IntroductionThe relationship between inflammatory and anti-inflammato�ry markers and telomere length (TL), a biological index of aging, is still poor�ly understood. By applying a 2-sample Mendelian randomization (MR), we
investigated the causal associations between adiponectin, bilirubin, C-reac�tive protein (CRP), leptin, and serum uric acid (SUA) with TL.Material and methodsMR was implemented by using summary-level data
from the largest ever genome-wide association studies (GWAS) conducted
on our interested exposure and TL. Inverse variance weighted method (IVW),
weighted median (WM)-based method, MR-Egger, MR-Robust Adjusted Pro�file Score (RAPS), and MR-Pleiotropy RESidual Sum and Outlier (PRESSO) were
applied. Sensitivity analysis was conducted using the leave-one-out method.ResultsWith regard to adiponectin, CRP, leptin, and SUA levels, we found no
effect on TL for all 4 types of tests (all p > 0.108). Results of the MR-Egger
(p = 0.892) and IVW (p = 0.124) showed that bilirubin had no effect on
telomere maintenance, whereas the results of the WM (p = 0.030) and RAPS
(p = 0.022) were negative, with higher bilirubin concentrations linked to
shorter TL. There was a low likelihood of heterogeneity for all the estima�tions, except for bilirubin (IVW p = 0.026, MR Egger p = 0.018). MR-PRESSO
highlighted no outlier. For all the estimations, we observed negligible inter�cepts that were indicative of low likelihood of the pleiotropy (all p > 0.161).
The results of leave-one-out method demonstrated that the links are not
driven because of single nucleotide polymorphisms (SNPs).ConclusionsOur results highlight that neither the anti-inflammatory nor
pro-inflammatory markers tested have any significant causal effect on TL.
The casual role of bilirubin on TL still needs to be investigated.