy people at oral therapeutic doses, amphetamine has been shown to increase muscle strength, acceleration, athletic performance in anaerobic conditions, and endurance (i.e. it delays the onset of fatigue), while improving reaction time. Amphetamine improves endurance and reaction time primarily through reuptake inhibition and release of dopamine in the central nervous system. Amphetamine and other dopaminergic drugs also increase power output at fixed levels of perceived exertion by overriding a “safety switch”, allowing the core temperature limit to increase in order to access a reserve capacity that is normally off-limits. At therapeutic doses, the adverse effects of amphetamine do not impede athletic performance; however, at much higher doses, amphetamine can induce effects that severely impair performance, such as rapid muscle breakdown and elevated body temperature.

Available Forms

Lisdexamfetamine is available as the dimesylate salt in the form of both oral capsules and chewable tablets. A dose of 50 mg of lisdexamfetamine dimesylate is approximately equimolar to a 20 mg dose of dextroamphetamine sulfate or to 15 mg dextroamphetamine free-base in terms of the amount of dextroamphetamine contained. Lisdexamfetamine capsules can be swallowed intact, or they can be opened and mixed into water, yogurt, or applesauce and consumed in that manner.

Contraindications

Pharmaceutical lisdexamfetamine is contraindicated in people with hypersensitivity to amphetamine products or any of the formulation’s inactive ingredients.[7] It is also contraindicated in patients who have used a monoamine oxidase inhibitor (MAOI) within the last 14 days. Amphetamine products are contraindicated by the United States Food and Drug Administration (USFDA) in people with a history of drug abuse, heart disease, or severe agitation or anxiety, or in those currently experiencing arteriosclerosis, glaucoma, hyperthyroidism, or severe hypertension. However, a European consensus statement on adult ADHD noted that stimulants do not worsen substance misuse in adults with ADHD and comorbid substance use disorder and should not be avoided in these individuals. In any case, the statement noted that immediate-release stimulants should be avoided in those with both ADHD and substance use disorder and that slower-release stimulant formulations like OROSTooltip osmotic-controlled release oral delivery system methylphenidate (Concerta) and lisdexamfetamine should be preferred due to their lower misuse potential. Prescribing information approved by the Australian Therapeutic Goods Administration further contraindicates anorexia.

Adverse Effects

Products containing lisdexamfetamine have a comparable drug safety profile to those containing amphetamine. The major side effects of lisdexamfetamine in short-term clinical trials (≥5% incidence) have included decreased appetite, insomnia, dry mouth, weight loss, irritability, upper abdominal pain, nausea, vomiting, diarrhoea, constipation, increased heart rate, anxiety, dizziness, and feeling jittery. Rates of side effects may vary in adults, adolescents, and children. Rare but serious side effects of lisdexamfetamine may include mania, sudden cardiac death in those with underlying heart problems, stimulant psychosis, and serotonin syndrome.

Interactions

  • Acidifying agents: Drugs or foods that acidify the urine, such as ascorbic acid, increase urinary excretion of dextroamphetamine, thus decreasing the half-life and effectiveness of dextroamphetamine in the body.
  • Alkalinising agents: Drugs or foods that alkalinise the urine, such as sodium bicarbonate, decrease urinary excretion of dextroamphetamine, thus increasing the half-life and effectiveness of dextroamphetamine in the body.
  • CYP2D6 inhibitors: Hydroxylation via the cytochrome P450 enzyme CYP2D6 is the major pathway of metabolism of dextroamphetamine. Potent CYP2D6 inhibitors, such as paroxetine, fluoxetine, bupropion, and duloxetine, among others, may inhibit the metabolism of dextroamphetamine and thereby increase exposure to it. Studies characterising this potential interaction are currently lacking. Concomitant use of lisdexamfetamine with CYP2D6 inhibitors may increase the risk of serotonin syndrome due to greater drug exposure.
  • Monoamine oxidase inhibitors: Concomitant use of MAOIs and central nervous system stimulants such as lisdexamfetamine can cause a hypertensive crisis.
  • Norepinephrine reuptake inhibitors (NRIs) like atomoxetine prevent norepinephrine release induced by amphetamines and have been found to reduce the stimulant, euphoriant, and sympathomimetic effects of dextroamphetamine in humans.

Pharmacology

Mechanism of Action

Lisdexamfetamine is an inactive prodrug that is converted in the body to dextroamphetamine, a pharmacologically active compound that is responsible for the drug’s activity. After oral ingestion, lisdexamfetamine is broken down by enzymes in red blood cells to form L-lysine, a naturally occurring essential amino acid, and dextroamphetamine. The half-life of this conversion is roughly 1 hour. The conversion of lisdexamfetamine to dextroamphetamine is not affected by gastrointestinal pH and is unlikely to be affected by alterations in normal gastrointestinal transit times. Studies show a linear relationship between peak plasma concentration of dextroamphetamine and lisdexamfetamine dose up to lisdexamfetamine doses of 250mg.

The optical isomers of amphetamine, i.e. dextroamphetamine and levoamphetamine, are TAAR1 agonists and vesicular monoamine transporter 2 inhibitors that can enter monoamine neurons; this allows them to release monoamine neurotransmitters (dopamine, norepinephrine, and serotonin, among others) from their storage sites in the presynaptic neuron, as well as prevent the reuptake of these neurotransmitters from the synaptic cleft.

Lisdexamfetamine was developed to provide a long-duration effect that is consistent throughout the day, with reduced potential for abuse. The attachment of the amino acid lysine slows down the relative amount of dextroamphetamine available in the bloodstream. Because no free dextroamphetamine is present in lisdexamfetamine capsules, dextroamphetamine does not become available through mechanical manipulation, such as crushing or simple extraction. A relatively sophisticated biochemical process is needed to produce dextroamphetamine from lisdexamfetamine. As opposed to Adderall, which contains amphetamine salts in a 3:1 dextro:levo ratio, lisdexamfetamine is a single-enantiomer dextroamphetamine formula. Studies conducted show that lisdexamfetamine dimesylate may have less abuse potential than dextroamphetamine and an abuse profile similar to diethylpropion at dosages that are FDA-approved for treatment of ADHD, but still has a high abuse potential when this dosage is exceeded by over 100%.

Pharmacokinetics

The oral bioavailability of amphetamine varies with gastrointestinal pH; it is well absorbed from the gut, and bioavailability is typically 90%. Amphetamine is a weak base with a pKa of 9.9; consequently, when the pH is basic, more of the drug is in its lipid soluble free base form, and more is absorbed through the lipid-rich cell membranes of the gut epithelium. Conversely, an acidic pH means the drug is predominantly in a water-soluble cationic (salt) form, and less is absorbed. Approximately 20% of amphetamine circulating in the bloodstream is bound to plasma proteins. Following absorption, amphetamine readily distributes into most tissues in the body, with high concentrations occurring in cerebrospinal fluid and brain tissue.

The half-lives of amphetamine enantiomers differ and vary with urine pH. At normal urine pH, the half-lives of dextroamphetamine and levoamphetamine are 9–11 hours and 11–14 hours, respectively. Highly acidic urine will reduce the enantiomer half-lives to 7 hours; highly alkaline urine will increase the half-lives up to 34 hours. The immediate-release and extended release variants of salts of both isomers reach peak plasma concentrations at 3 hours and 7 hours post-dose respectively. Amphetamine is eliminated via the kidneys, with 30–40% of the drug being excreted unchanged at normal urinary pH. When the urinary pH is basic, amphetamine is in its free base form, so less is excreted. When urine pH is abnormal, the urinary recovery of amphetamine may range from a low of 1% to a high of 75%, depending mostly upon whether urine is too basic or acidic, respectively. Following oral administration, amphetamine appears in urine within 3 hours. Roughly 90% of ingested amphetamine is eliminated 3 days after the last oral dose.

Lisdexamfetamine is a prodrug of dextroamphetamine. It is not as sensitive to pH as amphetamine when being absorbed in the gastrointestinal tract. Following absorption into the blood stream, lisdexamfetamine is completely converted by red blood cells to dextroamphetamine and the amino acid L-lysine by hydrolysis via undetermined aminopeptidase enzymes. This is the rate-limiting step in the bioactivation of lisdexamfetamine. The elimination half-life of lisdexamfetamine is generally less than 1 hour. Due to the necessary conversion of lisdexamfetamine into dextroamphetamine, levels of dextroamphetamine with lisdexamfetamine peak about one hour later than with an equivalent dose of immediate-release dextroamphetamine. Presumably due to its rate-limited activation by red blood cells, intravenous administration of lisdexamfetamine shows greatly delayed time to peak and reduced peak levels compared to intravenous administration of an equivalent dose of dextroamphetamine. The pharmacokinetics of lisdexamfetamine are similar regardless of whether it is administered orally, intranasally, or intravenously. Hence, in contrast to dextroamphetamine, parenteral use does not enhance the subjective effects of lisdexamfetamine. Because of its behaviour as a prodrug and its pharmacokinetic differences, lisdexamfetamine has a longer duration of therapeutic effect than immediate-release dextroamphetamine and shows reduced misuse potential.

CYP2D6, dopamine β-hydroxylase (DBH), flavin-containing monooxygenase 3 (FMO3), butyrate-CoA ligase (XM-ligase), and glycine N-acyltransferase (GLYAT) are the enzymes known to metabolise amphetamine or its metabolites in humans. Amphetamine has a variety of excreted metabolic products, including 4-hydroxyamphetamine, 4-hydroxynorephedrine, 4-hydroxyphenylacetone, benzoic acid, hippuric acid, norephedrine, and phenylacetone. Among these metabolites, the active sympathomimetics are 4-hydroxyamphetamine, 4-hydroxynorephedrine, and norephedrine. The main metabolic pathways involve aromatic para-hydroxylation, aliphatic alpha- and beta-hydroxylation, N-oxidation, N-dealkylation, and deamination.

Chemistry

Lisdexamfetamine is a substituted amphetamine with an amide linkage formed by the condensation of dextroamphetamine with the carboxylate group of the essential amino acid L-lysine. The reaction occurs with retention of stereochemistry, so the product lisdexamfetamine exists as a single stereoisomer. There are many possible names for lisdexamfetamine based on IUPAC nomenclature, but it is usually named as N-[(2S)-1-phenyl-2-propanyl]-L-lysinamide or (2S)-2,6-diamino-N-[(1S)-1-methyl-2-phenylethyl]hexanamide.

Amine functional groups are vulnerable to oxidation in air and so pharmaceuticals containing them are usually formulated as salts where this moiety has been protonated. This increases stability, water solubility, and, by converting a molecular compound to an ionic compound, increases the melting point and thereby ensures a solid product. In the case of lisdexamfetamine, this is achieved by reacting with two equivalents of methanesulfonic acid to produce the dimesylate salt, a water-soluble (792 mg mL−1) powder with a white to off-white colour.

Comparison to other Formulations

Lisdexamfetamine dimesylate is one marketed formulation delivering dextroamphetamine.

Society and Culture

Name

Lisdexamfetamine is the International Nonproprietary Name (INN) and is a contraction of L-lysine-dextroamphetamine.

As of November 2020, lisdexamfetamine is sold under the following brand names: Aduvanz, Elvanse, Juneve, Samexid, Tyvense, Venvanse, and Vyvanse.

Research

Depression

Amphetamine was used to treat depression starting in the 1930s and has been described as the first antidepressant. In clinical studies in the 1970s and 1980s, psychostimulants, including amphetamine and methylphenidate, were found to transiently improve mood in a majority of people with depression and to increase psychomotor activation in almost all individuals.

Some clinical trials that used lisdexamfetamine as an add-on therapy with a selective serotonin reuptake inhibitor (SSRI) or serotonin-norepinephrine reuptake inhibitor (SNRI) for treatment-resistant depression indicated that this is no more effective than the use of an SSRI or SNRI alone. Other studies indicated that psychostimulants potentiated antidepressants, and were under-prescribed for treatment-resistant depression. In those studies, patients showed significant improvement in energy, mood, and psychomotor activity. Clinical guidelines advise caution in the use of stimulants for depression and advise them only as second- or third-line adjunctive agents.

In February 2014, Shire announced that two late-stage clinical trials had found that Vyvanse was not an effective treatment for depression, and development for this indication was discontinued. A 2018 meta-analysis of randomised controlled trials of lisdexamfetamine for antidepressant augmentation in people with major depressive disorder—the first to be conducted—found that lisdexamfetamine was not significantly better than placebo in improving Montgomery–Åsberg Depression Rating Scale scores, response rates, or remission rates. However, there was indication of a small effect in improving depressive symptoms that approached trend-level significance. Lisdexamfetamine was well-tolerated in the meta-analysis. The quantity of evidence was limited, with only four trials included. In a subsequent 2022 network meta-analysis, lisdexamfetamine was significantly effective as an antidepressant augmentation for treatment-resistant depression.

Although lisdexamfetamine has shown limited effectiveness in the treatment of depression in clinical trials, a phase II clinical study found that the addition of lisdexamfetamine to an antidepressant improved executive dysfunction in people with mild major depressive disorder but persisting executive dysfunction.

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What is the Eating Disorder Diagnostic Scale?

Published on by Andrew MarshallLeave a comment

Introduction

The Eating Disorder Diagnostic Scale (EDDS) is a 22 item self-report questionnaire that assesses the presence of three eating disorders; anorexia nervosa, bulimia nervosa and binge eating disorder.

Outline

It was adapted by Stice et al. in 2000 from the validated structured psychiatric interview: The Eating Disorder Examination (EDE) and the eating disorder module of the Structured Clinical Interview for DSM-IV (SCID)16.

A study was made to complete the EDDS research; the process to create and finalise the questionnaire. A group of people eating-disorders researchers take a looked at a preliminary version of the questionnaire and made a final decision of which questions to put on the final questionnaire with the 22 questions.

  • The questionnaire starts off with questions about the patient’s feelings towards his/her physical appearance, specifically the weight.
  • Then, it proceeds to questions about having episodes of eating with a loss of control and how he/she felt after overeating.
  • The questions afterwards are about the patient’s experience on fasting, making themselves vomit and using laxatives to prevent weight gain.
  • It will then ask you how much body image problems impact your relationship and friendship with others.
  • Lastly, the questionnaire asks for the patient’s current weight, height, sex and age.

The EDDS questionnaire is used for researchers to provide some cures for the three types of eating disorder. It is more efficient than having an interview because it’s easier to get a result, from a group of participants, with the 22-questions questionnaire. Having to interview each participant is a harder and more time-consuming way to get a result. This questionnaire is also useful for primary care/ clinical purposes to identify patients with eating pathology.

In follow up studies of the reliability and validity of the EDDS, it was shown to be sufficiently sensitive to detect the effects of eating disorders prevention programs, response to such programs and the future onset of eating disorder pathology and depression. The EDDS shows both full and subthreshold diagnoses for anorexia nervosa, bulimia nervosa and binge eating disorder. EDDS is a continuous eating disorder symptom composite score. The PhenX Toolkit uses the EDDS for as an Eating Disorders Screener protocol.

Refer to:

Book: Binge Eating Disorder: Step-by-Step Guide to Prevention and Recovery from Binge Eating Disorder

Published on by Andrew MarshallLeave a comment

Book Title:

Binge Eating Disorder: Step-by-Step Guide to Prevention and Recovery from Binge Eating Disorder.

Author(s): Michael Miller and Ashley Victoria.

Year: 2018.

Edition: First (1st).

Publisher: CreateSpace Independent Publishing Platform.

Type(s): Paperback, Audiobook, and Kindle.

Synopsis:

Do you consume abnormally large amounts of food in one sitting? Do you doubt that your untimely binging is a problem? Are you someone who is not comfortable revealing that you suffer from binge eating disorder? If your answer to any of the above questions is a “YES” then you have got hold of the right book.

Binge eating is a serious disorder that masks itself as overeating and can go undetected for long periods of time. It may surprise you, but binge eating affects more people than bulimia and anorexia. Consuming abnormally large amounts of food in one sitting becomes a regular feature in the life of binge eaters. Most of these individuals don’t even recognise that there’s something wrong with them until they get overweight or obese.

Part of the reason why this happens is because there is a lack of awareness among people with regards to this disorder. The symptoms are often passed off as overeating and most people think that it’s normal for someone to eat until their guts hurt.

The very reason we wanted to come up with a book for people suffering from binge eating disorder was to spread awareness about it so they don’t face the issues many people did and ignore the problem.

Through the course of the book, we intend to openly discuss binge eating in detail. Until now if you thought that you might have to live with this disorder forever, this guide will prove you wrong. Here is a quick snapshot of what is covered in the book:

  • Details of BED (binge eating disorder).
  • Symptoms of BED.
  • Preventive measures.
  • Steps to eliminate the habit.
  • Facts on binge eating.
  • Role of the society, family and media towards eating disorders.
  • Habits that trigger binging.

What is an Other Specified Feeding or Eating Disorder?

Published on by Andrew Marshall1 Comment

Introduction

Other specified feeding or eating disorder (OSFED) is a DSM-5 category that, along with unspecified feeding or eating disorder (UFED), replaces the category formerly called eating disorder not otherwise specified (EDNOS) in the DSM-IV-TR.

It captures feeding disorders and eating disorders of clinical severity that do not meet diagnostic criteria for anorexia nervosa (AN), bulimia nervosa (BN), binge eating disorder (BED), avoidant/restrictive food intake disorder (ARFID), pica, or rumination disorder.

OSFED includes five examples:

  1. Atypical anorexia nervosa.
  2. Atypical bulimia nervosa of low frequency and/or limited duration.
  3. Binge eating disorder of low frequency and/or limited duration.
  4. Purging disorder.
  5. Night eating syndrome (NES).

Brief History

In 1980, DSM-III was the first DSM to include a category for eating disorders that could not be classified in the categories of AN, BN, or pica. This category was called Atypical Eating Disorder. Atypical Eating Disorder was described in one sentence in the DSM-III and received very little attention in the literature, as it was perceived to be uncommon compared to the other defined eating disorders. In DSM-III-R, published in 1987, the Atypical Eating Disorder category became known as Eating Disorder Not Otherwise Specified (EDNOS). DSM-III-R included examples of individuals who would meet criteria for EDNOS, in part to acknowledge the increasingly recognized heterogeneity of individuals within the diagnostic category.

In 1994, DSM-IV was published and expanded EDNOS to include six clinical presentations. These presentations included individuals who:

  • Met criteria for AN, but continued to menstruate;
  • Met criteria for AN, but still had weight in the normal range despite significant weight loss;
  • Met criteria for BN but did not meet frequency criterion for binge eating or purging;
  • Engaged in inappropriate compensatory behaviour after eating small amounts of food; or
  • Repeatedly chewed or spit out food, or who binged on food but did not subsequently purge.

A disadvantage of DSM-IV’s broad EDNOS category was that people with very different symptoms were still classified as having the same diagnosis, making it difficult to access care specific to the disorder and conduct research on the diversity of pathology within EDNOS. Furthermore, EDNOS was perceived as less severe than AN or BN, despite findings that individuals diagnosed with EDNOS share similarities with full-threshold AN or BN in the degree of eating pathology, general psychopathology, and physical health. This perception prevented people in need from seeking help or insurance companies from covering treatment costs. DSM-5, published in 2013, sought to address these issues by adding new diagnoses and revising existing criteria.

Epidemiology

Few studies to date have examined OSFED prevalence. The largest community study is by Stice (2013), who examined 496 adolescent females who completed annual diagnostic interviews over 8 years. Lifetime prevalence by age 20 for OSFED overall was 11.5%. 2.8% had atypical AN, 4.4% had subthreshold BN, 3.6% had subthreshold BED, and 3.4% had purging disorder. Peak age of onset for OSFED was 18-20 years. NES was not assessed in this study, but estimates from other studies suggest that it presents in 1% of the general population.

A few studies have compared the prevalence of EDNOS and OSFED and found that though the prevalence of atypical eating disorders decreased with the new classification system, the prevalence still remains high. For example, in a population of 215 young patients presenting for ED treatment, the diagnosis of EDNOS to OSFED decreased from 62.3% to 32.6%. In another study of 240 females in the US with a lifetime history of an eating disorder, the prevalence changed from 67.9% EDNOS to 53.3% OSFED. Although the prevalence appears to reduce when using the categorisations of EDNOS vs. OSFED, a high proportion of cases still receive diagnoses of atypical eating disorders, which creates difficulties in communication, treatment planning, and basic research.

Classification

The five OSFED examples that can be considered eating disorders include atypical AN, BN (of low frequency and/or limited duration), BED (of low frequency and/or limited duration), purging disorder, and NES. Of note, OSFED is not limited to these five examples, and can include individuals with heterogeneous eating disorder presentations (i.e. OSFED-other). Another term, UFED, is used to describe individuals for whom full diagnostic criteria are not met but the reason remains unspecified or the clinician does not have adequate information to make a more definitive diagnosis.

Atypical Anorexia NervosaIn atypical AN, individuals meet all of the criteria for AN, with the exception of the weight criterion: the individual’s weight remains within or above the normal range, despite significant weight loss.
Atypical Bulimia NervosaIn this sub-threshold version of BN, individuals meet all criteria for BN, with the exception of the frequency criterion: binge eating and inappropriate compensatory behaviours occur, on average, less than once a week and/or for fewer than 3 months.
Binge Eating Disorder of Low Frequency and/or Limited DurationIn this sub-threshold version of BED, individuals must meet all criteria for BED, with the exception of the frequency criterion: binge eating occurs, on average, less than once a week and/or for fewer than 3 months.
Purging DisorderIn purging disorder, purging behaviour aimed to influence weight or shape is present, but in the absence of binge eating.
Night Eating SyndromeIn NES, individuals have recurrent episodes of eating at night, such as eating after awakening from sleep or excess calorie intake after the evening meal. This eating behaviour is not culturally acceptable by group norms, such as the occasional late-night munchies after a gathering. NES includes an awareness and recall of the eating, is not better explained by external influences such as changes in the individual’s sleep-wake cycle, and causes significant distress and/or impairment of functioning.

Though not defined specifically in DSM-5, research criteria for this diagnosis proposed adding the following criteria (1) the consumption of at least 25% of daily caloric intake after the evening meal and/or (2) evening awakenings with ingestions at least twice per week.

Treatment

Few studies guide the treatment of individuals with OSFED. However, cognitive behavioural therapy (CBT), which focuses on the interplay between thoughts, feelings, and behaviours, has been shown to be the leading evidence-based treatment for the eating disorders of BN and BED. For OSFED, a particular cognitive behavioural treatment can be used called CBT-Enhanced (CBT-E), which was designed to treat all forms of eating disorders. This method focuses not only what is thought to be the central cognitive disturbance in eating disorders (i.e. over-evaluation of eating, shape, and weight), but also on modifying the mechanisms that sustain eating disorder psychopathology, such as perfectionism, core low self-esteem, mood intolerance, and interpersonal difficulties. CBT-E showed effectiveness in two studies (total N = 219) and well maintained over 60-week follow-up periods. CBT-E is not specific to individual types of eating disorders but is based on the concept that common mechanisms are involved in the persistence of atypical eating disorders, AN, and BN.

What is Binge Eating Disorder?

Published on by Andrew Marshall5 Comments

Introduction

Binge eating disorder (BED) is an eating disorder characterised by frequent and recurrent binge eating episodes with associated negative psychological and social problems, but without the compensatory behaviours common to Bulimia Nervosa, OSFED, or the Binge-Purge subtype of Anorexia Nervosa.

BED is a recently described condition, which was required to distinguish binge eating similar to that seen in bulimia nervosa but without characteristic purging. Individuals who are diagnosed with bulimia nervosa and binge eating disorder exhibit similar patterns of compulsive overeating, neurobiological features of dysfunctional cognitive control and food addiction, and biological and environmental risk factors. Some professionals consider BED to be a milder form of bulimia with the two conditions on the same spectrum.

Binge eating is one of the most prevalent eating disorders among adults, though there tends to be less media coverage and research about the disorder in comparison to anorexia nervosa and bulimia nervosa.

Brief History

The disorder was first described in 1959 by psychiatrist and researcher Albert Stunkard as “night eating syndrome” (NES). The term “binge eating” was coined to describe the same bingeing-type eating behaviour but without the exclusive nocturnal component.

There is generally less research on binge eating disorder in comparison to anorexia nervosa and bulimia nervosa.

Signs and Symptoms

Binge eating is the core symptom of BED; however, not everyone who binge eats has BED. An individual may occasionally binge eat without experiencing many of the negative physical, psychological, or social effects of BED. This may be considered disordered eating rather than a clinical disorder. Precisely defining binge eating can be problematic, however binge eating episodes in BED are generally described as having the following potential features:

  • Eating much faster than normal, perhaps in a short space of time.
  • Eating until feeling uncomfortably full.
  • Eating a large amount when not hungry.
  • Subjective loss of control over how much or what is eaten.
  • Binges may be planned in advance, involving the purchase of special binge foods, and the allocation of specific time for binging, sometimes at night.
  • Eating alone or secretly due to embarrassment over the amount of food consumed.
  • There may be a dazed mental state during the binge.
  • Not being able to remember what was eaten after the binge.
  • Feelings of guilt, shame or disgust following a food binge.

In contrast to bulimia nervosa, binge eating episodes are not regularly followed by activities intended to compensate for the amount of food consumed, such as self-induced vomiting, laxative or enema misuse, or strenuous exercise. BED is characterised more by overeating than dietary restriction. Those with BED often have poor body image and frequently diet, but are unsuccessful due to the severity of their binge eating.

Obesity is common in persons with BED, as is depression, low self-esteem, stress and boredom. Those with BED are also at risk of Non-alcoholic fatty liver disease, menstrual irregularities such as amenorrhea, and gastrointestinal problems such as acid reflux and heartburn.

Causes

As with other eating disorders, binge eating is an “expressive disorder” – a disorder that is an expression of deeper psychological problems. People who have binge eating disorder have been found to have higher weight bias internalisation, which includes low self-esteem, unhealthy eating patterns, and general body dissatisfaction. Binge eating disorder commonly develops as a result or side effect of depression, as it is common for people to turn to comfort foods when they are feeling down.

There was resistance to give binge eating disorder the status of a fully fledged eating disorder because many perceived binge eating disorder to be caused by individual choices. Previous research has focused on the relationship between body image and eating disorders, and concludes that disordered eating might be linked to rigid dieting practices. In the majority of cases of anorexia, extreme and inflexible restriction of dietary intake leads at some point to the development of binge eating, weight regain, bulimia nervosa, or a mixed form of eating disorder not otherwise specified. Binge eating may begin when individuals recover from an adoption of rigid eating habits. When under a strict diet that mimics the effects of starvation, the body may be preparing for a new type of behaviour pattern, one that consumes a large amount of food in a relatively short period of time.

Some studies show that BED aggregates in families and could be genetic. However, very few published studies around the genetics exist.

However, other research suggests that binge eating disorder can also be caused by environmental factors and the impact of traumatic events. One study showed that women with binge eating disorder experienced more adverse life events in the year prior to the onset of the development of the disorder, and that binge eating disorder was positively associated with how frequently negative events occur. Additionally, the research found that individuals who had binge eating disorder were more likely to have experienced physical abuse, perceived risk of physical abuse, stress, and body criticism. Other risk factors may include childhood obesity, critical comments about weight, low self-esteem, depression, and physical or sexual abuse in childhood. A systematic review concluded that bulimia nervosa and binge eating disorder are more impacted by family separations, a loss in their lives and negative parent-child interactions compared to those with anorexia nervosa. A few studies have suggested that there could be a genetic component to binge eating disorder, though other studies have shown more ambiguous results. Studies have shown that binge eating tends to run in families and a twin study by Bulik, Sullivan, and Kendler has shown a, “moderate heritability for binge eating” at 41%. More research must be done before any firm conclusions can be drawn regarding the heritability of binge eating disorder. Studies have also shown that eating disorders such as anorexia and bulimia reduce coping abilities, which makes it more likely for those suffering to turn to binge eating as a coping strategy.

A correlation between dietary restraint and the occurrence of binge eating has been shown in some research. While binge eaters are often believed to be lacking in self-control, the root of such behaviour might instead be linked to rigid dieting practices. The relationship between strict dieting and binge eating is characterised by a vicious circle. Binge eating is more likely to occur after dieting, and vice versa. Several forms of dieting include delay in eating (e.g. not eating during the day), restriction of overall calorie intake (e.g. setting calorie limit to 1,000 calories per day), and avoidance of certain types of food (e.g. “forbidden” food, such as sugar, carbohydrates, etc.). Strict and extreme dieting differs from ordinary dieting. Some evidence suggests the effectiveness of moderate calorie restriction in decreasing binge eating episodes among overweight individuals with binge eating disorder, at least in the short-term.

In the US it is estimated that 3.5% of young women and 30% to 40% of people who seek weight loss treatments, can be clinically diagnosed with binge eating disorder.

Diagnosis

International Classification of Diseases

BED was first included in the Diagnostic and Statistical Manual of Mental Disorders (DSM) in 1994 simply as a feature of eating disorder. In 2013 it gained formal recognition as a psychiatric condition in the DSM-5.

The 2017 update to the American version of the ICD-10 includes BED under F50.81. ICD-11 may contain a dedicated entry (6B62), defining BED as frequent, recurrent episodes of binge eating (once a week or more over a period of several months) which are not regularly followed by inappropriate compensatory behaviours aimed at preventing weight gain.

Diagnostic and Statistical Manual

Previously considered a topic for further research exploration, binge eating disorder was included in the DSM in 2013. Until 2013, binge eating disorder was categorized as an Eating Disorder Not Otherwise Specified, an umbrella category for eating disorders that don’t fall under the categories for anorexia nervosa or bulimia nervosa. Because it was not a recognised psychiatric disorder in the DSM-IV until 2013, it has been difficult to obtain insurance reimbursement for treatments. The disorder now has its own category under DSM-5, which outlines the signs and symptoms that must be present to classify a person’s behaviour as binge eating disorder. Studies have confirmed the high predictive value of these criteria for diagnosing BED.

According to the World Health Organization’s ICD-11 classification of BED, the severity of the disorder can be classified as mild (1-3 episodes/week), moderate (4-7 episodes/week), severe (8-13 episodes/week) and extreme (>14 episodes/week).

One study claims that the method for diagnosing BED is for a clinician to conduct a structured interview using the DSM-5 criteria or taking the Eating Disorder Examination. The Structured Clinical Interview takes no more than 75 minutes to complete and has a systematic approach which follows the DSM-5 criteria. The Eating Disorder Examination is a semi-structured interview which identifies the frequency of binges and associated eating disorder features.

Treatment

Counselling and certain medication, such as lisdexamfetamine and selective serotonin reuptake inhibitor (SSRIs), may help. Some recommend a multidisciplinary approach in the treatment of the disorder.

Counselling

Cognitive behavioural therapy (CBT) treatment has been demonstrated as a more effective form of treatment for BED than behavioural weight loss programmes. 50% of BED individuals achieve complete remission from binge eating and 68-90% will reduce the amount of binge eating episodes they have. CBT has also been shown to be an effective method to address self-image issues and psychiatric comorbidities (e.g. depression) associated with the disorder. The goal of CBT is to interrupt binge-eating behaviour, learn to create a normal eating schedule, change the perception around weight and shape and develop positive attitudes about one’s body. Although this treatment is successful in eliminating binge eating episodes, it does not lead to losing any weight. Recent reviews have concluded that psychological interventions such as psychotherapy and behavioural interventions are more effective than pharmacological interventions for the treatment of binge eating disorder. A meta-analysis concluded that psychotherapy based on CBT not only significantly improved binge-eating symptomatology but also reduced a client’s BMI significantly at posttreatment and longer than 6 and 12 months after treatment. There is the 12-step Overeaters Anonymous or Food Addicts in Recovery Anonymous. Behavioural weight loss treatment has been proven to be effective as a means to achieve weight loss amongst patients.

Medication

Lisdexamfetamine is a US Food and Drug Administration (FDA)-approved drug that is used for the treatment of moderate to severe binge eating disorder in adults.

Three other classes of medications are also used in the treatment of binge eating disorder: antidepressants, anticonvulsants, and anti-obesity medications. Antidepressant medications of the selective serotonin reuptake inhibitor (SSRI) have been found to effectively reduce episodes of binge eating and reduce weight. Similarly, anticonvulsant medications such as topiramate and zonisamide may be able to effectively suppress appetite. The long-term effectiveness of medication for binge eating disorder is currently unknown. For BED patients with manic episodes, risperidone is recommended. If BED patients have bipolar depression, lamotrigine is appropriate to use.

Trials of antidepressants, anticonvulsants, and anti-obesity medications suggest that these medications are superior to placebo in reducing binge eating. Medications are not considered the treatment of choice because psychotherapeutic approaches, such as CBT, are more effective than medications for binge eating disorder. A meta-analysis concluded that using medications did not reduce binge-eating episodes and BMI posttreatment at 6-12 months. This indicates a potential possibility of relapse after withdrawal from the medications. Medications also do not increase the effectiveness of psychotherapy, though some patients may benefit from anticonvulsant and anti-obesity medications, such as phentermine/topiramate, for weight loss.

Blocking opioid receptors leads to less food intake. Additionally, bupropion and naltrexone used together may cause weight loss. Combining these alongside psychotherapies like CBT may lead to better outcomes for BED.

Surgery

Bariatric surgery has also been proposed as another approach to treat BED and a recent meta-analysis showed that approximately two-thirds of individuals who seek this type of surgery for weight loss purposes have BED. Bariatric surgery recipients who had BED prior to receiving the surgery tend to have poorer weight-loss outcomes and are more likely to continue to exhibit eating behaviours characteristic of BED.

Lifestyle Interventions

Other treatments for BED include lifestyle interventions like weight training, peer support groups, and investigation of hormonal abnormalities.

Prognosis

Individuals suffering from BED often have a lower overall quality of life and commonly experience social difficulties. Early behaviour change is an accurate prediction of remission of symptoms later.

Individuals who have BED commonly have other comorbidities such as major depressive disorder, personality disorder, bipolar disorder, substance abuse, body dysmorphic disorder, kleptomania, irritable bowel syndrome, fibromyalgia, or an anxiety disorder. Individuals may also exhibit varying degrees of panic attacks and a history of attempted suicide.

While people of a healthy weight may overeat occasionally, an ongoing habit of consuming large amounts of food in a short period of time may ultimately lead to weight gain and obesity. Bingeing episodes usually include foods that are high in fat, sugar, and/or salt, but low in vitamins and minerals, as these types of foods tend to trigger the greatest chemical and emotional rewards. The main physical health consequences of this type of eating disorder are brought on by the weight gain resulting from calorie-laden bingeing episodes. Mental and emotional consequences of binge eating disorder include social weight stigma and emotional loss of control. Up to 70% of individuals with BED may also be obese, and therefore obesity-associated morbidities such as high blood pressure and coronary artery disease type 2 diabetes mellitus gastrointestinal issues (e.g. gallbladder disease), high cholesterol levels, musculoskeletal problems and obstructive sleep apnoea may also be present.

Epidemiology

General

The prevalence of BED in the general population is approximately 1-3%, with BED cases usually occurring between the ages of 12.4 and 24.7, but prevalence rates increase until the age of 40. Binge eating disorder is the most common eating disorder in adults.

The limited amount of research that has been done on BED shows that rates of binge eating disorder are fairly comparable among men and women. The lifetime prevalence of binge eating disorder has been observed in studies to be 2.0% for men and 3.5% for women, higher than that of the commonly recognised eating disorders anorexia nervosa and bulimia nervosa. However another systematic literature review found the prevalence average to be about 2.3% in women and about 0.3% in men. Lifetime prevalence rates for BED in women can range anywhere from 1.5 to 6 times higher than in men. One literature review found that point prevalence rates for BED vary from 0.1% to 24.1% depending on the sample. This same review also found that the 12-month prevalence rates vary between 0.1% to 8.8%.

Recent studies found that eating disorders which included anorexia nervosa, bulimia nervosa and binge-eating disorder are common among sexual and gender minority populations, including gay, lesbian, bisexual and transgender people. This could be due to the minority stress and discrimination this population experiences.

Due to limited and inconsistent information and research on ethnic and racial differences, prevalence rates are hard to determine for BED. Rates of binge eating disorder have been found to be similar among black women, white women, and white men, while some studies have shown that binge eating disorder is more common among black women than among white women. However, majority of the research done around BED is focused on White women. One literature review found information citing no difference between BED prevalence among Hispanic, African American, and White women while other information found that BED prevalence was highest among Hispanics followed by Black individuals and finally White people.

Worldwide Prevalence

Eating disorders have usually been considered something that was specific to Western countries. However, the prevalence of eating disorders is increasing in other non-Western countries. Though the research on binge eating disorders tends to be concentrated in North America, the disorder occurs across cultures. In the USA, BED is present in 0.8% of male adults and 1.6% of female adults in a given year.

The prevalence of BED is lower in Nordic countries compared to Europe in a study that included Finland, Sweden, Norway, and Iceland. The point prevalence ranged from 0.4 to 1.5% and the lifetime prevalence ranged from 0.7 to 5.8% for BED in women.

In a study that included Argentina, Brazil, Chile, Colombia, Mexico, and Venezuela, the point prevalence for BED was 3.53%. Therefore, this particular study found that the prevalence for BED is higher in these Latin American countries compared to Western countries.

The prevalence of BED in Europe ranges from <1 to 4%.

Co-Morbidities

BED is co-morbid with diabetes, hypertension, previous stroke, and heart disease in some individuals.

In people who have obsessive-compulsive disorder or bipolar I or II disorders, BED lifetime prevalence was found to be higher.

Additionally, 30 to 40% of individuals seeking treatment for weight-loss can be diagnosed with binge eating disorder.

Underreporting in Men

Eating disorders are oftentimes underreported in men. Underreporting could be a result of measurement bias due to how eating disorders are defined. The current definition for eating disorders focuses on thinness. However, eating disorders in men tend to centre on muscularity and would therefore warrant a need for a different measurement definition. Further research should focus on including more men in samples since previous research has focused primarily on women.