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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: OBJECTIVE, METHODS, RESULTS. Meshes: Autistic Disorder, Body Mass Index, Child, Child Nutritional Physiological Phenomena, Chromosome Deletion, Chromosome Disorders, Chromosomes, Human, Pair 16, Emotions, Feeding Behavior, Female, Humans, Hunger, Intellectual Disability, Male, Obesity.
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Are eating in the absence of hunger but not loss of control behaviors associated with 16p11.2 deletions? Context: The ∼600-kb BP4-BP5 16p11.2 deletion has been consistently associated with obesity. We studied two heritable disinhibited eating behaviors, eating in the absence of hunger (EAH) and loss of control (LOC), to better characterize the relationship between the deletion and obesity. Our study population included ninety-three 16p11.2 CNV carriers (64 with deletions and 29 with duplications) and their families. We performed analyses using linear mixed models and focused on deletion carriers. We confirmed previous associations between the 16p11.2 deletion and obesity (P < 0.0001) and between all EAH subscales and obesity (P < 0.05), after adjusting for confounders. We found significant associations between the deletion and EAH due to external cues (P = 0.004) and EAH due to boredom (P = 0.003), but not EAH due to fatigue/anxiety or negative affect. Conditioning BMI on the 16p11.2 deletion and each EAH behavior did not abolish the association between the deletion and obesity. LOC was underrepresented and not associated with the deletion.
assistant
We report evidence that the 16p11.2 deletion may influence specific obesity-associated disinhibited eating behaviors: EAH due to external trigger and EAH due to boredom. Prospective studies are needed to confirm the temporal order of EAH behaviors and obesity related to the deletion. Final Decision: yes