PDF(Pubmed)
Abstract：
UNASSIGNED: Observational studies have suggested a potential relationship between birthweight and telomere length. However, the causal link between these two parameters remains undefined. In this study, we use Mendelian Randomization (MR). This method employs genetic variants as instrumental variables, to explore the existence of causal associations and elucidate the causal relationship between birth weight and telomere length.
UNASSIGNED: We used 35 single nucleotide polymorphisms (SNPs) as instrumental variables for birth weight. These SNPs were identified from a meta-analysis involving 153,781 individuals. Furthermore, we obtained summary statistics for telomere length from a study conducted on 472,174 United Kingdom Biobank participants. To evaluate the causal estimates, we applied the random effect inverse variance weighted method (IVW) and several other MR methods, such as MR-Egger, weighted median, and MR-PRESSO, to verify the reliability of our findings.
UNASSIGNED: Our analysis supports a significant causal relationship between genetically predicted birth weight and telomer3e length. The inverse variance weighted analysis results for birth weight (Beta = 0.048; 95%CI = 0.023 to 0.073; p < 0.001) corroborate this association.
UNASSIGNED: Our study provides robust evidence supporting a causal link between higher birth weight and longer telomere length.
UNASSIGNED: We used 35 single nucleotide polymorphisms (SNPs) as instrumental variables for birth weight. These SNPs were identified from a meta-analysis involving 153,781 individuals. Furthermore, we obtained summary statistics for telomere length from a study conducted on 472,174 United Kingdom Biobank participants. To evaluate the causal estimates, we applied the random effect inverse variance weighted method (IVW) and several other MR methods, such as MR-Egger, weighted median, and MR-PRESSO, to verify the reliability of our findings.
UNASSIGNED: Our analysis supports a significant causal relationship between genetically predicted birth weight and telomer3e length. The inverse variance weighted analysis results for birth weight (Beta = 0.048; 95%CI = 0.023 to 0.073; p < 0.001) corroborate this association.
UNASSIGNED: Our study provides robust evidence supporting a causal link between higher birth weight and longer telomere length.
摘要：
■观察性研究表明出生体重和端粒长度之间存在潜在的关系。然而,这两个参数之间的因果联系仍然未定义。在这项研究中,我们使用孟德尔随机化（MR）。这种方法采用遗传变异作为工具变量，探讨因果关系的存在，阐明出生体重与端粒长度之间的因果关系。
■我们使用35个单核苷酸多态性（SNP）作为出生体重的辅助变量。这些SNP是从涉及153,781名个体的荟萃分析中鉴定的。此外，我们从一项针对472,174名英国Biobank参与者的研究中获得了端粒长度的汇总统计数据.为了评估因果估计，我们应用了随机效应逆方差加权法(IVW)和其他几种MR方法，比如MR-Egger，加权中位数，和MR-PRESSO,以验证我们研究结果的可靠性。
■我们的分析支持遗传预测的出生体重与端粒3e长度之间的显着因果关系。出生体重的逆方差加权分析结果（Beta=0.048;95CI=0.023至0.073;p<0.001）证实了这种关联。
■我们的研究提供了有力的证据，支持较高的出生体重和较长的端粒长度之间的因果关系。
■我们使用35个单核苷酸多态性（SNP）作为出生体重的辅助变量。这些SNP是从涉及153,781名个体的荟萃分析中鉴定的。此外，我们从一项针对472,174名英国Biobank参与者的研究中获得了端粒长度的汇总统计数据.为了评估因果估计，我们应用了随机效应逆方差加权法(IVW)和其他几种MR方法，比如MR-Egger，加权中位数，和MR-PRESSO,以验证我们研究结果的可靠性。
■我们的分析支持遗传预测的出生体重与端粒3e长度之间的显着因果关系。出生体重的逆方差加权分析结果（Beta=0.048;95CI=0.023至0.073;p<0.001）证实了这种关联。
■我们的研究提供了有力的证据，支持较高的出生体重和较长的端粒长度之间的因果关系。
