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Fat brains, greedy genes, and parent power: A biobehavioural risk model of child and adult obesity

机译:肥胖的大脑,贪婪的基因和父母的力量:儿童和成人肥胖的生物行为风险模型

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We live in a world replete with opportunities to overeat highly calorific, palatable foods - yet not everyone becomes obese. Why? We propose that individuals show differences in appetitive traits (e.g. food cue responsiveness, satiety sensitivity) that manifest early in life and predict their eating behaviours and weight trajectories. What determines these traits? Parental feeding restriction is associated with higher child adiposity, pressure to eat with lower adiposity, and both strategies with less healthy eating behaviours, while authoritative feeding styles coincide with more positive outcomes. But, on the whole, twin and family studies argue that nature has a greater influence than nurture on adiposity and eating behaviour, and behavioural investigations of genetic variants that are robustly associated with obesity (e.g. FTO) confirm that genes influence appetite. Meanwhile, a growing body of neuroimaging studies in adults, children and high risk populations suggests that structural and functional variation in brain networks associated with reward, emotion and control might also predict appetite and obesity, and show genetic influence. Together these different strands of evidence support a biobehavioural risk model of obesity development. Parental feeding recommendations should therefore acknowledge the powerful - but modifiable - contribution of genetic and neurological influences to children's eating behaviour.
机译:我们生活在一个充满机会的世界,过量食用高热量,可口的食物-但并非所有人都变得肥胖。为什么?我们建议个体在生活早期表现出食欲特征(例如食物提示反应性,饱腹感)方面的差异,并预测其饮食行为和体重轨迹。是什么决定了这些特征?父母的进食限制与儿童肥胖,较高的饮食压力和较低的肥胖有关,并且两种策略都具有不良的健康饮食行为,而权威的喂养方式与更积极的结果相吻合。但是,总体而言,双胞胎和家庭研究认为,自然对肥胖和饮食行为的影响远大于营养对肥胖的影响,对与肥胖有密切关系的遗传变异的行为研究(例如FTO)证实了基因对食欲的影响。同时,越来越多的成年人,儿童和高危人群的神经影像学研究表明,与奖赏,情感和控制有关的大脑网络的结构和功能变异也可能预测食欲和肥胖,并显示出遗传影响。这些不同的证据共同支持肥胖症发展的生物行为风险模型。因此,父母的喂养建议应该承认遗传和神经学影响对儿童饮食行为的强大但可修改的贡献。

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