Enhanced cognitive behavior therapy for severe and extreme anorexia nervosa: An outpatient case series.

OBJECTIVE: The study aimed to assess outcomes in patients with severe and extreme anorexia nervosa managed with enhanced cognitive behavior therapy (CBT-E) in a real-world outpatient setting. METHOD: Thirty patients with anorexia nervosa and body mass index (BMI) <16 aged ≥17 years were recruited from consecutive referrals to an eating disorder service clinic offering outpatient CBT-E. BMI and Eating Disorder Examination Questionnaire (EDE-Q), Brief Symptom Inventory (BSI), and Clinical Impairment Assessment (CIA) scores were recorded at admission, end of treatment, and 20- and 60-week follow-ups for treatment completers. RESULTS: Twenty patients (66.7%) completed the treatment and showed both considerable weight gain (Cohen's f = 1.43), and significantly reduced scores for clinical impairment (f = 1.26) and eating-disorder (f = 1.03) and general psychopathology (f = 0.99). Changes remained stable at both follow-ups. About half of the patients who completed treatment had a BMI ≥18.5 at the end of treatment and follow-ups. DISCUSSION: CBT-E seems suitable and promising for patients with severe and extreme anorexia nervosa seeking treatment in a real-world clinical setting, provided that their medical conditions are stable, and they have no current major depressive episodes or substance abuse; it may represent a valid alternative to inpatient treatment for those who are able to sustain engagement in a full course of outpatient treatment.

Effectiveness of enhanced cognitive behavioral therapy (CBT-E) in the treatment of anorexia nervosa: a prospective multidisciplinary study.

BACKGROUND: Anorexia nervosa (AN) is a debilitating psychiatric disorder associated with a wide array of negative health complications and psychiatric comorbidity. Existing evidence for AN treatment in adults is weak, and no empirically supported treatment has been reliably established. The primary objective of this study is to gain knowledge about the effectiveness of enhanced cognitive behavioral therapy (CBT-E) for anorexia nervosa delivered in a public hospital setting. Baseline predictors of treatment outcome and dropout are studied. Furthermore, there will be collected blood and stool samples for a general biobank to be able to initiate research on possible pathophysiological mechanisms underlying AN. METHODS: The study will assess the potency of outpatient CBT-E in a sample of patients suffering from AN (age >16) admitted to the Section for Eating Disorders at the Department for Psychosomatic Medicine, Haukeland University Hospital in Bergen, Norway. The study has a longitudinal design with five main assessment time points: before treatment, at 3 months, at the end of treatment, at 20 weeks, and at 12 months follow-up including biobank samples. A control group without an eating disorder will also be recruited. DISCUSSION: Treatment research in a public hospital setting is important for gaining knowledge about the transportability of treatments evaluated in research clinics into ordinary clinical practice. Furthermore, biological material from the thoroughly described patient cohort will serve as a basis for further research on the pathophysiological mechanisms in AN. TRIAL REGISTRATION: ClinicalTrials.gov Identifier: NCT02745067 . Registered 14 April 2016. .

Are the Effects of Malnutrition on the Gut Microbiota-Brain Axis the Core Pathologies of Anorexia Nervosa?

Anorexia nervosa (AN) is a disabling, costly, and potentially deadly illness. Treatment failure and relapse after treatment are common. Several studies have indicated the involvement of the gut microbiota-brain (GMB) axis. This narrative review hypothesizes that AN is driven by malnutrition-induced alterations in the GMB axis in susceptible individuals. According to this hypothesis, initial weight loss can voluntarily occur through dieting or be caused by somatic or psychiatric diseases. Malnutrition-induced alterations in gut microbiota may increase the sensitivity to anxiety-inducing gastrointestinal hormones released during meals, one of which is cholecystokinin (CCK). The experimental injection of a high dose of its CCK-4 fragment in healthy individuals induces panic attacks, probably via the stimulation of CCK receptors in the brain. Such meal-related anxiety attacks may take part in developing the clinical picture of AN. Malnutrition may also cause increased effects from appetite-reducing hormones that also seem to have roles in AN development and maintenance. The scientific background, including clinical, microbiological, and biochemical factors, of AN is discussed. A novel model for AN development and maintenance in accordance with this hypothesis is presented. Suggestions for future research are also provided.

Anorexia nervosa: Outpatient treatment and medical management.

Anorexia nervosa (AN) is a disabling, costly and potentially deadly illness. Treatment failure and relapse are common after completing treatment, and a substantial proportion of patients develop severe and enduring AN. The time from AN debut to the treatment initiation is normally unreasonably long. Over the past 20 years there has been empirical support for the efficacy of several treatments for AN. Moreover, outpatient treatment with family-based therapy or individual psychotherapy is associated with good outcomes for a substantial proportion of patients. Early intervention improves outcomes and should be a priority for all patients. Outpatient treatment is usually the best format for early intervention, and it has been demonstrated that even patients with severe or extreme AN can be treated as outpatients if they are medically stable. Inpatient care is more disruptive, more costly, and usually has a longer waiting list than does outpatient care. The decision as to whether to proceed with outpatient treatment or to transfer the patient for inpatient therapy may be difficult. The core aim of this opinion review is to provide the knowledge base needed for performing safe outpatient treatment of AN. The scientific essentials for outpatient treatment are described, including how to assess and manage the medical risks of AN and how to decide when transition to inpatient care is indicated. The following aspects are discussed: early intervention, outpatient treatment of AN, including outpatient psychotherapy for severe and extreme AN, how to determine when outpatient treatment is safe, and when transfer to inpatient healthcare is indicated. Emerging treatments, ethical issues and outstanding research questions are also addressed.

BMI at Discharge from Treatment Predicts Relapse in Anorexia Nervosa: A Systematic Scoping Review.

BACKGROUND: Anorexia nervosa (AN) has high rates of enduring disease and mortality. Currently, there is insufficient knowledge on the predictors of relapse after weight normalization and this is why a systematic literature review was performed. METHODS: PubMed, EMBASE, PsychInfo, and Cochrane databases were searched for literature published until 13 July 2021. All study designs were eligible for inclusion if they focused on predictors of relapse after weight normalization in AN. Individual study definitions of relapse were used, and in general, this was either a drop in BMI and/or reccurrence of AN symptoms. RESULTS: The database search identified 11,507 publications, leaving 9511 publications after the removal of duplicates and after a review of abstracts and titles; 191 were selected for full-text review. Nineteen publications met the criteria and included 1398 AN patients and 39 healthy controls (HC) from adults and adolescents (ages range 11-73 years). The majority used a prospective observational study design (12 studies), a few used a retrospective observational design (6 studies), and only one was a non-randomized control trial (NRCT). Sample sizes ranged from 16 to 191 participants. BMI or measures of body fat and leptin levels at discharge were the strongest predictors of relapse with an approximate relapse rate of 50% at 12 months. Other predictors included signs of eating disorder psychopathology at discharge. CONCLUSIONS: BMI at the end of treatment is a predictor of relapse in AN, which is why treatment should target a BMI well above 20. Together with the time to relapse, these outcomes are important to include in the evaluation of current and novel treatments in AN and for benchmarking.

Enhanced cognitive behaviour therapy (CBT-E) for severe and extreme anorexia nervosa in an outpatient eating disorder unit at a public hospital: a quality-assessment study.

BACKGROUND: The aim of this quality-assessment study was to determine the outcome of patients with severe and extreme anorexia nervosa (AN) in a real-world outpatient setting. METHODS: Twenty-one adults with AN and a body mass index (BMI) of < 16 were recruited from consecutive referrals to an outpatient clinic at a public hospital in Western Norway. All enrolled patients were provided with enhanced cognitive behaviour therapy (CBT-E) to treat their AN, commencing between January 2013 and December 2016. Their BMI was recorded at baseline, at the end of CBT-E and 1 year after the end of treatment. RESULTS: Ten patients completed the CBT-E treatment and achieved a large weight gain with the change remaining stable at follow-up. Eleven patients did not complete the treatment but had a significant increase in BMI at the premature end of treatment. One year after end of therapy 14/21 (66.7%) of the patients had BMI above 18.5 kg/m2. No severe complications were observed during therapy. CONCLUSIONS: Although 52.4% of the patients did not complete outpatient CBT-E, the findings of this quality-assessment study support previous findings indicating that CBT-E may represent a valid alternative to inpatient treatment in patients with severe and extreme AN.

Implementation of enhanced cognitive behaviour therapy (CBT-E) for adults with anorexia nervosa in an outpatient eating-disorder unit at a public hospital.

BACKGROUND: Anorexia nervosa (AN) in adults is difficult to treat, and no current treatment is supported by robust evidence. A few studies, most of which were performed by highly specialized research units, have indicated that enhanced cognitive behaviour therapy (CBT-E) for eating disorders can be effective. However, the dropout rate is high and the evidence from non-research clinical units is sparse. METHODS: This quality assessment project implemented CBT-E in an outpatient setting at a public hospital. Forty-four patients with AN started therapy. Each patient received at least 40 sessions of CBT-E over a 12-month period. Their body mass index (BMI) was recorded at baseline and after 3, 6 and 12 months. Reasons for not starting therapy or for leaving therapy prematurely were recorded. RESULTS: Half (n = 22) of the 44 patients who started outpatient CBT-E did not complete the treatment. In the remaining sample there was a large (and statistically significant) weight gain after 12 months. The percentage of patients achieving the target BMI of > 18.5 kg/m2 was 36.4, 50.0 and 77.3% after 3, 6 and 12 months, respectively. CONCLUSIONS: This quality assessment project shows that it is possible to establish effective CBT-E in an outpatient eating-disorder unit at a public hospital. Although half of the patients did not complete CBT-E, the remaining patients achieved a significant increase in BMI at 1 year after the start of therapy.

[Somatic investigation and treatment of eating disorders]. / Somatisk utredning og behandling av spiseforstyrrelser.

Eating disorders are associated with several medical complications. Growth retardation and osteoporosis can cause permanent sequelae if treatment is delayed. Severe eating disorders are associated with significant mortality. Cardiac arrhythmias are the most common somatic cause of death. Hypokalaemia is a common complication and is associated with increased risk of cardiac arrhythmias. Occasionally, overzealous refeeding may induce a potentially life-threatening condition, the refeeding syndrome. In any patient with severe eating disorder, a physician should perform diagnostic evaluation including assessment of possible somatic complications. This is necessary in order to determine where and how the patient should be treated. Most of the somatic complications of eating disorders are partly or completely reversible if the patient receives adequate treatment in time.

Malignancy: Insulin-like Growth Factor-1 (IGF-1) is a Costimulator of the Expansion of Lineage Committed Cells Derived from Peripheral Blood Mobilized CD34+ Cells in Multiple Myeloma Patients.

The effect of insulin-like growth factor-1 (IGF-1) on highly enriched human apheresis CD34(+) progenitor cells was investigated in vitro. The progenitor cells were mobilized by treatment with cyclophosphamide + granulocyte - colony stimulating factor (G-CSF) in patients with multiple myeloma. CD34(+) cells were cultured for 7 days in serumfree medium containing stem cell factor (SCF), granulocyte-macrophage colony stimulating factor (GM-CSF) and interleukin-3 (IL-3), and this is referred to as cytokine-dependent proliferation. After 7 days of cytokine-dependent proliferation the total number of viable cells increased 1.6-8.2 times, and subsets of cells expressing the granulocyte marker CD15, the myelomonocytic marker CD64 and the erythrocyte phenotype CD71(high) /CD64(-) were detected among the in vitro cultured cells. Addition of G-CSF together with SCF + IL-3 + GM-CSF increased the number of CD15(+) and CD64(+) cells, but without altering the number of erythroid cells. IGF-1 caused a dose-dependent increase in the number of CD15(+), CD64(+) and CD71(high) /CD64(-) cells, and this increase was detected when cells were cultured in both SCF + IL-3 + GM-CSF alone and G-CSF + SCF + IL-3 + GM-CSF. A minor subset of CD34(+) cells could still be detected among in vitro cultured cells and the number of CD34(+) cells was not altered by adding G-CSF and/or IGF-1. Morphologically recognizable mature granulocytes or erythroid cells could not be detected for any of the combinations investigated. We conclude that IGF-1 can enhance the in vitro proliferation of committed progenitor cells derived from apheresis CD34(+) cells.