Polaprezinc (Zinc-L-Carnosine Complex) as an Add-on Therapy for Binge Eating Disorder and Bulimia Nervosa, and the Possible Involvement of Zinc Deficiency in These Conditions: A Pilot Study.

BACKGROUND: Zinc plays an important role in appetite regulation. L-Carnosine, an endogenous dipeptide, may also regulate eating behavior via its histaminergic and antiglutamatergic properties. Polaprezinc (zinc-L-carnosine complex) is a medication for gastric ulcers. A small case series reported successful treatment of binge eating with add-on polaprezinc. METHODS: This was an open trial of add-on polaprezinc in patients with binge eating disorder (BED; n = 22) or bulimia nervosa (BN; n = 7) receiving antidepressants. A 4-week baseline period was followed by a 16-week polaprezinc treatment at 150 mg/d (containing 34 mg zinc and 116 mg L-carnosine) in addition to ongoing psychotropic medications. We also assessed their zinc status via a laboratory index and zinc deficiency-related symptoms. RESULTS: At the study end, both conditions showed a significant reduction in the 4-week frequency of combined objective and subjective binge eating episodes, the 4-week frequency of days when at least 1 such episode occurred (only in BED), several aspects of eating disorder psychopathology (rated by the Eating Disorder Examination-Questionnaire), and comorbid depressive symptoms (rated by the 16-item Quick Inventory of Depressive Symptomatology [Self-Report]). Serum copper/zinc ratio decreased from 1.4 to 1.1 on average in both conditions. All patients had multiple zinc deficiency-related symptoms at baseline that substantially improved after polaprezinc treatment. Overall, the effectiveness of polaprezinc was greater in BED patients than in BN patients, with minor adverse effects. CONCLUSIONS: These findings offer preliminary evidence for the effectiveness of polaprezinc in treating BED and BN and suggest the involvement of zinc deficiency in these conditions.

A Double-Blind, Randomized Pilot Trial of Chromium Picolinate for Overweight Individuals with Binge-Eating Disorder: Effects on Glucose Regulation.

PURPOSE: Chromium treatment has been shown to improve glucose regulation in some populations. The purpose of this study was to evaluate whether chromium picolinate (CrPic) supplementation improves glucose regulation in overweight individuals with binge-eating disorder (BED). METHODS: In this double-blinded randomized pilot trial, participants (N = 24) were randomized to high (HIGH, 1000 mcg/day, n = 8) or moderate (MOD, 600 mcg/day, n = 9) dose of CrPic or placebo (PL, n = 7) for 6 months. Participants completed an oral glucose tolerance test (OGTT) at baseline, 3 months, and 6 months. Fixed effects models were used to estimate mean change in glucose area under the curve (AUC), insulinAUC, and insulin sensitivity index (ISI). RESULTS: Results revealed a significant group and time interaction (p < 0.04) for glucoseAUC, with glucoseAUC increasing significantly in the PL group (p < 0.02) but decreasing significantly in the MOD group (p < 0.03) at 6 months. InsulinAUC increased significantly over time (main effect, p < 0.02), whereas ISI decreased significantly over time (main effect, p < 0.03). CONCLUSION: As anticipated, a moderate dose of CrPic was associated with improved glycemic control, whereas PL was associated with decreased glycemic control. It was unexpected that the improved glycemic control seen in the MOD dose group was not seen in the HIGH dose group. However, although participants randomized to the HIGH dose group did not have improved glycemic control, they had better glycemic control than participants randomized to the PL group. These findings support the need for larger trials.

A double-blind, randomized pilot trial of chromium picolinate for binge eating disorder: results of the Binge Eating and Chromium (BEACh) study.

OBJECTIVE: Chromium treatment has been shown to improve mood, appetite, and glucose regulation in various psychiatric and medical patient populations. The authors propose that chromium may be useful in the treatment of binge eating disorder (BED). METHOD: Twenty-four overweight adults with BED were enrolled in a 6-month double-blind placebo-controlled trial and randomly assigned to receive either 1000mcg chromium/day ("high dose"; n=8) or 600mcg chromium/day ("moderate dose"; n=9) as chromium picolinate or placebo (n=7). Mixed linear regression models were used to estimate mean change in binge frequency and related psychopathology, weight, symptoms of depression, and fasting glucose. RESULTS: Fasting glucose was significantly reduced in both chromium groups compared to the placebo group; similarly, numerically, but not significantly, greater reductions in binge frequency, weight, and symptoms of depression were observed in those treated with chromium versus placebo, although statistical power was limited in this pilot trial. For fasting glucose, the findings suggest a dose response with larger effects in the high dose compared to moderate dose group. CONCLUSION: These initial findings support further larger trials to determine chromium's efficacy in maintaining normal glucose regulation, reducing binge eating and related psychopathology, promoting modest weight loss, and reducing symptoms of depression in individuals with BED. Studies designed to link the clinical effects of chromium with changes in underlying insulin, serotonin, and dopamine pathways may be especially informative. If efficacious, chromium supplementation may provide a useful, low-cost alternative to or augmentation strategy for selective serotonin reuptake inhibitors, which have partial efficacy in BED. ClinicalTrials.gov NCT00904306.

World Federation of Societies of Biological Psychiatry (WFSBP) guidelines for the pharmacological treatment of eating disorders.

OBJECTIVES: The treatment of eating disorders is a complex process that relies not only on the use of psychotropic drugs but should include also nutritional counselling, psychotherapy and the treatment of the medical complications, where they are present. In this review recommendations for the pharmacological treatment of eating disorders (anorexia nervosa (AN), bulimia nervosa (BN), binge eating disorder (BED)) are presented, based on the available literature. METHODS: The guidelines for the pharmacological treatment of eating disorders are based on studies published between 1977 and 2010. A search of the literature included: anorexia nervosa bulimia nervosa, eating disorder and binge eating disorder. Many compounds have been studied in the therapy of eating disorders (AN: antidepressants (TCA, SSRIs), antipsychotics, antihistaminics, prokinetic agents, zinc, Lithium, naltrexone, human growth hormone, cannabis, clonidine and tube feeding; BN: antidepressants (TCA, SSRIs, RIMA, NRI, other AD), antiepileptics, odansetron, d-fenfluramine Lithium, naltrexone, methylphenidate and light therapy; BED: antidepressants (TCA, SSRIs, SNRIs, NRI), antiepileptics, baclofen, orlistat, d-fenfluramine, naltrexone). RESULTS: In AN 20 randomized controlled trials (RCT) could be identified. For zinc supplementation there is a grade B evidence for AN. For olanzapine there is a category grade B evidence for weight gain. For the other atypical antipsychotics there is grade C evidence. In BN 36 RCT could be identified. For tricyclic antidepressants a grade A evidence exists with a moderate-risk-benefit ratio. For fluoxetine a category grade A evidence exists with a good risk-benefit ratio. For topiramate a grade 2 recommendation can be made. In BED 26 RCT could be identified. For the SSRI sertraline and the antiepileptic topiramate a grade A evidence exists, with different recommendation grades. CONCLUSIONS: Additional research is needed for the improvement of the treatment of eating disorders. Especially for anorexia nervosa there is a need for further pharmacological treatment strategies.

Multivariate therapeutic approach to binge-eating disorder: combined nutritional, psychological and pharmacological treatment.

Treatment for binge-eating disorder (BED) is directed towards either the physical or psychopathological impairments, and often does not cover all the alterations characterizing the disease. In 30 BED patients, we monitored the effects of three types of 6-month treatment, randomly assigned to one of the three treatment groups, each consisting of 10 patients. Group 1 received a 1700-kcal diet (21% proteins, 27% lipids, 52% carbohydrate), cognitive-behavioural therapy (CBT), sertraline (50-150 mg/day) and topiramate (25-150 mg/day); group 2 received the same diet, CBT, sertraline; and group 3 received nutritional counselling and CBT. Binge frequency and weight were assessed every month. The Eating Disorder Inventory-2, the Symptoms Check List-90-Revised (SCL-90-R) and the Personality Diagnostic Questionnaire-4-Revised (PDQ-4-R) were administered before and after treatment. Binge frequency and excessive weight decreased significantly only in group 1 patients, in whom improvement was noted in total Eating Disorder Inventory-2 scores and the subitems 'bulimia', 'drive for thinness', 'maturity fear', 'ascetism', in total SCL-90-R scores and in the subitem 'somatization', in PDQ-4-R subitems 'schizotypic personality' and 'dependent personality'. Group 2 patients improved on the SCL-90-R subitems 'depression' and 'interpersonal relationship' and in the PDQ-4-R 'schizoid personality'. Combination therapy seems to be the only fully effective treatment in BED patients.