ABSTRACT
Background and Objectives: The NUCB2 gene and its polymorphisms were identified as novel players in the regulation of food intake, potentially leading to obesity (OBE) and altered eating behaviors. Naltrexone/bupropion SR (NB) showed good efficacy and tolerability for treating OBE and altered eating behaviors associated with binge eating disorder (BED). This prospective study investigates the influence of NUCB2 gene polymorphism on NB treatment response in OBE and BED. Materials and Methods: Body mass index (BMI), eating (EDE-Q, BES, NEQ, GQ, Y-FAS 2.0) and general psychopathology (BDI, STAI-S) were evaluated at baseline (t0) and after 16 weeks (t1) of NB treatment in patients with OBE and BED (Group 1; N = 22) vs. patients with OBE without BED (Group 2; N = 20). Differences were evaluated according to the rs757081 NUCB2 gene polymorphism. Results: NUCB2 polymorphism was equally distributed between groups. Although weight at t0 was higher in Group 1, weight loss was similar at t1 in both groups. BMI was not influenced by NUCB2 polymorphism. In Group 1, the CG-genotype reported significant improvement in eating psychopathology while the GG-genotype reported improvement only for FA. No differences were observed in Group 2. Conclusions: Patients diagnosed with BED and treated with NB exhibited a more favorable treatment response within the CG-genotype of the NUCB2 polymorphism.
ABSTRACT
BACKGROUND: Impaired metabolic response such as blood glucose fast fluctuations may be hypothesized in binge eating disorder (BED) and food addiction (FA) by virtue of the repetitive consumption of highly processed food. Conversely, rapid changes in plasma glucose (i.e., hypoglycemia) may trigger craving for the same food products. The investigation of early glycemic disturbances in BED and FA could enhance the understanding of the metabolic mechanisms involved in the maintenance of the disorders. Present study investigated hypoglycemia events during a 5-h-long oral glucose tolerance test (OGTT) in people with BED, FA, and the comorbid phenotype. Further, the association between the severity of eating psychopathology and the variability in hypoglycaemia events was explored. METHODS: Two-hundred participants with high weight and no diabetes completed the extended OGTT and were screened for BED, FA, BED-FA, or no-BED/FA. The four groups were compared in hypoglycemia events, OGTT-derived measures, and eating psychopathology. The association between predictors (eating psychopathology), confounders (demographics, metabolic features), and the outcomes (hypoglycemia, early/late hypoglycemia, severe hypoglycemia, reactive hypoglycemia) was examined through logistic regression. RESULTS: Hypoglycemia in general, and reactive hypoglycemia were highly frequent (79% and 28% of the sample, respectively). Hypoglycemia events (< 70 mg/dL) were equally experienced among groups, whilst severe hypoglycemia (< 54 mg/dL) was more frequent in BED at the late stage of OGTT (5 h; χ2 = 1.120, p = .011). The FA and BED groups exhibited significantly higher number of reactive hypoglycemia (χ2 = 13.898, p = .003), in different times by diagnosis (FA: 210'-240'; BED: at the 270'). FA severity was the only predictor of early and reactive hypoglycemia. CONCLUSIONS: People with BED or FA are prone to experiencing reactive hypoglycemia; FA severity may predict early and symptomatic hypoglycemia events. This can further reinforce disordered eating behaviours by promoting addictive responses, both biologically and behaviourally. These results inform professionals dealing with eating disorders about the need to refer patients for metabolic evaluation. On the other hand, clinicians dealing with obesity should screen for and address BED and FA in patients seeking care for weight loss.
Impairment in blood glucose control may be attended in binge eating disorder (BED) and food addiction (FA), two distinct eating disorders which are characterized by the recurrent consumption of highly palatable food rich in high-glucose index carbohydrates. Conversely, rapid changes in blood glucose, such as hypoglycemia, may intensify craving for high-calorie products, thus reinforcing pathological eating behaviours. This study investigated the presence of hypoglycemia events in people suffering from BED, FA, both, or no eating disorder, and explored whether the severity of eating behaviours correlated with a higher probability of having hypoglycemia. Results showed that people with BED and FA experienced more episodes of symptomatic hypoglycemia than those with obesity but no eating disorder. The severity of binge eating was associated with more severe hypoglycemia events, indicated by lower plasma glucose values. Lastly, people with severe FA were more prone to experiencing early post-meal hypoglycemia accompanied by symptoms. These results inform professionals dealing with eating disorders about the need to refer patients for metabolic evaluation. On the other hand, clinicians dealing with obesity should screen for and address BED and FA in patients seeking care for weight loss.
ABSTRACT
PURPOSE: Binge eating disorder (BED) has a considerable clinical relevance by virtue of its high numerous psychiatric and medical comorbidities; among the latter, the most frequent is obesity. Available treatments for BED have shown frequent relapse of binges or weight regain in the long term. The new combination of naltrexone and bupropion sustained release (NB) has proved to be effective for weight loss among obese patients. As NB acts on hypothalamic and reward circuits, that seem involved in the pathogenesis and maintenance of BED symptoms, this study aims to evaluate the efficacy of NB in improving pathological eating behavior and losing weight in BED patients. METHODS: In this preliminary study, 23 obese-BED patients and a control group of 20 obese non-BED patients (respectively, Groups 1 and 2) who had previously undergone at least 5 unsuccessful weight-loss programs were treated with NB in addition to modified life style. Evaluation at t0 and after 16 weeks of treatment (t1) included anthropometric measurement, eating behavior assessment and psychopathological questionnaires (EDE-Q, BES, YFAS, BDI and STAI). RESULTS: A significant and similar weight loss (ΔBMI% ≈ 8%) was evident for both groups. Pathological eating behavior (i.e., binge, grazing, emotional eating, craving for carbohydrates, and post-dinner eating), BES score and YFAS severity significantly improved, especially among BED. NB was well tolerated and drop-out rate was low. CONCLUSION: Treatment with NB, in addition to a reduced-calorie diet and increased physical activity, seems an effective and well-tolerated option for improving pathological eating behavior and losing weight in obese-BED patients. LEVEL OF EVIDENCE: Level III case-control study.