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Walk Faster, Age More Slowly – Fight Aging!


Walking speed is one of the long-standing simple biomarkers of aging, predating modern medicine. Measures of physical capacity correlate with the onset of frailty and increased risk of mortality. People become weaker and walk more slowly as they lose fitness and strength with the progression of aging. With the ongoing development of new measures of biological age, including epigenetic clocks and combinations of simple measures such as phenotypic age, researchers have some interest in comparing the new with the old.


In today’s open access paper, researcher use the technique of Mendelian randomization to try to derive some indication of causation regarding walking speed and degenerative aging. They conclude that the data is supportive of a causal relationship between a faster walking pace and slower pace of aging. This fits well with current thought on the merits of mild physical activity on long-term health and mortality. The use of accelerometers in epidemiological studies has shown that even a modest level of activity in later life correlates with significant improvements versus being sedentary.


Effects of walking on epigenetic age acceleration: a Mendelian randomization study



Walking stands as the most prevalent physical activity in the daily lives of individuals and is closely associated with physical functioning and the aging process. Nonetheless, the precise cause-and-effect connection between walking and aging remains unexplored. The epigenetic clock emerges as the most promising biological indicator of aging, capable of mirroring the biological age of the human body and facilitating an investigation into the association between walking and aging. Our primary objective is to investigate the causal impact of walking with epigenetic age acceleration (EAA).



This represents the inaugural large-scale two-sample Mendelian randomization (MR) study uncovering the causal link between walking and epigenetic aging. Our results illuminate a consistent and significant causal association, indicating that increased walking speed correlates with the deceleration of epigenetic aging. Essentially, brisk walking appears to exert a beneficial influence on slowing down the aging process. Notably, this causal relationship persists uniformly across all four classical epigenetic clocks.



In contrast, alternate facets of walking, including walking duration and frequency over the past four weeks, did not exhibit resilient causality concerning accelerated epigenetic aging. Additionally, a comparative analysis using sedentary behavior revealed that leisurely sedentary behavior induced GrimAge EAA. While no conclusive causal link was identified in the analysis of sedentary behavior on the remaining three epigenetic clocks, the heightened correlation of GrimAge with behavioral lifestyle suggests a potential association between sedentary behavior and accelerated aging.

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