Department of Psychology and Logopedics, Faculty of Medicine, University of Helsinki, Helsinki, Finland.
Helsinki Collegium for Advanced Studies, University of Helsinki, Helsinki, Finland.
Int J Obes (Lond). 2018 Apr;42(4):866-871. doi: 10.1038/ijo.2017.174. Epub 2017 Jul 31.
The life-course development of body mass index (BMI) may be driven by interactions between genes and obesity-inducing social environments. We examined whether lower parental or own education accentuates the genetic risk for higher BMI over the life course, and whether diet and physical activity account for the educational differences in genetic associations with BMI.
SUBJECTS/METHODS: The study comprised 2441 participants (1319 women, 3-18 years at baseline) from the prospective, population-based Cardiovascular Risk in Young Finns Study. BMI (kg/m) trajectories were calculated from 18 to 49 years, using data from six time points spanning 31 years. A polygenic risk score for BMI was calculated as a weighted sum of risk alleles in 97 single-nucleotide polymorphisms. Education was assessed via self-reports, measured prospectively from participants in adulthood and from parents when participants were children. Diet and physical activity were self-reported in adulthood.
Mean BMI increased from 22.6 to 26.6 kg/m during the follow-up. In growth curve analyses, the genetic risk score was associated with faster BMI increase over time (b=0.02, (95% CI, 0.01-0.02, P<0.001)). The association between the genetic risk score and BMI was more pronounced among those with lower educational level in adulthood (b=-0.12 (95% CI, -0.23-0.01); P=0.036)). No interaction effect was observed between the genetic risk score and parental education (b=0.05 (95% CI, -0.09-0.18; P=0.51)). Diet and physical activity explained little of the interaction effect between the genetic risk score and adulthood education.
In this prospective study, the association of a risk score of 97 genetic variants with BMI was stronger among those with low compared with high education. This suggests lower education in adulthood accentuates the risk of higher BMI in people at genetic risk.
人体体重指数（BMI）的一生发展轨迹可能是由基因与肥胖诱发的社会环境之间的相互作用所驱动的。我们研究了父母或自身教育程度较低是否会加剧一生中遗传因素对 BMI 升高的风险，以及饮食和体育活动是否会导致遗传关联与 BMI 之间的教育差异。
受试者/方法：该研究纳入了前瞻性、基于人群的芬兰心血管风险青年研究中的 2441 名参与者（女性 1319 名，基线时年龄 3-18 岁）。使用跨越 31 年的 6 个时间点的数据，从 18 岁到 49 岁计算 BMI（kg/m）轨迹。BMI 的多基因风险评分是通过 97 个单核苷酸多态性中的风险等位基因的加权和计算得出的。教育程度通过参与者成年后的自我报告和参与者儿童时期的父母报告来评估。饮食和体育活动在成年后通过自我报告进行评估。
在随访期间，平均 BMI 从 22.6 增加到 26.6 kg/m。在生长曲线分析中，遗传风险评分与随时间的 BMI 增加呈正相关（b=0.02，（95%CI，0.01-0.02，P<0.001））。在教育程度较低的成年人中，遗传风险评分与 BMI 的关联更为明显（b=-0.12（95%CI，-0.23-0.01）；P=0.036））。未观察到遗传风险评分与父母教育之间存在交互作用（b=0.05（95%CI，-0.09-0.18；P=0.51））。饮食和体育活动仅能部分解释遗传风险评分与成年教育之间的交互作用效应。
在这项前瞻性研究中，与 97 个遗传变异风险评分与 BMI 的关联在教育程度较低的人群中比在教育程度较高的人群中更强。这表明，成年时的低教育程度会加剧遗传风险人群 BMI 升高的风险。
