Eating disorder symptoms and their associations with anthropometric and psychiatric polygenic scores.

Eating disorder symptoms and their associations with anthropometric and psychiatric polygenic scores.
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DOI:
10.1002/erv.2889
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发表时间:
2022-05
影响因子:
5.3
通讯作者:
Micali, Nadia
Micali, Nadia
中科院分区:
心理学2区
文献类型:
--
作者:
Abdulkadir, Mohamed;Huebel, Christopher;Herle, Moritz;Loos, Ruth J. F.;Breen, Gerome;Bulik, Cynthia M.;Micali, Nadia

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进食障碍(艾德)症状在普通人群中普遍存在,但其与精神、代谢和人体测量特征的共同遗传基础尚不清楚。在此,我们在雅芳父母和儿童纵向研究(ALSPAC)中研究了与神经性厌食症相关的多基因评分(PGSs)特征是否也与青少年艾德症状相关。ALSPAC研究共纳入8654名具有基因型数据和至少一种表型测量的参与者。我们将来自25个特征(16个精神特征,4个代谢特征,5个人体测量特征)的PGS与8个艾德症状相关联,包括禁食减肥等行为和对身体不满等认知。较高的注意缺陷多动障碍PGS和较低的教育程度PGS与禁食减肥有关。较高的失眠PGS与身体不满增加有关。我们没有发现代谢特征PGS和任何艾德症状之间存在关联的证据。无脂肪质量、脂肪质量和体脂百分比PGSs与暴饮暴食、过度运动、禁食减肥、身体不满以及体重和形状问题呈正相关。艾德症状在遗传上与精神和人体测量学相关,但与代谢特征无关。我们的研究结果为未来的遗传学研究提供了见解,研究为什么一些有艾德症状的个体会发展成阈值ED,而另一些则不会。一些饮食失调症状(即,暴饮暴食、禁食减肥和身体不满意)与精神和人体测量多基因评分显著相关,强调了这些特征的遗传复杂性。一般人群中存在的进食障碍症状和阈值进食障碍可能部分病因相关(即,精神和人体测量起源),但代谢遗传因素可以区分症状和阈值进食障碍。因此,代谢紊乱可能是催化剂,使一些人的发展轨迹,导致阈值饮食失调。
Eating disorder (ED) symptoms are prevalent in the general population, but their shared genetic underpinnings with psychiatric, metabolic, and anthropometric traits are not known. Here, we examined if polygenic scores (PGSs) of traits associated with anorexia nervosa are also associated with adolescent ED symptoms in the Avon Longitudinal Study of Parents and Children (ALSPAC). A total of 8654 participants with genotype data and at least one phenotypic measure were included from the ALSPAC study. We associated PGS from 25 traits (16 psychiatric, 4 metabolic, and 5 anthropometric) with eight ED symptoms, including behaviours such as fasting for weight loss and cognitions such as body dissatisfaction. Higher attention deficit hyperactivity disorder PGS and lower educational attainment PGS were associated with fasting for weight loss. Higher insomnia PGS was associated with increased body dissatisfaction. We found no evidence of an association between metabolic trait PGS and any ED symptom. Fat‐free mass, fat mass, and body fat percentage PGSs, were positively associated with binge eating, excessive exercise, fasting for weight loss, body dissatisfaction, and weight and shape concern. ED symptoms are genetically associated with psychiatric and anthropometric, but not with metabolic traits. Our findings provide insights for future genetic research investigating on why some individuals with ED symptoms progress to develop threshold EDs while others do not. Several eating disorder symptoms (i.e., binge eating, fasting for weight loss, and body dissatisfaction) in this study were significantly associated with both psychiatric and anthropometric polygenic scores emphasising the genetic complexity of these traits. Eating disorder symptoms as present in the general population and threshold eating disorders may be partially etiologically related (i.e., psychiatric and anthropometric origins), but metabolic genetic factors may differentiate between symptoms and threshold eating disorders. Metabolic disturbances could therefore be the catalyst that puts some individuals on a developmental trajectory leading to threshold eating disorders.
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