Longitudinal association of a body mass index (BMI) genetic risk score with growth and BMI changes across the life course: The Cardiovascular Risk in Young Finns Study

Longitudinal association of a body mass index (BMI) genetic risk score with growth and BMI changes across the life course: The Cardiovascular Risk in Young Finns Study
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DOI:
10.1038/s41366-020-0611-x
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发表时间:
2020-06-03
影响因子:
4.9
通讯作者:
Magnussen, Costan G.
Magnussen, Costan G.
中科院分区:
医学2区
文献类型:
--
作者:
Buscot, Marie-Jeanne;Wu, Feitong;Magnussen, Costan G.

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背景与成人体重指数(BMI)相关的遗传风险评分在整个生命过程中对BMI水平的作用尚不清楚。我们研究了97个单核苷酸多态性加权遗传风险评分(wGRS 97)是否与不同生命阶段BMI的年龄相关进展以及早期生命过程中BMI的不同发展轨迹相关。方法2188名1980年以前出生的芬兰青年心血管风险研究参与者,他们的基因型数据和身高和体重的客观测量从6岁到49岁收集了8次。使用个体生长曲线分析、潜在类生长混合模型和泊松修正回归来检查关联性。结果wGRS 97从6岁开始与BMI相关,在30岁时观察到峰值效应量(女性:1.14 kg/m2;男性:1.09 kg/m2),BMI随着wGRS 97标准差的增加而增加。wGRS 97和BMI之间的关联在儿童期随着年龄的增长而增强,但在青春期放缓,特别是在女性中,并在35-40岁时减弱。较高的wGRS 97与儿童期和成年期的BMI速度增加相关,但与成年期的BMI变化无关。与属于“正常稳定”的生命过程轨迹组(从儿童到成年的正常BMI)相比,wGRS 97高一个标准差与属于不太有利的生命过程BMI轨迹组的风险增加13-127%相关。结论:对较高成人BMI具有遗传易感性的个体在儿童期/青春期的BMI增加水平较高且增加速度加快,并且具有较不利的生命过程BMI轨迹的风险增加。
Background The role of genetic risk scores associated with adult body mass index (BMI) on BMI levels across the life course is unclear. We examined if a 97 single nucleotide polymorphism weighted genetic risk score (wGRS97) associated with age-related progression in BMI at different life stages and distinct developmental trajectories of BMI across the early life course. Methods 2188 Cardiovascular Risk in Young Finns Study participants born pre-1980 who had genotype data and objective measurements of height and weight collected up to 8 times from age 6 to 49 years. Associations were examined using Individual Growth Curve analysis, Latent Class Growth Mixture Modelling, and Poisson modified regression. Results The wGRS97 associated with BMI from age 6 years with peak effect sizes observed at age 30 years (females: 1.14 kg/m(2); males: 1.09 kg/m(2) higher BMI per standard deviation increase in wGRS97). The association between wGRS97 and BMI became stronger with age in childhood but slowed in adolescence, especially in females, and weakened at age 35-40 years. A higher wGRS97 associated with an increased BMI velocity in childhood and adulthood, but not with BMI change in adulthood. Compared with belonging to a 'normal stable' life-course trajectory group (normal BMI from childhood to adulthood), a one standard deviation higher wGRS97 associated with a 13-127% increased risk of belonging to a less favourable life-course BMI trajectory group. Conclusions Individuals with genetic susceptibility to higher adult BMI have higher levels and accelerated rates of increase in BMI in childhood/adolescence, and are at increased risk of having a less favourable life-course BMI trajectory.