I'm not even sure how to parse this. > Therefore, the aim of this study was to investigate the association between self-reported walking pace and LTL in middle

I'm not even sure how to parse this. > Therefore, the aim of this study was to investigate the association between self-reported walking pace and LTL in middle-aged adults. This included harnessing previously defined genetic instruments for both walking pace and LTL to undertake bi-directional Mendelian randomisation (MR) analyses to help clarify the causal nature and relative importance of any observed associations. So what is "bi-directional Mendelian randomisation" [1] https://academic.oup.com/ije/article/48/3/907/5531241 https://academic.oup.com/ije/article/48/3/907/5531241 > Where the causal relationship between two related phenotypes is unknown, bidirectional Mendelian randomization can be used to orient the causal direction(s) of effect using two independent sets of genetic variants related to each of the phenotypes. So the headline tells me walking will make me live longer because the telomeres aren't shortening as fast. But the MR tells me that there are genetic variants causing the walking pace trait, and the walking pace trait causes the telomere trait because it is also associated with the walking genetic variant. So am I to understand that the walking itself without the genetic variant for walking would not cause the teleomere change?