Menzies Institute for Medical Research, University of Tasmania, Hobart, Tasmania, Australia.
Department of Medicine, University of Turku and Division of Medicine, Turku University Hospital, Turku, Finland.
Int J Obes (Lond). 2020 Aug;44(8):1733-1742. doi: 10.1038/s41366-020-0611-x. Epub 2020 Jun 3.
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.
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.
The wGRS97 associated with BMI from age 6 years with peak effect sizes observed at age 30 years (females: 1.14 kg/m; males: 1.09 kg/m 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.
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.
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。我们研究了一个与 BMI 在不同生命阶段随年龄进展相关的 97 个单核苷酸多态性加权遗传风险评分(wGRS97),以及 BMI 在生命早期的不同发育轨迹和不同的 BMI 发展轨迹。
共有 2188 名出生于 1980 年之前的年轻芬兰人心血管风险研究参与者,他们有基因型数据,并且从 6 岁到 49 岁期间身高和体重的客观测量数据被采集了 8 次。使用个体生长曲线分析、潜在类别增长混合模型和泊松修正回归来检验关联。
wGRS97 与 6 岁时的 BMI 相关,在 30 岁时达到最大效应量(女性:wGRS97 每增加一个标准差,BMI 增加 1.14kg/m;男性:wGRS97 每增加一个标准差,BMI 增加 1.09kg/m)。wGRS97 与 BMI 的关联在儿童期随年龄增长而增强,但在青春期减缓,尤其是在女性中,在 35-40 岁时减弱。wGRS97 较高与儿童期和成年期 BMI 速度增加有关,但与成年期 BMI 变化无关。与属于“正常稳定”生命历程轨迹组(儿童期到成年期 BMI 正常)相比,wGRS97 增加一个标准差,与属于不太有利的生命历程 BMI 轨迹组的风险增加 13-127%相关。
具有较高成人 BMI 遗传易感性的个体在儿童/青少年时期 BMI 水平较高且增长速度较快,并且发生不太有利的生命历程 BMI 轨迹的风险增加。