Tag: Bulimia Nervosa

What is the Eating Disorder Diagnostic Scale?

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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:

What is Fluoxetine?

Published on by Andrew Marshall26 Comments

Introduction

Fluoxetine, sold under the brand names Prozac and Sarafem among others, is an antidepressant of the selective serotonin reuptake inhibitor (SSRI) class. It is used for the treatment of major depressive disorder, obsessive–compulsive disorder (OCD), bulimia nervosa, panic disorder, and premenstrual dysphoric disorder. It is also approved for treatment of major depressive disorder in adolescents and children 8 years of age and over. It has also been used to treat premature ejaculation. Fluoxetine is taken by mouth.

Common side effects include indigestion, trouble sleeping, sexual dysfunction, loss of appetite, dry mouth, and rash. Serious side effects include serotonin syndrome, mania, seizures, an increased risk of suicidal behaviour in people under 25 years old, and an increased risk of bleeding. Discontinuation syndrome is less likely to occur with fluoxetine than with other antidepressants, but it still happens in many cases. Fluoxetine taken during pregnancy is associated with significant increase in congenital heart defects in the newborns. It has been suggested that fluoxetine therapy may be continued during breastfeeding if it was used during pregnancy or if other antidepressants were ineffective. Its mechanism of action is unknown, but some hypothesize that it is related to serotonin activity in the brain.

Fluoxetine was discovered by Eli Lilly and Company in 1972, and entered medical use in 1986. It is on the World Health Organisation’s List of Essential Medicines. It is available as a generic medication. In 2018, it was the 23rd most commonly prescribed medication in the United States, with more than 25 million prescriptions. Lilly also markets fluoxetine in a fixed-dose combination with olanzapine as olanzapine/fluoxetine (Symbyax).

Brief History

The work which eventually led to the discovery of fluoxetine began at Eli Lilly and Company in 1970 as a collaboration between Bryan Molloy and Robert Rathbun. It was known at that time that the antihistamine diphenhydramine shows some antidepressant-like properties. 3-Phenoxy-3-phenylpropylamine, a compound structurally similar to diphenhydramine, was taken as a starting point, and Molloy synthesized a series of dozens of its derivatives. Hoping to find a derivative inhibiting only serotonin reuptake, an Eli Lilly scientist, David T. Wong, proposed to retest the series for the in vitro reuptake of serotonin, norepinephrine and dopamine. This test, carried out by Jong-Sir Horng in May 1972, showed the compound later named fluoxetine to be the most potent and selective inhibitor of serotonin reuptake of the series. Wong published the first article about fluoxetine in 1974. A year later, it was given the official chemical name fluoxetine and the Eli Lilly and Company gave it the trade name Prozac. In February 1977, Dista Products Company, a division of Eli Lilly & Company, filed an Investigational New Drug application to the US Food and Drug Administration (FDA) for fluoxetine.

Fluoxetine appeared on the Belgian market in 1986. In the US, the FDA gave its final approval in December 1987, and a month later Eli Lilly began marketing Prozac; annual sales in the US reached $350 million within a year. Worldwide sales eventually reached a peak of $2.6 billion a year.

Lilly tried several product line extension strategies, including extended release formulations and paying for clinical trials to test the efficacy and safety of fluoxetine in premenstrual dysphoric disorder and rebranding fluoxetine for that indication as “Sarafem” after it was approved by the FDA in 2000, following the recommendation of an advisory committee in 1999. The invention of using fluoxetine to treat PMDD was made by Richard Wurtman at MIT; the patent was licensed to his startup, Interneuron, which in turn sold it to Lilly.

To defend its Prozac revenue from generic competition, Lilly also fought a five-year, multimillion-dollar battle in court with the generic company Barr Pharmaceuticals to protect its patents on fluoxetine, and lost the cases for its line-extension patents, other than those for Sarafem, opening fluoxetine to generic manufacturers starting in 2001. When Lilly’s patent expired in August 2001, generic drug competition decreased Lilly’s sales of fluoxetine by 70% within two months.

In 2000 an investment bank had projected that annual sales of Sarafem could reach $250M/year. Sales of Sarafem reached about $85M/year in 2002, and in that year Lilly sold its assets connected with the drug for $295M to Galen Holdings, a small Irish pharmaceutical company specializing in dermatology and women’s health that had a sales force tasked to gynaecologists’ offices; analysts found the deal sensible since the annual sales of Sarafem made a material financial difference to Galen, but not to Lilly.

Bringing Sarafem to market harmed Lilly’s reputation in some quarters. The diagnostic category of PMDD was controversial since it was first proposed in 1987, and Lilly’s role in retaining it in the appendix of the DSM-IV-TR, the discussions for which got under way in 1998, has been criticised. Lilly was criticised for inventing a disease in order to make money, and for not innovating but rather just seeking ways to continue making money from existing drugs. It was also criticised by the FDA and groups concerned with women’s health for marketing Sarafem too aggressively when it was first launched; the campaign included a television commercial featuring a harried woman at the grocery store who asks herself if she has PMDD.

Medical Uses

Fluoxetine is frequently used to treat major depressive disorder, OCD, post-traumatic stress disorder (PTSD), bulimia nervosa, panic disorder, premenstrual dysphoric disorder, and trichotillomania. It has also been used for cataplexy, obesity, and alcohol dependence, as well as binge eating disorder. Fluoxetine seems to be ineffective for social anxiety disorder. Studies do not support a benefit in children with autism, though there is but tentative evidence for its benefit in adult autism.

Depression

Efficacy of fluoxetine for acute and maintenance treatment of major depressive disorder in adults as well as children and adolescents (8 to 18 years) was established in multiple clinical trials. In addition to being effective for depression in 6-week long double-blind controlled trials, fluoxetine was better than placebo for the prevention of depression recurrence, when the patients, who originally responded to fluoxetine, were treated for a further 38 weeks. Efficacy of fluoxetine for geriatric as well as paediatric depression was also demonstrated in placebo-controlled trials.

Fluoxetine is as effective as tricyclic antidepressants but is better tolerated. It is less effective than sertraline, mirtazapine, and venlafaxine. According to a network analysis of clinical trials, fluoxetine may belong to the group of less effective antidepressants; however, its acceptability is higher than any other antidepressant, except agomelatine.

Obsessive-Compulsive Disorder

The efficacy of fluoxetine in the treatment of OCD was demonstrated in two randomised multicentre phase III clinical trials. The pooled results of these trials demonstrated that 47% of completers treated with the highest dose were “much improved” or “very much improved” after 13 weeks of treatment, compared to 11% in the placebo arm of the trial. The American Academy of Child and Adolescent Psychiatry state that SSRIs, including fluoxetine, should be used as first-line therapy in children, along with cognitive behavioural therapy (CBT), for the treatment of moderate to severe OCD.

Panic Disorder

The efficacy of fluoxetine in the treatment of panic disorder was demonstrated in two 12-week randomised multicentre phase III clinical trials that enrolled patients diagnosed with panic disorder, with or without agoraphobia. In the first trial, 42% of subjects in the fluoxetine-treated arm were free of panic attacks at the end of the study, vs. 28% in the placebo arm. In the second trial, 62% of fluoxetine treated patients were free of panic attacks at the end of the study, vs. 44% in the placebo arm.

Bulimia Nervosa

A 2011 systematic review discussed seven trials which compared fluoxetine to a placebo in the treatment of bulimia nervosa, six of which found a statistically significant reduction in symptoms such as vomiting and binge eating. However, no difference was observed between treatment arms when fluoxetine and psychotherapy were compared to psychotherapy alone.

Premenstrual Dysphoric Disorder

Fluoxetine is used to treat premenstrual dysphoric disorder, a condition where individuals have affective and somatic symptoms monthly during the luteal phase of menstruation. Taking fluoxetine 20 mg/d can be effective in treating PMDD, though doses of 10mg/d have also been prescribed effectively.

Impulsive Aggression

Fluoxetine is considered a first-line medication for the treatment of impulsive aggression of low intensity. Fluoxetine reduced low intensity aggressive behaviour in patients in intermittent aggressive disorder and borderline personality disorder. Fluoxetine also reduced acts of domestic violence in alcoholics with a history of such behaviour.

Special Populations

In children and adolescents, fluoxetine is the antidepressant of choice due to tentative evidence favouring its efficacy and tolerability. In pregnancy, fluoxetine is considered a category C drug by the US Food and Drug Administration (FDA). Evidence supporting an increased risk of major foetal malformations resulting from fluoxetine exposure is limited, although the Medicines and Healthcare products Regulatory Agency (MHRA) of the UK has warned prescribers and patients of the potential for fluoxetine exposure in the first trimester (during organogenesis, formation of the foetal organs) to cause a slight increase in the risk of congenital cardiac malformations in the newborn. Furthermore, an association between fluoxetine use during the first trimester and an increased risk of minor foetal malformations was observed in one study.

However, a systematic review and meta-analysis of 21 studies – published in the Journal of Obstetrics and Gynaecology Canada – concluded:

“the apparent increased risk of fetal cardiac malformations associated with maternal use of fluoxetine has recently been shown also in depressed women who deferred SSRI therapy in pregnancy, and therefore most probably reflects an ascertainment bias. Overall, women who are treated with fluoxetine during the first trimester of pregnancy do not appear to have an increased risk of major fetal malformations.”

Per the FDA, infants exposed to SSRIs in late pregnancy may have an increased risk for persistent pulmonary hypertension of the newborn. Limited data support this risk, but the FDA recommends physicians consider tapering SSRIs such as fluoxetine during the third trimester. A 2009 review recommended against fluoxetine as a first-line SSRI during lactation, stating, “Fluoxetine should be viewed as a less-preferred SSRI for breastfeeding mothers, particularly with newborn infants, and in those mothers who consumed fluoxetine during gestation.” Sertraline is often the preferred SSRI during pregnancy due to the relatively minimal foetal exposure observed and its safety profile while breastfeeding.

Adverse Effects

Side effects observed in fluoxetine-treated persons in clinical trials with an incidence >5% and at least twice as common in fluoxetine-treated persons compared to those who received a placebo pill include abnormal dreams, abnormal ejaculation, anorexia, anxiety, asthenia, diarrhoea, dry mouth, dyspepsia, flu syndrome, impotence, insomnia, decreased libido, nausea, nervousness, pharyngitis, rash, sinusitis, somnolence, sweating, tremor, vasodilation, and yawning. Fluoxetine is considered the most stimulating of the SSRIs (that is, it is most prone to causing insomnia and agitation). It also appears to be the most prone of the SSRIs for producing dermatologic reactions (e.g. urticaria (hives), rash, itchiness, etc.).

Sexual Dysfunction

Sexual dysfunction, including loss of libido, anorgasmia, lack of vaginal lubrication, and erectile dysfunction, are some of the most commonly encountered adverse effects of treatment with fluoxetine and other SSRIs. While early clinical trials suggested a relatively low rate of sexual dysfunction, more recent studies in which the investigator actively inquires about sexual problems suggest that the incidence is >70%. On the 11th of June 2019 the Pharmacovigilance Risk Assessment Committee of the European Medicines Agency concluded that there is a possible causal association between SSRI use and long-lasting sexual dysfunction that persists despite discontinuation of SSRI, including fluoxetine, and that the labels of these drugs should be updated to include a warning.

Discontinuation Syndrome

Fluoxetine’s longer half-life makes it less common to develop discontinuation syndrome following cessation of therapy, especially when compared to antidepressants with shorter half-lives such as paroxetine. Although gradual dose reductions are recommended with antidepressants with shorter half-lives, tapering may not be necessary with fluoxetine.

Pregnancy

Antidepressant exposure (including fluoxetine) is associated with shorter average duration of pregnancy (by three days), increased risk of preterm delivery (by 55%), lower birth weight (by 75 g), and lower Apgar scores (by <0.4 points). There is 30-36% increase in congenital heart defects among children whose mothers were prescribed fluoxetine during pregnancy, with fluoxetine use in the first trimester associated with 38-65% increase in septal heart defects.

Suicide

In 2007 the FDA required all antidepressants to carry a black box warning stating that antidepressants increase the risk of suicide in people younger than 25. This warning is based on statistical analyses conducted by two independent groups of FDA experts that found a 2-fold increase of the suicidal ideation and behaviour in children and adolescents, and 1.5-fold increase of suicidality in the 18-24 age group. The suicidality was slightly decreased for those older than 24, and statistically significantly lower in the 65 and older group. This analysis was criticized by Donald Klein, who noted that suicidality, that is suicidal ideation and behaviour, is not necessarily a good surrogate marker for completed suicide, and it is still possible, while unproven, that antidepressants may prevent actual suicide while increasing suicidality.

There is less data on fluoxetine than on antidepressants as a whole. For the above analysis on the antidepressant level, the FDA had to combine the results of 295 trials of 11 antidepressants for psychiatric indications to obtain statistically significant results. Considered separately, fluoxetine use in children increased the odds of suicidality by 50%, and in adults decreased the odds of suicidality by approximately 30%. Similarly, the analysis conducted by the UK MHRA found a 50% increase of odds of suicide-related events, not reaching statistical significance, in the children and adolescents on fluoxetine as compared to the ones on placebo. According to the MHRA data, for adults fluoxetine did not change the rate of self-harm and statistically significantly decreased suicidal ideation by 50%.

QT Prolongation

Fluoxetine can affect the electrical currents that heart muscle cells use to coordinate their contraction, specifically the potassium currents Ito and IKs that repolarise the cardiac action potential. Under certain circumstances, this can lead to prolongation of the QT interval, a measurement made on an electrocardiogram reflecting how long it takes for the heart to electrically recharge after each heartbeat. When fluoxetine is taken alongside other drugs that prolong the QT interval, or by those with a susceptibility to long QT syndrome, there is a small risk of potentially lethal abnormal heart rhythms such as Torsades de Pointes. As of 2019, the drug reference site CredibleMeds lists Fluoxetine as leading to a conditional risk of arrhythmias.

Overdose

In overdose, most frequent adverse effects include:

  • Nervous system effects:
    • Anxiety.
    • Nervousness.
    • Insomnia.
    • Drowsiness.
    • Fatigue or asthenia.
    • Tremor.
    • Dizziness or lightheadedness.
  • Gastrointestinal effects:
    • Anorexia (symptom).
    • Nausea.
    • Diarrhoea.
    • Vasodilation.
    • Dry mouth.
    • Abnormal vision.
  • Other effects:
    • Abnormal ejaculation.
    • Rash.
    • Sweating.
    • Decreased libido.

Interactions

Contraindications include prior treatment (within the past 5-6 weeks, depending on the dose) with MAOIs such as phenelzine and tranylcypromine, due to the potential for serotonin syndrome. Its use should also be avoided in those with known hypersensitivities to fluoxetine or any of the other ingredients in the formulation used. Its use in those concurrently receiving pimozide or thioridazine is also advised against.

In some cases, use of dextromethorphan-containing cold and cough medications with fluoxetine is advised against, due to fluoxetine increasing serotonin levels, as well as the fact that fluoxetine is a cytochrome P450 2D6 inhibitor, which causes dextromethorphan to not be metabolized at a normal rate, thus increasing the risk of serotonin syndrome and other potential side effects of dextromethorphan.

Patients who are taking anticoagulants or NSAIDS must be careful when taking fluoxetine or other SSRIs, as they can sometimes increase the blood-thinning effects of these medications.

Fluoxetine and norfluoxetine inhibit many isozymes of the cytochrome P450 system that are involved in drug metabolism. Both are potent inhibitors of CYP2D6 (which is also the chief enzyme responsible for their metabolism) and CYP2C19, and mild to moderate inhibitors of CYP2B6 and CYP2C9. In vivo, fluoxetine and norfluoxetine do not significantly affect the activity of CYP1A2 and CYP3A4. They also inhibit the activity of P-glycoprotein, a type of membrane transport protein that plays an important role in drug transport and metabolism and hence P-glycoprotein substrates such as loperamide may have their central effects potentiated. This extensive effect on the body’s pathways for drug metabolism creates the potential for interactions with many commonly used drugs.

Its use should also be avoided in those receiving other serotonergic drugs such as monoamine oxidase inhibitors, tricyclic antidepressants, methamphetamine, amphetamine, MDMA, triptans, buspirone, serotonin–norepinephrine reuptake inhibitors and other SSRIs due to the potential for serotonin syndrome to develop as a result.

There is also the potential for interaction with highly protein-bound drugs due to the potential for fluoxetine to displace said drugs from the plasma or vice versa hence increasing serum concentrations of either fluoxetine or the offending agent.

Pharmacology

Pharmacodynamics

Fluoxetine is a selective serotonin reuptake inhibitor (SSRI) and does not appreciably inhibit norepinephrine and dopamine reuptake at therapeutic doses. It does, however, delay the reuptake of serotonin, resulting in serotonin persisting longer when it is released. Large doses in rats have been shown to induce a significant increase in synaptic norepinephrine and dopamine. Thus, dopamine and norepinephrine may contribute to the antidepressant action of fluoxetine in humans at supratherapeutic doses (60-80 mg). This effect may be mediated by 5HT2C receptors, which are inhibited by higher concentrations of fluoxetine.

Fluoxetine increases the concentration of circulating allopregnanolone, a potent GABAA receptor positive allosteric modulator, in the brain. Norfluoxetine, a primary active metabolite of fluoxetine, produces a similar effect on allopregnanolone levels in the brains of mice. Additionally, both fluoxetine and norfluoxetine are such modulators themselves, actions which may be clinically-relevant.

In addition, fluoxetine has been found to act as an agonist of the σ1-receptor, with a potency greater than that of citalopram but less than that of fluvoxamine. However, the significance of this property is not fully clear. Fluoxetine also functions as a channel blocker of anoctamin 1, a calcium-activated chloride channel. A number of other ion channels, including nicotinic acetylcholine receptors and 5-HT3 receptors, are also known to be inhibited at similar concentrations.

Fluoxetine has been shown to inhibit acid sphingomyelinase, a key regulator of ceramide levels which derives ceramide from sphingomyelin.

Mechanism of Action

Fluoxetine elicits antidepressant effect by inhibiting serotonin re-uptake in the synapse by binding to the re-uptake pump on the neuronal membrane to increase serotonin availability and enhance neurotransmission. Norfluoxetine and desmethylfluoxetine are metabolites of fluoxetine and also act as serotonin re-uptake inhibitors, increasing the duration of action of the drug.

Pharmacokinetics

The bioavailability of fluoxetine is relatively high (72%), and peak plasma concentrations are reached in 6-8 hours. It is highly bound to plasma proteins, mostly albumin and α1-glycoprotein. Fluoxetine is metabolised in the liver by isoenzymes of the cytochrome P450 system, including CYP2D6. The role of CYP2D6 in the metabolism of fluoxetine may be clinically important, as there is great genetic variability in the function of this enzyme among people. CYP2D6 is responsible for converting fluoxetine to its only active metabolite, norfluoxetine. Both drugs are also potent inhibitors of CYP2D6.

The extremely slow elimination of fluoxetine and its active metabolite norfluoxetine from the body distinguishes it from other antidepressants. With time, fluoxetine and norfluoxetine inhibit their own metabolism, so fluoxetine elimination half-life increases from 1 to 3 days, after a single dose, to 4 to 6 days, after long-term use. Similarly, the half-life of norfluoxetine is longer (16 days) after long-term use. Therefore, the concentration of the drug and its active metabolite in the blood continues to grow through the first few weeks of treatment, and their steady concentration in the blood is achieved only after four weeks. Moreover, the brain concentration of fluoxetine and its metabolites keeps increasing through at least the first five weeks of treatment. The full benefit of the current dose a patient receives is not realised for at least a month following ingestion. For example, in one 6-week study, the median time to achieving consistent response was 29 days. Likewise, complete excretion of the drug may take several weeks. During the first week after treatment discontinuation, the brain concentration of fluoxetine decreases by only 50%, The blood level of norfluoxetine four weeks after treatment discontinuation is about 80% of the level registered by the end of the first treatment week, and, seven weeks after discontinuation, norfluoxetine is still detectable in the blood.

Measurement in Body Fluids

Fluoxetine and norfluoxetine may be quantitated in blood, plasma or serum to monitor therapy, confirm a diagnosis of poisoning in a hospitalised person or assist in a medicolegal death investigation. Blood or plasma fluoxetine concentrations are usually in a range of 50-500 μg/L in persons taking the drug for its antidepressant effects, 900-3000 μg/L in survivors of acute overdosage and 1000-7000 μg/L in victims of fatal overdosage. Norfluoxetine concentrations are approximately equal to those of the parent drug during chronic therapy, but may be substantially less following acute overdosage, since it requires at least 1-2 weeks for the metabolite to achieve equilibrium.

Usage

In 2010, over 24.4 million prescriptions for generic fluoxetine were filled in the United States, making it the third-most prescribed antidepressant after sertraline and citalopram. In 2011, 6 million prescriptions for fluoxetine were filled in the United Kingdom.

Society and Culture

American Airline Pilots

Beginning 05 April 2010, fluoxetine became one of four antidepressant drugs that the US Federal Aviation Authority (FAA) permitted for pilots with authorisation from an aviation medical examiner. The other permitted antidepressants are sertraline (Zoloft), citalopram (Celexa), and escitalopram (Lexapro). These four remain the only antidepressants permitted by FAA as of 02 December 2016.

Sertraline, citalopram and escitalopram are the only antidepressants permitted for EASA medical certification, as of January 2019.

Environmental Effects

Fluoxetine has been detected in aquatic ecosystems, especially in North America. There is a growing body of research addressing the effects of fluoxetine (among other SSRIs) exposure on non-target aquatic species.

In 2003, one of the first studies addressed in detail the potential effects of fluoxetine on aquatic wildlife; this research concluded that exposure at environmental concentrations was of little risk to aquatic systems if a hazard quotient approach was applied to risk assessment. However, they also stated the need for further research addressing sub-lethal consequences of fluoxetine, specifically focusing on study species’ sensitivity, behavioural responses, and endpoints modulated by the serotonin system.

Since 2003, a number of studies have reported fluoxetine-induced impacts on a number of behavioural and physiological endpoints, inducing antipredator behaviour, reproduction, and foraging at or below field-detected concentrations. However, a 2014 review on the ecotoxicology of fluoxetine concluded that, at that time, a consensus on the ability of environmentally realistic dosages to affect the behaviour of wildlife could not be reached.

Politics

During the 1990 campaign for Governor of Florida, it was disclosed that one of the candidates, Lawton Chiles, had depression and had resumed taking fluoxetine, leading his political opponents to question his fitness to serve as Governor.

What is the Bulimia Test-Revised?

Published on by Andrew MarshallLeave a comment

Introduction

The Bulimia Test-Revised (BULIT-R) is a 36 item self-report questionnaire to assess the presence of bulimic symptoms.

Background

The Bulimia Test (BULIT) was devised by Smith and Thelen in 1984. It was a self-reported questionnaire measure of bulimia that was based on the Diagnostic and Statistical Manual of Mental Disorders III (DSM III) criteria for bulimia (Smiht & Thelen, 1984).

It was then revised (Bulimia Test-Revised, BULIT-R) in 1991 to accommodate the Diagnostic and Statistical Manual of Mental Disorders-III-Revised (DSM-III-R) criteria of bulimia nervosa, using a 28-item, self-report, multiple-choice scale was developed by comparing responses of clinically identified female bulimics with those of female college students (Thelen et al., 1991).

The results of retesting and diagnostic judgements based on interviews showed that the BULIT-R was a reliable and valid predictor of bulimia nervosa in a nonclinical population.

The test has been validated for use in both males and females.

Scoring

The BULIT-R contains 36 multiple choice questions with five possible responses, 28 of which factor into the total score, questions 6,11, 19, 20, 27, 29, 31 and 36 are not scored.

Items 2,5,7,8,10, 12, 13, 14, 15, 16, 17, 21, 23, 26, 28, 30, 32, 35 are reversed scored. Scores range from 29-140 with those greater than 104 being indicative of bulimia nervosa.

References

Smith, M.C. & Thelen, M.H. (1984) Development and Validation of a Test for Bulimia. Journal of Consulting and Clinical Psychology. 52, pp.863-872

Thelen, M.H., Farmer, J., Wonderlich, S. & Smith, M. (1991) A Revision of the Bulimia Test: The BULIT-R. Psychological Assessment: A Journal of Consulting and Clinical Psychology. 3(1), pp.119-124. https://doi.org/10.1037/1040-3590.3.1.119

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.

What is an Eating Disorder Inventory?

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Introduction

The Eating Disorder Inventory (EDI) is a self-report questionnaire used to assess the presence of eating disorders:

  • Anorexia nervosa both restricting and binge-eating/purging type;
  • Bulimia nervosa; and
  • Eating disorder not otherwise specified including binge eating disorder.

The original questionnaire consisted of 64 questions, divided into eight subscales. It was created in 1984 by David M. Garner and others. There have been two subsequent revisions by Garner:

  • The Eating Disorder Inventory-2 (EDI-2); and
  • The Eating Disorder Inventory-3 (EDI-3).

Diagnostic Use

The Eating Disorder Inventory is a diagnostic tool designed for use in a clinical setting to assess the presence of an eating disorder. It is generally used in conjunction with other psychological tests such as the Beck Depression Inventory. Depression has been shown to yield higher scores on the EDI-3.

Eating Disorder Inventory

The Eating Disorder Inventory (EDI) comprises 64 questions, divided into eight subscales. Each question is on a 6-point scale (ranging from “always” to “never”), rated 0-3. The score for each sub-scale is then summed. The 8 subscale scores on the EDI are:

  • Drive for thinness: an excessive concern with dieting, preoccupation with weight, and fear of weight gain.
  • Bulimia: episodes of binge eating and purging.
  • Body dissatisfaction: not being satisfied with one’s physical appearance.
  • Ineffectiveness: assesses feelings of inadequacy, insecurity, worthlessness and having no control over their lives.
  • Perfectionism: not being satisfied with anything less than perfect.
  • Interpersonal distrust: reluctance to form close relationships.
  • Interoceptive awareness: “measures the ability of an individual to discriminate between sensations and feelings, and between the sensations of hunger and satiety”.
  • Maturity fears: The fear of facing the demands of adult life.

Eating Disorder Inventory-2

The first revision of the EDI was in 1991. The 1991 version, Eating Disorder Inventory-2 (EDI-2) is used for both males and females over age 12. The EDI-2 retains the original format of the EDI with the inclusion of 27 new items divided into three additional subscales:

  • Asceticism: reflects the avoidance of sexual relationships.
  • Impulse regulation: shows the ability to regulate impulsive behaviour, especially the binge behaviour.
  • Social insecurity: estimates social fears and insecurity.

Eating Disorder Inventory-3

The latest revision to the Eating Disorder Inventory was released in 2004. It contains the original items of the first version as well as EDI-2, and was also enhanced to reflect more modern theories related to the diagnosis of eating disorders. It was designed for use with females ages 13-53 years, and can be administered in 20 minutes. It contains 91 items divided into twelve subscales rated on a 0-4 point scoring system. Three items on the EDI-3 are specific to eating disorders, and 9 are general psychological scales that are relevant to eating disorders. The inventory yields six composite scores: eating disorder risk, ineffectiveness, interpersonal problems, affective problems, overcontrol, and general psychological maladjustment.

Eating Disorder Symptom Checklist

The Eating Disorder Symptom Checklist is a separate self-report form used to measure the frequency of symptoms (i.e., binge eating; the use of laxatives, diet pills; exercise patterns). The information provided by the checklist aids in determining whether patients meets the diagnostic criteria as set forth in the Diagnostic and Statistical Manual of Mental Disorders IV-TR for an eating disorder.

Eating Disorder Referral Form

The Eating Disorder Referral Form is an abbreviated form of the EDI-3 for use in non-clinical settings such as the allied health professions. It contains 25 questions from the EDI-3 that are specific to eating disorder risk. It also includes questions specific to the behavioural patterns of someone with or at risk of developing an eating disorder. The referral form utilizes indexes based on body mass index in identifying at risk patients.

What is the SCOFF Questionnaire?

Published on by Andrew Marshall1 Comment

Introduction

The SCOFF questionnaire utilises an acronym in a simple five question test devised for use by non-professionals to assess the possible presence of an eating disorder.

Scoff is also an alternative/slang word for food.

Background

It was devised by John F. Morgan, Fiona Reid, and J Hubert Lacey in 1999.

The original SCOFF questionnaire was devised for use in the United Kingdom, thus the original acronym needs to be adjusted for users in the United States and Canada.

The letters in the full acronym are taken from key words in the questions:

  • Do you make yourself Sick because you feel uncomfortably full?
  • Do you worry that you have lost Control over how much you eat?
  • Have you recently lost more than One stone (14 lb/6.5 kg) in a 3-month period?
  • Do you believe yourself to be Fat when others say you are too thin?
  • Would you say that Food dominates your life?

Notes

  • The “S” stands for “Sick”:
    • In British English means specifically to “vomit”.
    • In American English and Canadian English it is synonymous with “ill”.
  • The “O” is used in the acronym to denote “one stone”.
    • A “stone” is an Imperial unit of weight which made up of 14 lbs (equivalent to 6.35 kg).

All participants (in Morgan and colleagues research) found the questions and the term “SCOFF” acceptable. Setting the threshold at two or more yes answers to all five questions provided 100% sensitivity for anorexia and bulimia, separately and combined (all patients: 95% confidence interval, 96.9%-100.0%; patients with bulimia: 92.6%-100.0%; and patients with anorexia: 94.7%-100.0%), with a specificity of 87.5% (79.2%-93.4%) for controls.

Scoring

One point is assigned for every “yes”; a score greater than two (≥2) indicates a possible case of anorexia nervosa or bulimia nervosa.

Reference

Morgan, J.F., Reid, F. & Lacy, J.H. (2000) The SCOFF Questionnaire. Western Journal of Medicine. 172(3), pp.164-165.

What is Orthorexia Nervosa?

Published on by Andrew Marshall2 Comments

Orthorexia nervosa (also known as orthorexia) is a proposed eating disorder characterised by an excessive preoccupation with eating healthy food.

The term was introduced in 1997 by American physician Steven Bratman, M.D. He suggested that some people’s dietary restrictions intended to promote health may paradoxically lead to unhealthy consequences, such as social isolation, anxiety, loss of ability to eat in a natural, intuitive manner, reduced interest in the full range of other healthy human activities, and, in rare cases, severe malnutrition or even death.

In 2009, Ursula Philpot, chair of the British Dietetic Association and senior lecturer at Leeds Metropolitan University, described people with orthorexia nervosa as being “solely concerned with the quality of the food they put in their bodies, refining and restricting their diets according to their personal understanding of which foods are truly ‘pure’.” This differs from other eating disorders, such as anorexia nervosa and bulimia nervosa, where those affected focus on the quantity of food eaten.

Orthorexia nervosa also differs from anorexia nervosa in that it does not disproportionally affect one gender. Studies have found that orthorexia nervosa is equally found in both men and women with no significant gender differences at all. Furthermore, research has found significant positive correlations between ON and both narcissism and perfectionism, but no significant correlation between ON and self esteem. This shows that high-ON individuals likely take pride over their healthy eating habits over others and that is the driving force behind their orthorexia as opposed to body image like anorexia.

Orthorexia nervosa is not recognised as an eating disorder by the American Psychiatric Association, and so is not mentioned as an official diagnosis in the widely used Diagnostic and Statistical Manual of Mental Disorders (DSM).

Brief History

In a 1997 article in the magazine Yoga Journal, the American physician Steven Bratman coined the term “orthorexia nervosa” from the Greek ορθο- (ortho, “right” or “correct”), and όρεξις (orexis, “appetite”), literally meaning ‘correct appetite’, but in practice meaning ‘correct diet’. The term is modelled on anorexia, literally meaning “without appetite”, as used in the definition of the condition anorexia nervosa. (In both terms, “nervosa” indicates an unhealthy psychological state.) Bratman described orthorexia as an unhealthy fixation with what the individual considers to be healthy eating. Beliefs about what constitutes healthy eating commonly originate in one or another dietary theory such as raw foods veganism or macrobiotics, but are then taken to extremes, leading to disordered eating patterns and psychological and/or physical impairment. Bratman based this proposed condition on his personal experiences in the 1970s, as well as behaviours he observed among his patients in the 1990s. In 2000, Bratman, with David Knight, authored the book Health Food Junkies, which further expanded on the subject.

Following the publication of the book, in 2004 a team of Italian researchers from La Sapienza University of Rome, published the first empirical study attempting to develop a tool to measure the prevalence of orthorexia, known as the ORTO-15.

In 2015, responding to news articles in which the term orthorexia is applied to people who merely follow a non-mainstream theory of healthy eating, Bratman specified the following: “A theory may be conventional or unconventional, extreme or lax, sensible or totally wacky, but, regardless of the details, followers of the theory do not necessarily have orthorexia. They are simply adherents of a dietary theory. The term ‘orthorexia’ only applies when an eating disorder develops around that theory.” Bratman elsewhere clarifies that with a few exceptions, most common theories of healthy eating are followed safely by the majority of their adherents; however, “for some people, going down the path of a restrictive diet in search of health may escalate into dietary perfectionism.” Karin Kratina, PhD, writing for the National Eating Disorders Association, summarises this process as follows: “Eventually food choices become so restrictive, in both variety and calories, that health suffers – an ironic twist for a person so completely dedicated to healthy eating.”

Although orthorexia is not recognised as a mental disorder by the American Psychiatric Association, and it is not listed in the DSM-5, as of January 2016, four case reports and more than 40 other articles on the subject have been published in a variety of peer-reviewed journals internationally. According to a study published in 2011, two-thirds of a sample of 111 Dutch-speaking eating disorder specialists felt they had observed the syndrome in their clinical practice.

According to the Macmillan English Dictionary, the word is entering the English lexicon. The concept of orthorexia as a newly developing eating disorder has attracted significant media attention in the 21st century.

Signs and Symptoms

Symptoms of orthorexia nervosa include “obsessive focus on food choice, planning, purchase, preparation, and consumption; food regarded primarily as source of health rather than pleasure; distress or disgust when in proximity to prohibited foods; exaggerated faith that inclusion or elimination of particular kinds of food can prevent or cure disease or affect daily well-being; periodic shifts in dietary beliefs while other processes persist unchanged; moral judgment of others based on dietary choices; body image distortion around sense of physical “impurity” rather than weight; persistent belief that dietary practices are health-promoting despite evidence of malnutrition.”

Cause(s)

There has been no investigation into whether there may be a biological cause specific to orthorexia nervosa. It may be a food-centred manifestation of obsessive-compulsive disorder (OCD), which has a lot to do with control.

Diagnosis

In 2016, formal criteria for orthorexia were proposed in the peer-reviewed journal Eating Behaviours by Thom Dunn and Steven Bratman. These criteria are as follows:

  • Criterion A:
    • Obsessive focus on “healthy” eating, as defined by a dietary theory or set of beliefs whose specific details may vary; marked by exaggerated emotional distress in relationship to food choices perceived as unhealthy; weight loss may ensue, but this is conceptualised as an aspect of ideal health rather than as the primary goal.
    • As evidenced by the following:
      1. Compulsive behaviour and/or mental preoccupation regarding affirmative and restrictive dietary practices believed by the individual to promote optimum health. (Footnotes to this criteria add: Dietary practices may include use of concentrated “food supplements.” Exercise performance and/or fit body image may be regarded as an aspect or indicator of health.)
      2. Violation of self-imposed dietary rules causes exaggerated fear of disease, sense of personal impurity and/or negative physical sensations, accompanied by anxiety and shame.
      3. Dietary restrictions escalate over time, and may come to include elimination of entire food groups and involve progressively more frequent and/or severe “cleanses” (partial fasts) regarded as purifying or detoxifying. This escalation commonly leads to weight loss, but the desire to lose weight is absent, hidden or subordinated to ideation about healthy food.
  • Criterion B:
    • The compulsive behaviour and mental preoccupation becomes clinically impairing by any of the following:
      1. Malnutrition, severe weight loss or other medical complications from restricted diet.
      2. Intrapersonal distress or impairment of social, academic or vocational functioning secondary to beliefs or behaviours about healthy diet.
      3. Positive body image, self-worth, identity and/or satisfaction excessively dependent on compliance with self-defined “healthy” eating behaviour.

A diagnostic questionnaire has been developed for orthorexia sufferers, similar to questionnaires for other eating disorders, named the ORTO-15. However, Dunn and Bratman critique this survey tool as lacking appropriate internal and external validation.

Epidemiology

Results across scientific findings have yet to find a definitive conclusion to support whether nutrition students and professionals are at higher risk than other population subgroups, due to differing results in the research literature. There are only a few notable scientific works that, in an attempt to explore the breadth and depth of the still vaguely-understood illness, have tried to identify which groups in society are most vulnerable to its onset. This includes a 2008 German study, which based its research on the widespread suspicion that the most nutritionally-informed, such as university nutrition students, are a potential high-risk group for eating disorders, due to a substantial accumulation of knowledge on food and its relationship to health; the idea being that the more one knows about health, the more likely an unhealthy fixation about being healthy can develop. This study also inferred that orthorexic tendencies may even fuel a desire to study the science, indicating that many within this field might suffer from the disorder before commencing the course. However the results found that the students in the study, upon initial embarkation of their degree, did not have higher orthorexic values than other non-nutrition university students, and thus the report concluded that further research is needed to clarify the relationship between food-education and the onset of ON.

Similarly, in a Portuguese study on nutrition tertiary students, the participants’ orthorexic scores (according to the ORTO-15 diagnostic questionnaire) actually decreased as they progressed through their course, as well as the overall risk of developing an eating disorder being low at 4.2%. The participants also answered questionnaires to provide insight into their eating behaviours and attitudes, and despite this study finding that nutrition and health-science students tend to have more restrictive eating behaviours, these studies however found no evidence to support that these students have “more disturbed or disordered eating patterns than other students” These two aforementioned studies conclude that the more understanding of food one has is not necessarily a risk factor for ON, explaining that the data gathered suggests dietetics professionals are not at significant risk of it.

However, these epidemiologic studies have been critiqued as using a fundamentally flawed survey tool that inflates prevalence rates. Scholars have questioned both the reliability and validity of the ORTO-15.

Most scientific findings tend to agree, however, young adults and adolescents are extremely susceptible to developing eating disorders. One study found that there was no relationship between BOT score and college major, which may indicate the prevalence of mental health issues and eating disorders on college campuses and that health and science majors are no longer the only ones affected More studies have also been conducted on the link between increased Instagram use and Orthorexia nervosa. The social media based healthy community has recently grown in popularity especially on platforms such as Instagram. The hashtag #food is one of the top 25 most popular hashtags on Instagram. A study that investigated this relationship found that increased use of Instagram correlated between symptoms of ON with no other social media platform having the same effect. With young adults and adolescents making up the majority of social media users, exposure to this type of content can lead to developing unhealthy behaviour.