Appetite, reward sensitivity and the development of disordered eating behaviours: nature via nurture.

几十年的双胞胎和家庭研究已经确定，饮食失调（EDs）有很强的遗传基础，根据ED类型的不同，遗传率估计在39-74%之间。更重要的是，大规模的基因组研究开始识别特定的常见基因变异。环境也起着至关重要的作用，众所周知，环境因素（如创伤经历、社会压力等）经常“触发”ED症状的发作（基因-环境相互作用）。然而，影响ED和ED症状的具体环境因素，如暴饮暴食，在很大程度上仍是未知的。一系列社会、认知和行为特征的个体差异被假设为易患ed，并介导对ed的遗传和环境影响。然而，以往对急症的研究主要集中在社会/心理风险因素上，而对行为特征的关注远远不够。相比之下，肥胖研究主要集中在食欲特征等行为特征上。特别是，这一领域的研究已经确定，食物线索反应是肥胖的一个关键易感风险因素。奖励敏感性和食物成瘾症状之间的联系也引起了人们的兴趣。然而，食欲特征和奖励敏感性作为饮食失调症状（如暴饮暴食）的易感风险因素尚未被探索。EDs研究的另一个限制是依赖于诊断为EDs的临床样本。由于ed的人群患病率较低，样本往往较小，并且集中在可能不具有代表性的高度精选群体上。众所周知，ED症状是连续存在的，基于人群的研究将症状作为连续的结果，因此有助于阐明ED的病因。大型纵向研究是必要的，以确定在ED症状发作之前的危险因素，但很少。

Decades of twin and family studies have established that eating disorders (EDs) have a strong genetic basis, with heritability estimates in the range of 39-74% depending on the ED type. What is more, large-scale genomic studies are starting to identify specific common genetic variants involved. The environment also plays a crucial role, and it is well known that environmental factors (such as traumatic experiences, social pressures etc.) often 'trigger' the onset of ED symptoms (gene-environment interaction). However, the specific environmental factors on both EDs and ED symptoms such as binge eating are still largely unknown. Individual differences in a range of social, cognitive and behavioural traits are hypothesised to predispose to EDs, and to mediate the genetic and environmental influences on EDs. However, previous research on EDs has mainly focused on social/psychological risk factors, while behavioural traits have received far less attention. In contrast, obesity research has focused largely on behavioural traits such as appetitive traits. In particular, research from this field has established that food cue responsiveness is a key predisposing risk factor for obesity. The link between reward sensitivity and food addiction symptoms has also been of interest. However, appetitive traits and reward sensitivity as predisposing risk factors for disordered eating symptoms (such as binge-eating) have not yet been explored. A further limitation of EDs research has been the reliance on clinical samples with diagnosed EDs. Samples have tended to be small due to the low population prevalence of EDs, and focused on highly select groups who may not be representative. It is well recognised that ED symptoms exist on a continuum and population-based research into symptoms as continuous outcomes would therefore help to elucidate the aetiology of EDs. Large longitudinal studies are necessary for identifying risk factors that precede the onset of ED symptoms, but are rare.