“…Binge eating, characterized by eating a large amount of food in a short period of time, as well as a sense of lack of control over food intake, is the most common behavioral manifestation present in a variety of eating disorders (Attia et al, 2013; Kessler et al, 2013). Data suggest that individuals who engage in binge eating behavior develop AUD, overweight/obesity, and worsening depressive symptoms over the course of time (Franko et al, 2005; Sonneville et al, 2013).…”
Binge eating disorder and alcohol use disorder (AUD) frequently co-occur in the presence of other psychiatric conditions. Data suggest that binge eating engages similar behavioral and neurochemical processes common to AUD, which might contribute to the etiology or maintenance of alcoholism. However, it is unclear how binge feeding behavior and alcohol intake interact to promote initiation or maintenance of AUD. We investigated the impact of binge-like feeding on alcohol intake and anxiety-like behavior in male Long Evans rats. Rats received chow (controls) or extended intermittent access (24 hr twice a week; Int-HFD) to a nutritionally complete high-fat diet for six weeks. Standard rodent chow was available ad-libitum to all groups and food intake was measured. Following HFD exposure, 20.0% ethanol, 2.0% sucrose intake and endocrine peptide levels were evaluated. Anxiety-like behavior was measured using a light-dark (LD) box apparatus. Rats in the Int-HFD group displayed a binge-like pattern of feeding (alternations between caloric overconsumption and voluntary caloric restriction). Surprisingly, alcohol intake was significantly attenuated in the Int-HFD group whereas sugar consumption was unaffected. Plasma acyl-ghrelin levels were significantly elevated in the Int-HFD group, whereas glucagon-like peptide-1 levels did not change. Moreover, rats in the Int-HFD group spent more time in the light side of the LD box compared to controls, indicating that binge-like feeding induced anxiolytic effects. Collectively, these data suggest that intermittent access to HFD attenuates alcohol intake through reducing anxiety-like behavior, a process potentially controlled by elevated plasma ghrelin levels.
“…Binge eating, characterized by eating a large amount of food in a short period of time, as well as a sense of lack of control over food intake, is the most common behavioral manifestation present in a variety of eating disorders (Attia et al, 2013; Kessler et al, 2013). Data suggest that individuals who engage in binge eating behavior develop AUD, overweight/obesity, and worsening depressive symptoms over the course of time (Franko et al, 2005; Sonneville et al, 2013).…”
Binge eating disorder and alcohol use disorder (AUD) frequently co-occur in the presence of other psychiatric conditions. Data suggest that binge eating engages similar behavioral and neurochemical processes common to AUD, which might contribute to the etiology or maintenance of alcoholism. However, it is unclear how binge feeding behavior and alcohol intake interact to promote initiation or maintenance of AUD. We investigated the impact of binge-like feeding on alcohol intake and anxiety-like behavior in male Long Evans rats. Rats received chow (controls) or extended intermittent access (24 hr twice a week; Int-HFD) to a nutritionally complete high-fat diet for six weeks. Standard rodent chow was available ad-libitum to all groups and food intake was measured. Following HFD exposure, 20.0% ethanol, 2.0% sucrose intake and endocrine peptide levels were evaluated. Anxiety-like behavior was measured using a light-dark (LD) box apparatus. Rats in the Int-HFD group displayed a binge-like pattern of feeding (alternations between caloric overconsumption and voluntary caloric restriction). Surprisingly, alcohol intake was significantly attenuated in the Int-HFD group whereas sugar consumption was unaffected. Plasma acyl-ghrelin levels were significantly elevated in the Int-HFD group, whereas glucagon-like peptide-1 levels did not change. Moreover, rats in the Int-HFD group spent more time in the light side of the LD box compared to controls, indicating that binge-like feeding induced anxiolytic effects. Collectively, these data suggest that intermittent access to HFD attenuates alcohol intake through reducing anxiety-like behavior, a process potentially controlled by elevated plasma ghrelin levels.
“…It is important to note that the DSM-5 Eating Disorders Work Group specifically decided not to make obesity a psychiatric diagnosis, stating that “genetic, physiological, behavioral, and environmental factors that vary across individuals contribute to the development of obesity; thus, obesity per se is not considered a mental disorder” (page 1238) [6]. It would therefore be unfortunate if DSM-5 changes inadvertently pathologized normative eating behaviors among individuals with obesity, who already face discrimination in the workplace, health care facilities, educational institutions, the media, and interpersonal relationships [7].…”
Background. DSM-5 revisions have been criticized in the popular press for overpathologizing normative eating patterns—particularly among individuals with obesity. To evaluate the evidence for this and other DSM-5 critiques, we compared the point prevalence and interrater reliability of DSM-IV versus DSM-5 eating disorders (EDs) among adults seeking weight-loss treatment. Method. Clinicians (n = 2) assigned DSM-IV and DSM-5 ED diagnoses to 100 participants via routine clinical interview. Research assessors (n = 3) independently conferred ED diagnoses via Structured Clinical Interview for DSM-IV and a DSM-5 checklist. Results. Research assessors diagnosed a similar proportion of participants with EDs under DSM-IV (29%) versus DSM-5 (32%). DSM-5 research diagnoses included binge eating disorder (9%), bulimia nervosa (2%), subthreshold binge eating disorder (5%), subthreshold bulimia nervosa (2%), purging disorder (1%), night eating syndrome (6%), and other (7%). Interrater reliability between clinicians and research assessors was “substantial” for both DSM-IV (κ = 0.64, 84% agreement) and DSM-5 (κ = 0.63, 83% agreement). Conclusion. DSM-5 ED criteria can be reliably applied in an obesity treatment setting and appear to yield an overall ED point prevalence comparable to DSM-IV.
“…In the fourth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV) [5] three EDs are recognized: anorexia nervosa (AN), bulimia nervosa (BN) and a residual diagnostic category called eating disorder not otherwise specified (EDNOS) including binge eating disorder (BED). In the new edition, DSM-5 [6], BED has been added as a new official diagnosis [7]. Prior to the official recognition of BED as a specific DSM-5 ED, several studies into the efficacy of specific BED interventions have been performed [8], utilizing DSM-IV research criteria.…”
BackgroundWhile eating disorder not otherwise specified (EDNOS) is the most common eating disorder (ED) diagnosis in routine clinical practice, no specific treatment methods for this diagnosis have yet been developed and studied. Enhanced cognitive behavioral therapy (CBT-E) has been described and put to the test as a transdiagnostic treatment protocol for all EDs, including EDNOS. Initial research in the UK suggests that CBT-E is more effective for EDs, especially bulimia nervosa (BN) and EDNOS, than the earlier version of CBT. These positive results of CBT-E have to be replicated in more detail, preferably by independent researchers in different countries. Being the first Dutch study into CBT-E, the results from this national multicenter study – on three sites specialized in EDs – will deliver important information about the effectiveness of CBT-E in several domains of ED pathology, while providing input for the upcoming update of the Dutch Multidisciplinary Guideline for the Treatment of Eating Disorders.Methods/designA multicenter randomized controlled trial will be conducted. One hundred and thirty-two adult outpatients (aged 18 years and older) with an ED diagnosis and a Body Mass index (BMI) of between 17.5 and 40 will be randomly allocated to the control or the intervention group. Subjects in the control group will receive Treatment as Usual (standard outpatient treatment provided at the participating sites). Subjects in the intervention group will receive 20 sessions of CBT-E in 20 weeks. The design is a 2 (group) × 5 (time) repeated measures factorial design in which neither therapists nor patients will be blinded for treatment allocation. The primary outcome measure is recovery from the ED. Secondary outcome measures include ED psychopathology, common mental disorders, anxiety and depressive symptoms, health-related quality of life, health care use and productivity loss. Self-esteem, perfectionism and interpersonal problems will be examined as putative predictors and mediators of the effect of treatment. Also, an economic evaluation from a societal perspective will be undertaken. All relevant effects, direct and indirect costs will be included. Utility scores will measure the effects. Measurements will take place at pretreatment, 6 weeks, 20 weeks, 40 weeks and 80 weeks.DiscussionThis effectiveness study into CBT-E has the aim of broadening the scope and generalizability of former studies. If CBT-E appears to be at least as effective as traditional diagnosis-specific treatments for a broad range of ED patients, training in one protocol would be sufficient for clinicians to treat patients with different kinds of EDs. It gives the opportunity to offer treatment for a severe mental disorder with fewer resources, thereby increasing the accessibility of specialized care for patients with an ED.Trial registrationNetherlands Trial Register, NTR4485. Registered on 2 April 2014.Electronic supplementary materialThe online version of this article (doi:10.1186/s13063-016-1716-3) contains supplementary material, wh...
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