一项青少年队列研究中饮食行为与精神病理、脑成熟和肥胖遗传风险的关系

Xinyang Yu, Zuo Zhang, Moritz Herle, Tobias Banaschewski, Gareth J. Barker, Arun L. W. Bokde, Herta Flor, Antoine Grigis, Hugh Garavan, Penny Gowland, Andreas Heinz, Rüdiger Brühl, Jean-Luc Martinot, Marie-Laure Paillère Martinot, Eric Artiges, Frauke Nees, Dimitri Papadopoulos Orfanos, Hervé Lemaître, Tomáš Paus, Luise Poustka, Sarah Hohmann, Nathalie Holz, Christian Bäuchl, Michael N. Smolka, Nilakshi Vaidya, Henrik Walter, Robert Whelan, Ulrike Schmidt, Gunter Schumann, Sylvane Desrivières, on behalf of the IMAGEN consortium
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摘要

不健康的饮食是饮食失调(EDs)和肥胖的一个危险因素,通常与情绪和行为问题并存;然而,其潜在的神经生物学机制尚不清楚。通过分析纵向IMAGEN青少年队列的数据,我们研究了饮食行为、使用多基因评分(pgs)的高体重指数(BMI)遗传易感性以及ed相关精神病理和大脑成熟轨迹(14-23岁)之间的关系。聚类分析确定了23岁(N = 996)的3个饮食群体:限制性、情绪化/不受控制和健康饮食。BMI PGS、ED症状轨迹、内化和外化问题以及大脑成熟度将这些组区分开来。在限制性进食者和情绪化/不受控制的进食者中,大脑中几个区域的体积和厚度下降不那么明显。较小的小脑体积减少唯一地介导了BMI PGS对限制性饮食的影响,而多个脑区较小的体积减少介导了外化问题升高与情绪性/不受控制的饮食之间的关系,独立于BMI。这些发现揭示了遗传风险、脑成熟延迟和ED症状行为的独特贡献。这项研究确定了不同的饮食行为特征,并将它们与饮食失调症状、高体重指数的遗传倾向和青春期大脑成熟联系起来。
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Relationships of eating behaviors with psychopathology, brain maturation and genetic risk for obesity in an adolescent cohort study
Unhealthy eating, a risk factor for eating disorders (EDs) and obesity, often coexists with emotional and behavioral problems; however, the underlying neurobiological mechanisms are poorly understood. Analyzing data from the longitudinal IMAGEN adolescent cohort, we investigated associations between eating behaviors, genetic predispositions for high body mass index (BMI) using polygenic scores (PGSs), and trajectories (ages 14–23 years) of ED-related psychopathology and brain maturation. Clustering analyses at age 23 years (N = 996) identified 3 eating groups: restrictive, emotional/uncontrolled and healthy eaters. BMI PGS, trajectories of ED symptoms, internalizing and externalizing problems, and brain maturation distinguished these groups. Decreasing volumes and thickness in several brain regions were less pronounced in restrictive and emotional/uncontrolled eaters. Smaller cerebellar volume reductions uniquely mediated the effects of BMI PGS on restrictive eating, whereas smaller volumetric reductions across multiple brain regions mediated the relationship between elevated externalizing problems and emotional/uncontrolled eating, independently of BMI. These findings shed light on distinct contributions of genetic risk, protracted brain maturation and behaviors in ED symptomatology. This study identifies distinct eating behavior profiles and links them to eating disorder symptoms, genetic predispositions for high body mass index and brain maturation during adolescence.
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