Wang W X, Huang N H, Lyu J, Yu C Q, Guo Y, Pei P, Du H D, Chen J S, Chen Z M, Huang T, Li Liming
Department of Epidemiology and Biostatistics, School of Public Health, Beijing 100191, China.
Department of Epidemiology and Biostatistics, School of Public Health, Beijing 100191, China Peking University Center for Public Health and Epidemic Preparedness & Response, Beijing 100191, China Key Laboratory of Molecular Cardiovascular Sciences, Ministry of Education, Beijing 100191, China.
Zhonghua Liu Xing Bing Xue Za Zhi. 2022 Apr 10;43(4):445-451. doi: 10.3760/cma.j.cn112338-20210413-00309.
To examine the associations of childhood obesity, assessed by genetic variations of childhood body mass index (BMI), with the risk of adult ischemic heart disease (IHD) and major coronary event (MCE). More than 69 000 participants from the China Kadoorie Biobank were genotyped. After excluding those with coronary heart disease, stroke, or cancer at baseline, a total of 64 454 participants were included in this study. Based on genome-wide significant single nucleotide polymorphisms (SNPs), childhood BMI genetic risk score were constructed for every participant and divided into quintiles, with the lowest quintile as the low genetic risk group and the highest quintile as the high genetic risk group. Cox proportional hazards regression models were used to estimate the association between genetic predisposition to childhood obesity and the risk of ischemic heart disease. During a median of 10.7 years of follow-up, 7 073 incident cases of IHD and 1 845 cases of MCE were documented. After adjusting for sex, age, region, and the first ten genetic principal components, the s (95%s) for IHD and MCE in the high genetic risk group were 1.10 (1.02-1.18) and 1.10 (0.95-1.27), compared with the low genetic risk group. IHD risk increased by 4% (2%-6%) for each one standard deviation increase in genetic risk score (trend =0.001). After further adjustment for baseline BMI, the differences between genetic risk groups were not statistically significant, but there was still a linear trend between genetic risk score and IHD risk (trend =0.019). IHD risk increased with genetic predisposition to childhood obesity, suggesting that childhood obesity is an important risk factor for the development of IHD in China. As an easily identifiable feature, changes of childhood BMI should be monitored regularly to realize early intervention of IHD in adults.
通过儿童体重指数（BMI）的基因变异评估儿童肥胖与成人缺血性心脏病（IHD）风险和主要冠状动脉事件（MCE）之间的关联。对来自中国嘉道理生物银行的69000多名参与者进行了基因分型。在排除基线时患有冠心病、中风或癌症的参与者后，本研究共纳入64454名参与者。基于全基因组显著单核苷酸多态性（SNP），为每位参与者构建儿童BMI遗传风险评分，并分为五等份，最低五等份为低遗传风险组，最高五等份为高遗传风险组。采用Cox比例风险回归模型估计儿童肥胖的遗传易感性与缺血性心脏病风险之间的关联。在中位10.7年的随访期间，记录了7073例IHD事件病例和1845例MCE病例。在调整性别、年龄、地区和前十个遗传主成分后，高遗传风险组IHD和MCE的s（95%置信区间）分别为1.10（1.02 - 1.18）和1.10（0.95 - 1.27），与低遗传风险组相比。遗传风险评分每增加一个标准差，IHD风险增加4%（2% - 6%）（趋势 = 0.001）。在进一步调整基线BMI后，遗传风险组之间的差异无统计学意义，但遗传风险评分与IHD风险之间仍存在线性趋势（趋势 = 0.019）。IHD风险随着儿童肥胖的遗传易感性增加，表明儿童肥胖是中国IHD发生的重要危险因素。作为一个易于识别的特征，应定期监测儿童BMI的变化，以实现对成人IHD的早期干预。
