The aim of this study was to provide an update of the most recent (since January 2014) enhanced cognitive behavioural therapy (CBT-E) effectiveness studies (randomized controlled trials and open trials) on bulimia nervosa, binge eating disorder and transdiagnostic samples.
In particular, changes in leptin and ghrelin occur in patients with anorexia or bulimia nervosa and have been suggested to represent not only homeostatic adaptations to an altered energy balance but to contribute also to the acquisition and/or maintenance of persistent starvation, binge eating and physical hyperactivity, which are potentially rewarding for ED patients.
Mood intolerance, a maintenance factor of BN but external to eating disorder pathological features (typically addressed within CBT), emerged as the primary clinical variable distinguishing the severity groups showing a differential treatment response.
Moreover, findings demonstrate that, in addition to being the front-running treatment for BN symptoms, CBT might also be the most effective psychotherapy for improving the symptoms of depression that commonly co-occur in BN.
Sixty-six men and women with DSM-5 binge-eating disorder (BED) or bulimia nervosa (BN) were randomized to receive eight sessions of CBT-GSH + Noom (n = 33) or CBT-GSH (n = 33) over 12 weeks.
The purpose of this investigation was to examine the indirect effects of Integrative Cognitive-Affective Therapy (ICAT-BN) and Cognitive-Behavioral Therapy-Enhanced (CBT-E) on bulimia nervosa (BN) treatment outcome through three hypothesized maintenance variables: emotion regulation, self-directed behavior, and self-discrepancy.
This study: (1) assessed the role of leptin, melanocortin, and neurotrophin genetic variants in conferring risk for AN and BN; and (2) explored the involvement of these genes in body mass index (BMI) variations within AN and BN.
Up to now, polymorphisms and variations in various genes (e.g. genes for 5-HT receptors, leptin gene, melanocortin MC(4) receptor gene) have been assessed for association and transmission disequilibrium pertaining to anorexia nervosa and/or bulimia nervosa.
There were no significant group differences in COMTVal158Met alleles and genotype frequencies between patients and controls, for all EDs pooled together [range of odds ratios (ORs): 0.96-1.04, p-values: 0.46-0.97, I<sup>2</sup> = 0%] and when analysing separately patients with AN (ORs: 0.94-1.04, p-values: 0.31-0.61, I<sup>2</sup> = 0%) or BN (ORs: 0.80-1.09, p-values: 0.28-0.64, I<sup>2</sup> = 0-44%).
We explored the influence of interactions between polymorphisms acting upon postsynaptic receptors (DRD2 TaqA1 rs1800497 and DRD4 7R) and dopamine regulators (COMTrs4680 and DAT1) on the expression of eating symptoms and personality traits in women with bulimia-spectrum eating disorders.
Eighty women receiving treatment for serious ED (52 for anorexia nervosa, 28 for bulimia nervosa) and 116 age-matched females in the control group underwent COMT genotyping for polymorphism in exon 4 (codon 158).
We explored the influence of interactions between polymorphisms acting upon postsynaptic receptors (DRD2 TaqA1 rs1800497 and DRD4 7R) and dopamine regulators (COMT rs4680 and DAT1) on the expression of eating symptoms and personality traits in women with bulimia-spectrum eating disorders.
Our findings suggest that although DRD4 may not be associated with the diagnosis of BN, its variants are associated with a history of childhood ADHD in BN probands.
The polymorphism -1438G>A in the serotonin 2A receptor or 5-hydroxytriptamine (5-HT) type 2A receptor (5-HTR2A) gene has been associated with alterations in food intake such as anorexia and bulimia.
We explored the effect of allelic variations within the 5-HT2A receptor gene promoter polymorphism -1438G/A on trait impulsiveness and serotonin function in women with BN.