Separating the genetics of childhood and adult obesity: a validation study of genetic scores for body mass index in adolescence and adulthood in the HUNT Study.
Separating the genetics of childhood and adult obesity: a validation study of genetic scores for body mass index in adolescence and adulthood in the HUNT Study.
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DOI：
10.1093/hmg/ddaa256
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发表时间：
2021-02-25
影响因子：
3.5
通讯作者：
Vie GÅ
中科院分区：
文献类型：
--
作者：
Brandkvist M;Bjørngaard JH;Ødegård RA;Åsvold BO;Smith GD;Brumpton B;Hveem K;Richardson TG;Vie GÅ
从生命历程的角度来看，导致儿童肥胖的遗传和环境因素可能对日后的健康产生持久影响。然而，肥胖轨迹在整个生命历程中如何变化仍不明确。最近，理查森等人针对体重指数（BMI）创建了有力的早期生命和成年基因评分，以全面尝试区分儿童期和成年期的肥胖。儿童期评分是使用对40 - 69岁成年人进行的基于问卷调查的数据得出的，这些数据涉及他们10岁时的相对体型，这使其容易出现回忆和错误分类偏差。因此，我们试图利用1963年至2019年挪威HUNT研究中66963名个体在青春期和成年期测量的BMI数据来验证儿童期和成年期的评分。儿童期评分在青春期和成年早期的预测性能更好，而成年期评分在成年期的预测性能更好。在12 - 15.9岁年龄组中，儿童期多基因风险评分（PRS）解释的方差为6.7%，而成人PRS为2.4%。在24 - 29.9岁年龄组中，成人PRS解释的方差为3.9%，儿童期PRS为3.6%。我们的研究结果支持，驱动BMI的遗传因素在幼年和成年时有所不同。在多变量孟德尔随机化框架内，经过验证的儿童期基因评分现在可用于确定儿童肥胖对后期疾病的影响。
From a life-course perspective, genetic and environmental factors driving childhood obesity may have a lasting influence on health later in life. However, how obesity trajectories vary throughout the life-course remains unknown. Recently, Richardson et al. created powerful early life and adult gene scores for body mass index (BMI) in a comprehensive attempt to separate childhood and adult obesity. The childhood score was derived using questionnaire-based data administered to adults aged 40–69 regarding their relative body size at age 10, making it prone to recall and misclassification bias. We therefore attempted to validate the childhood and adult scores using measured BMI data in adolescence and adulthood among 66 963 individuals from the HUNT Study in Norway from 1963 to 2019. The predictive performance of the childhood score was better in adolescence and early adulthood, whereas the predictive performance of the adult score was better in adulthood. In the age group 12–15.9 years, the variance explained by the childhood polygenic risk score (PRS) was 6.7% versus 2.4% for the adult PRS. In the age group 24–29.9 years, the variance explained by the adult PRS was 3.9% versus 3.6% for the childhood PRS. Our findings support that genetic factors driving BMI differ at young age and in adulthood. Within the framework of multivariable Mendelian randomization, the validated childhood gene score can now be used to determine the consequence of childhood obesity on later disease.
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