Management of eating disorders for people with higher weight: clinical practice guideline.

INTRODUCTION: The prevalence of eating disorders is high in people with higher weight. However, despite this, eating disorders experienced by people with higher weight have been consistently under-recognised and under-treated, and there is little to guide clinicians in the management of eating disorders in this population. AIM: The aim of this guideline is to synthesise the current best practice approaches to the management of eating disorders in people with higher weight and make evidence-based clinical practice recommendations. METHODS: The National Eating Disorders Collaboration Steering Committee auspiced a Development Group for a Clinical Practice Guideline for the treatment of eating disorders for people with higher weight. The Development Group followed the 'Guidelines for Guidelines' process outlined by the National Health and Medical Research Council and aim to meet their Standards to be: 1. relevant and useful for decision making; 2. transparent; 3. overseen by a guideline development group; 4. identifying and managing conflicts of interest; 5. focused on health and related outcomes; 6. evidence informed; 7. making actionable recommendations; 8. up-to-date; and, 9. accessible. The development group included people with clinical and/or academic expertise and/or lived experience. The guideline has undergone extensive peer review and consultation over an 18-month period involving reviews by key stakeholders, including experts and organisations with clinical academic and/or lived experience. RECOMMENDATIONS: Twenty-one clinical recommendations are made and graded according to the National Health and Medical Research Council evidence levels. Strong recommendations were supported for psychological treatment as a first-line treatment approach adults (with bulimia nervosa or binge-eating disorder), adolescents and children. Clinical considerations such as weight stigma, interprofessional collaborative practice and cultural considerations are also discussed. CONCLUSIONS: This guideline will fill an important gap in the need to better understand and care for people experiencing eating disorders who also have higher weight. This guideline acknowledges deficits in knowledge and consequently the reliance on consensus and lower levels of evidence for many recommendations, and the need for research particularly evaluating weight-neutral and other more recent approaches in this field.

The objective of this project was to develop recommendations and clinical considerations to guide clinicians in the management of people experiencing eating disorders who also have higher weight. A Guideline Development Group was formed containing members with academic and/or clinical expertise and people with a lived experience of eating disorder. The guideline was not only informed by reviews of the scientific literature but also clinical expertise and lived expertise. This guideline has undergone extensive review and consultation over an 18-month period involving reviews by key stakeholders, including experts and organisations with clinical, academic and/or lived expertise. The guideline outlines a set of recommendations for clinical practice including the strong recommendation for psychological treatment to be offered as the first treatment for an eating disorder in people who are of higher weight. Considerations in clinical practice including weight stigma, care by professionals from disparate disciplines, and cultural considerations are also discussed. The Guideline Development Group acknowledges a lack of available research evidence specific to people experiencing an eating disorder who are also of higher weight and consequently some recommendations relied on consensus of group members taking into account the expert reviews. The Group also identified areas where additional research is necessary such as research evaluating weigh-neutral and other more recent approached in the field.

Effects of starvation and short-term refeeding on gastric emptying and postprandial blood glucose regulation in adolescent girls with anorexia nervosa.

Postprandial glucose is reduced in malnourished patients with anorexia nervosa (AN), but the mechanisms and duration for this remain unclear. We examined blood glucose, gastric emptying, and glucoregulatory hormone changes in malnourished patients with AN and during 2 wk of acute refeeding compared with healthy controls (HCs). Twenty-two female adolescents with AN and 17 age-matched female HCs were assessed after a 4-h fast. Patients were commenced on a refeeding protocol of 2,400 kcal/day. Gastric emptying (13C-octanoate breath test), glucose absorption (3-O-methylglucose), blood glucose, plasma glucagon-like peptide-1 (GLP-1), glucose-dependent insulinotropic polypeptide (GIP), insulin, C-peptide, and glucagon responses to a mixed-nutrient test meal were measured on admission and 1 and 2 wk after refeeding. HCs were assessed once. On admission, patients had slower gastric emptying, lower postprandial glucose and insulin, and higher glucagon and GLP-1 than HCs ( P < 0.05). In patients with AN, the rise in glucose (0-30 min) correlated with gastric emptying ( P < 0.05). With refeeding, postprandial glucose and 3-O-methylglucose were higher, gastric emptying faster, and baseline insulin and C-peptide less ( P < 0.05), compared with admission. After 2 wk of refeeding, postprandial glucose remained lower, and glucagon and GLP-1 higher, in patients with AN than HCs ( P < 0.05) without differences in gastric emptying, baseline glucagon, or postprandial insulin. Delayed gastric emptying may underlie reduced postprandial glucose in starved patients with AN; however, postprandial glucose and glucoregulatory hormone changes persist after 2 wk of refeeding despite improved gastric emptying. Future research should explore whether reduced postprandial glucose in AN is related to medical risk by examining associated symptoms alongside continuous glucose monitoring during refeeding.

Appetite Perceptions, Gastrointestinal Symptoms, Ghrelin, Peptide YY and State Anxiety Are Disturbed in Adolescent Females with Anorexia Nervosa and Only Partially Restored with Short-Term Refeeding.

Factors underlying disturbed appetite perception in anorexia nervosa (AN) are poorly characterized. We examined in patients with AN whether fasting and postprandial appetite perceptions, gastrointestinal (GI) hormones, GI symptoms and state anxiety (i) differed from healthy controls (HCs) and (ii) were modified by two weeks of refeeding. 22 female adolescent inpatients with restricting AN, studied on hospital admission once medically stable (Wk0), and after one (Wk1) and two (Wk2) weeks of high-calorie refeeding, were compared with 17 age-matched HCs. After a 4 h fast, appetite perceptions, GI symptoms, state anxiety, and plasma acyl-ghrelin, cholecystokinin (CCK), peptide tyrosine tyrosine (PYY) and pancreatic polypeptide (PP) concentrations were assessed at baseline and in response to a mixed-nutrient test-meal (479 kcal). Compared with HCs, in patients with AN at Wk0, baseline ghrelin, PYY, fullness, bloating and anxiety were higher, and hunger less, and in response to the meal, ghrelin, bloating and anxiety were greater, and hunger less (all p < 0.05). After two weeks of refeeding, there was no change in baseline or postprandial ghrelin or bloating, or postprandial anxiety, but baseline PYY, fullness and anxiety decreased, and baseline and postprandial hunger increased (p < 0.05). We conclude that in AN, refeeding for 2 weeks was associated with improvements in PYY, appetite and baseline anxiety, while increased ghrelin, bloating and postprandial anxiety persisted.

Effects of dipeptidyl peptidase IV inhibition on glycemic, gut hormone, triglyceride, energy expenditure, and energy intake responses to fat in healthy males.

Fat is the most potent stimulus for glucagon-like peptide-1 (GLP-1) secretion. The aims of this study were to determine whether dipeptidyl peptidase IV (DPP-IV) inhibition would enhance plasma active incretin [glucose-dependent insulinotropic polypeptide (GIP), GLP-1] concentrations and modulate the glycemic, gut hormone, triglyceride, energy expenditure, and energy intake responses to intraduodenal fat infusion. In a double-blind, randomized, placebo-controlled crossover design, 16 healthy lean males received 50 mg vildagliptin (V), or matched placebo (P), before intraduodenal fat infusion (2 kcal/min, 120 min). Blood glucose, plasma insulin, glucagon, active GLP-1, and GIP and peptide YY (PYY)-(3-36) concentrations; resting energy expenditure; and energy intake at a subsequent buffet meal (time = 120-150 min) were quantified. Data are presented as areas under the curve (0-120 min, means ± SE). Vildagliptin decreased glycemia (P: 598 ± 8 vs. V: 573 ± 9 mmol·l⁻¹·min⁻¹, P < 0.05) during intraduodenal lipid. This was associated with increased insulin (P: 15,964 ± 1,193 vs. V: 18,243 ± 1,257 pmol·l⁻¹·min⁻¹, P < 0.05), reduced glucagon (P: 1,008 ± 52 vs. V: 902 ± 46 pmol·l⁻¹·min⁻¹, P < 0.05), enhanced active GLP-1 (P: 294 ± 40 vs. V: 694 ± 78 pmol·l⁻¹·min⁻¹) and GIP (P: 2,748 ± 77 vs. V: 4,256 ± 157 pmol·l⁻¹·min⁻¹), and reduced PYY-(3-36) (P: 9,527 ± 754 vs. V: 4,469 ± 431 pM/min) concentrations compared with placebo (P < 0.05, for all). Vildagliptin increased resting energy expenditure (P: 1,821 ± 54 vs. V: 1,896 ± 65 kcal/day, P < 0.05) without effecting energy intake. Vildagliptin 1) modulates the effects of intraduodenal fat to enhance active GLP-1 and GIP, stimulate insulin, and suppress glucagon, thereby reducing glycemia and 2) increases energy expenditure. These observations suggest that the fat content of a meal, by enhancing GLP-1 and GIP secretion, may contribute to the response to DPP-IV inhibition.

Timing is everything: the onset of depression and acute coronary syndrome outcome.

BACKGROUND: Conflicting findings have emerged from studies examining the impact of depression on death and readmission following a coronary event, possibly reflecting differences in the measurement of "depression" and the onset of depression in relation to the coronary event. The aim of this study was to examine the relationship between the timing of the depressive episode and 1-year cardiovascular outcome in recruited patients with acute coronary syndrome (ACS). METHODS: Patients hospitalized with ACS (N = 489) were recruited and assessed for lifetime and current depression by the Composite International Diagnostic Interview (CIDI) depression schedule. Patients were reinterviewed at 1 and 12 months by telephone to assess depression status and cardiovascular outcomes (ACS readmission and cardiac mortality). Mortality registers were also checked. RESULTS: Cardiovascular outcome was not associated with the presence of lifetime depression before the ACS admission or with existing depression at the time of the ACS admission. In contrast, depression that developed in the month after the ACS event showed a strong relationship with subsequent cardiovascular outcome, even after controlling for traditional cardiac risk factors. Outcome over the 12 months was more strongly predicted by the timing of depression onset than whether the depression was a first-ever (incident) or recurrent episode. CONCLUSIONS: Only a depressive episode that commenced following an ACS admission was associated with a poorer cardiovascular outcome. If confirmed, this finding would narrow the list of causal mechanisms previously proposed to account for the relationship between depression and coronary events.

A validation study of two brief measures of depression in the cardiac population: the DMI-10 and DMI-18.

The authors report on the psychometric characteristics and clinical efficacy of two versions of a recently developed screening measure of depression (the DMI-18 and DMI-10) in the cardiac population. Patients with acute coronary syndrome or heart failure (N = 322) completed the DMI measures, psychosocial questionnaires, and a semistructured clinical interview during the hospital stay. The DMI-18 and DMI-10 measures have adequate psychometric properties, demonstrating high sensitivity and specificity when evaluated against clinical judgment based on a semistructured interview. The DMI-18 and DMI-10 are appropriate for use as screening instruments in cardiac patients.

Low levels of docosahexaenoic acid identified in acute coronary syndrome patients with depression.

As deficiencies in n-3 PUFAs have been linked separately to depression and to cardiovascular disease, they could act as a higher order variable contributing to the established link between depression and cardiovascular disease. We therefore examine the relationship between depression and omega-3 polyunsaturated fatty acids (n-3 PUFA), including total n-3 PUFA, docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA), in patients with acute coronary syndrome (ACS). Plasma phospholipid levels of n-3 PUFA were measured in 100 patients hospitalized with ACS. Current major depressive episode was assessed by the Composite International Diagnostic Interview (CIDI). Depression severity was assessed by the 18-item Depression in the Medically Ill (DMI-18) measure. Patients clinically diagnosed with current depression had significantly lower mean total n-3 PUFA and DHA levels. Higher DMI-18 depression severity scores were significantly associated with lower DHA levels, with similar but non-significant trends observed for EPA and total n-3 PUFA levels. The finding that low DHA levels were associated with depression variables in ACS patients may explain links demonstrated between cardiovascular health and depression, and may have prophylactic and treatment implications.