Shapiro Ilona, Youssim Iaroslav, Israel Salomon, Friedlander Yechiel, Hochner Hagit
Braun School of Public Health, Hebrew University of Jerusalem, Jerusalem, Israel Department of Psychology, The Hebrew University of Jerusalem, Jerusalem, Israel.
Am J Epidemiol. 2025 May 7;194(5):1410-1417. doi: 10.1093/aje/kwae344.
Biological age (BA), reflecting aging-related health decline beyond chronological age, varies among individuals. While previous research explored associations of maternal pregnancy-related body size with offspring health outcomes, its implications for BA in young adults remain unclear. Utilizing longitudinal data of 1148 mother-offspring pairs from the Jerusalem Perinatal Study, we analyzed associations of maternal prepregnancy BMI and gestational weight gain (GWG) with offspring using the Klemera-Doubal method (KDM)-based BA at age 32 and potential familial life-course underlying mechanisms. Maternal pregnancy-related body size, adjusted for sociodemographic/lifestyle factors was associated with offspring BA (βmaternal prepregnancy BMI = 0.183; 95% CI, 0.098-0.267; βGWG = 0.093; 95% CI, 0.021-0.165). Association of GWG with BA was largely direct (90%; 95% CI, 44%-100%), while association with maternal prepregnancy BMI was partially mediated through adolescent BMI (36%; 95% CI, 18%-75%), with both associations eliminated after adjustment for offspring adult BMI. Associations persisted after adjusting for offspring polygenic risk score for BMI (βmaternal prepregnancy BMI = 0.128; 95% CI, 0.023-0.234; βGWG = 0.102; 95% CI, 0.006-0.198), and somewhat altered after adjustment for maternal cardiometabolic conditions (βmaternal prepregnancy BMI = 0.144; 95% CI, 0.059-0.230). Impact on GWG associations was negligible. Thus, perinatal obesogenic environment contributes to offspring BA beyond sociodemographic factors and maternal cardiometabolic history, yet intergenerational transmission of obesity seems to underlie these associations. Nonetheless, the period between adolescence and young adulthood could be targeted for weight-reducing interventions, ultimately promoting healthy aging.
生物年龄（BA）反映了超越实际年龄的与衰老相关的健康衰退，个体之间存在差异。虽然先前的研究探讨了母亲孕期相关身体大小与后代健康结局的关联，但其对年轻成年人BA的影响仍不明确。利用耶路撒冷围产期研究中1148对母婴的纵向数据，我们使用基于克莱梅拉-杜巴尔方法（KDM）的32岁时的BA以及潜在的家庭生命历程潜在机制，分析了母亲孕前BMI和孕期体重增加（GWG）与后代的关联。调整社会人口统计学/生活方式因素后的母亲孕期相关身体大小与后代BA相关（母亲孕前BMI的β = 0.183；95%置信区间，0.098 - 0.267；GWG的β = 0.093；95%置信区间，0.021 - 0.165）。GWG与BA的关联在很大程度上是直接的（90%；95%置信区间，44% - 100%），而与母亲孕前BMI的关联部分通过青少年BMI介导（36%；95%置信区间，18% - 75%），在调整后代成人BMI后，这两种关联均消失。在调整后代BMI的多基因风险评分后，关联仍然存在（母亲孕前BMI的β = 0.128；95%置信区间，0.023 - 0.234；GWG的β = 0.102；95%置信区间，0.006 - 0.198），在调整母亲心脏代谢状况后，关联有所改变（母亲孕前BMI的β = 0.144；95%置信区间，0.059 - 0.230）。对GWG关联的影响可忽略不计。因此，围产期致肥胖环境对后代BA的影响超出了社会人口统计学因素和母亲心脏代谢病史，但肥胖的代际传递似乎是这些关联的基础。尽管如此，青春期到年轻成年期这段时间可作为减重干预的目标，最终促进健康衰老。
