Sporadic fasting reduces attentional control without altering overall executive function in a binary classification task.

Diets with intermittent fasting are an efficient method for producing clinically significant weight loss and preventing the development of obesity. However, individuals following intermittent fasting must face the difficulty of avoiding eating when experiencing the feeling of hunger. In this study, we investigated which aspects of executive function were affected following a prolonged period of food deprivation in participants that have never previously undergone intermittent fasting. Twenty-six participants with normal weight performed two binary classification tasks (Stop Signal (SST) and Go/NoGo) after either a 12 h fasting or a nonfasting period in separate sessions. We measured their performance in several underlying decision-making processes, such as response inhibition and attentional control. In line with previous studies, our results revealed that decision-making processes to resolve the classification task were unaffected by fasting. Response inhibition, as indexed by the stop signal reaction time in the SST, remained as well unaltered after food deprivation. Rather, we observed a higher error rate in NoGo trials following a fasting period, which was associated with disrupted attentional control. Overall, these results indicate that when a hunger feeling reaches consciousness, it induces deficits over certain aspects of attentional control. Our findings hint at the importance of structured behavioral change strategies to cope with fasting-induced difficulties in attentional control, to help achieve weight management goals through successful self-monitoring of food intake.

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.