16p11.2 Locus modulates response to satiety before the onset of obesity.

BACKGROUND: The 600 kb BP4-BP5 copy number variants (CNVs) at the 16p11.2 locus have been associated with a range of neurodevelopmental conditions including autism spectrum disorders and schizophrenia. The number of genomic copies in this region is inversely correlated with body mass index (BMI): the deletion is associated with a highly penetrant form of obesity (present in 50% of carriers by the age of 7 years and in 70% of adults), and the duplication with being underweight. Mechanisms underlying this energy imbalance remain unknown. OBJECTIVE: This study aims to investigate eating behavior, cognitive traits and their relationships with BMI in carriers of 16p11.2 CNVs. METHODS: We assessed individuals carrying a 16p11.2 deletion or duplication and their intrafamilial controls using food-related behavior questionnaires and cognitive measures. We also compared these carriers with cohorts of individuals presenting with obesity, binge eating disorder or bulimia. RESULTS: Response to satiety is gene dosage-dependent in pediatric CNV carriers. Altered satiety response is present in young deletion carriers before the onset of obesity. It remains altered in adolescent carriers and correlates with obesity. Adult deletion carriers exhibit eating behavior similar to that seen in a cohort of obesity without eating disorders such as bulimia or binge eating. None of the cognitive measures are associated with eating behavior or BMI. CONCLUSIONS: These findings suggest that abnormal satiety response is a strong contributor to the energy imbalance in 16p11.2 CNV carriers, and, akin to other genetic forms of obesity, altered satiety responsiveness in children precedes the increase in BMI observed later in adolescence.

CYP2D6 polymorphism in patients with eating disorders.

CYP2D6 polymorphism is associated with variability in drug response, endogenous metabolism (that is, serotonin), personality, neurocognition and psychopathology. The relationship between CYP2D6 genetic polymorphism and the risk of eating disorders (ED) was analyzed in 267 patients with ED and in 285 controls. A difference in the CYP2D6 active allele distribution was found between these groups. Women carrying more than two active genes (ultrarapid metabolizers) (7.5 vs 4.6%) or two (67 vs 58.9%) active genes were more frequent among patients with ED, whereas those with one (20.6 vs 30.2%) or zero active genes (4.9 vs 6.3%) were more frequent among controls (P<0.05). Although further research is needed, present findings suggest an association between CYP2D6 and ED. CYP2D6 allele distribution in patients with ED seems related to increased enzyme activity.

Cognitive behavioral therapy for compulsive buying behavior: Predictors of treatment outcome.

BACKGROUND: Compulsive buying behavior (CBB) is receiving increasing consideration in both consumer and psychiatric-epidemiological research, yet empirical evidence on treatment interventions is scarce and mostly from small homogeneous clinical samples. OBJECTIVES: To estimate the short-term effectiveness of a standardized, individual cognitive behavioral therapy intervention (CBT) in a sample of n=97 treatment-seeking patients diagnosed with CBB, and to identify the most relevant predictors of therapy outcome. METHOD: The intervention consisted of 12 individual CBT weekly sessions, lasting approximately 45minutes each. Data on patients' personality traits, psychopathology, sociodemographic factors, and compulsive buying behavior were used in our analysis. RESULTS: The risk (cumulative incidence) of poor adherence to the CBT program was 27.8%. The presence of relapses during the CBT program was 47.4% and the dropout rate was 46.4%. Significant predictors of poor therapy adherence were being male, high levels of depression and obsessive-compulsive symptoms, low anxiety levels, high persistence, high harm avoidance and low self-transcendence. CONCLUSION: Cognitive behavioral models show promise in treating CBB, however future interventions for CBB should be designed via a multidimensional approach in which patients' sex, comorbid symptom levels and the personality-trait profiles play a central role.

Modulation of Irisin and Physical Activity on Executive Functions in Obesity and Morbid obesity.

Whether the executive profile is different between obesity (OB) and morbid obesity (MO) remains unclear. Recent evidence suggests that physical activity (PA) can act as a cognitive enhancer. Irisin is a recently discovered hormone associated with some of the positive effects of PA. The objective of the study was to investigate the executive profile in OB and MO, and to explore the role of PA and irisin. 114 participants were included (21 OB, 44 MO and 49 healthy controls-HC) in the study and assessed with the Wisconsin Card Sorting Test, Stroop Color and Word Test, and Iowa Gambling Task. All participants were female, aged between 18 and 60 years. Results showed a similar dysfunctional profile on decision making in OB and MO compared with HC. Thus, no specific neuropsychological profiles between OB and MO can be clearly observed in our sample. However, a negative correlation was found between irisin and executive functioning. These results demonstrate a specific executive profile in OB and a relevant and negative modulation of irisin on executive functioning. Although irisin might be a promising target for the treatment of obesity, its effects on cognition might be considered when thinking about its therapeutic use.

Specific eating disorder clusters based on social anxiety and novelty seeking.

While social avoidance and distress (SAD), a key aspect of social phobia related to behavioral inhibition, is high in different eating disorders (EDs), novelty seeking (NS) is mainly linked to bulimic disorders. Since heterogeneity in NS levels (low/high) exists in social phobia and in about 55% of ED with a highly disturbed personality, we examined ED types based on SAD and NS and their relationships to eating and comorbid features. Scores of 825 ED women on SAD and NS were submitted to cluster analysis. Five clinically differentiated ED clusters emerged: two without SAD (45%) and three with high SAD and low (13%), mid (34%), high NS (8%) levels. High vs. low SAD groups showed greater eating and social impairment, ineffectiveness, ascetism, suicide attempts, and lower education. Among SAD clusters, "SAD-low NS" had the lowest rate of binge eating, vomit, substance use, stealing and compulsive buying, whereas "SAD-high NS" presented the opposite pattern. However, no differences across SAD clusters were found with regard to ED diagnostic category distribution or history of treatment. Findings show that SAD-ED types present heterogeneity of NS and greater severity.