ARE SCREENS MAKING US AGE FASTER? THE EPIGENETIC COST OF DIGITAL SEDENTARISM

liviupoenaru
il y a 4 jours
3 min de lecture

Dec. 18, 2025

THE MENTAL FORECAST

What if leisure screen time is not merely eroding attention and mental health, but actively accelerating biological aging at the molecular level?This question is no longer speculative. Genetic epidemiology now forces a revision of how digital lifestyles are understood. Leisure screen time can no longer be treated as a neutral behavioral choice or a simple correlate of inactivity; it now appears as a causal biological exposure. Using Mendelian randomization, Zhao et al. (2025) demonstrate that genetically predicted sedentary behavior — including leisure screen time — significantly accelerates GrimAge epigenetic aging. Because Mendelian randomization reduces confounding and reverse causality, this finding positions screen-based sedentarism not merely as a social habit but as a driver of molecular aging processes embedded in human biology.

GrimAge is among the most clinically meaningful epigenetic clocks available, as it was designed to predict mortality and age-related disease rather than chronological age alone. Acceleration of GrimAge reflects cumulative dysregulation across inflammatory, metabolic, and neuroendocrine systems. A comprehensive review of stress-induced biological aging shows that chronic stress exposures alter immune function, promote systemic inflammation, and dysregulate hypothalamic–pituitary–adrenal axis signaling, leaving durable epigenetic marks that accelerate aging trajectories (Polsky et al., 2022). The causal association between sedentary behavior and GrimAge acceleration therefore suggests that prolonged screen exposure may biologically function as a persistent stressor rather than a passive absence of movement.

Crucially, Zhao et al. (2025) show that the effect of sedentary behavior on biological aging remains robust after adjustment for leisure-time physical activity. This indicates that screen time exerts an influence that cannot be fully explained by reduced movement alone. Prolonged visual engagement, sustained attentional capture, cognitive overload, and reward-driven interaction — core properties of digital environments — likely impose continuous neurophysiological demands that overlap with established stress-aging pathways. Screen-based sedentarism thus appears as a compound exposure, combining physical immobility with chronic cognitive and affective activation.

The broader epidemiological literature supports this interpretation. Large population-based studies consistently associate extended sitting time with increased all-cause mortality and cardiometabolic risk, even among individuals who meet recommended physical activity levels (Stamatakis et al., 2019). Mendelian-randomization findings now converge with these observations by providing causal genetic evidence that sedentary behavior contributes directly to biological aging. This convergence suggests that the health burden of digital sedentarism is not merely behavioral but structurally embedded in contemporary environments.

Importantly, genetic evidence also reveals a countervailing biological pathway. Mendelian-randomization analyses demonstrate that increased walking behavior causally reduces epigenetic age acceleration, indicating that embodied movement exerts a protective effect on biological aging processes (Chen et al., 2024). This bidirectional pattern reinforces causal interpretation: while sedentary screen exposure accelerates epigenetic aging, regular walking appears to decelerate it. Biological aging thus responds not only to energy expenditure but to the quality of sensorimotor and environmental interaction.

For THE MENTAL FORECAST, the implications are both clinical and civilizational. If leisure screen time causally accelerates biological aging at the epigenetic level, digital environments must be understood as structurally stressful systems rather than neutral tools of productivity or entertainment. What is culturally framed as efficiency may already be registered biologically as accelerated wear. Until experimental biomarker studies catch up, converging genetic, epidemiological, and stress-biology evidence delivers a clear signal: contemporary digital sedentarism is not only reshaping attention and beliefs — it is reshaping the pace of biological aging itself.

Liviu Poenaru

References

Zhao, X., Wu, X., He, L., Xiao, J., Xiang, R., Sha, L., Tang, M., Hao, Y., Qu, Y., Xiao, C., Qin, C., Hou, J., Deng, Q., Zhu, J., & Zheng, S. (2025). Leisure-time physical activity, sedentary behavior, and biological aging: Evidence from genetic correlation and Mendelian randomization analyses. Scandinavian Journal of Medicine & Science in Sports. https://doi.org/10.1111/sms.70014

Polsky, L. R., Rentscher, K. E., & Carroll, J. E. (2022). Stress-induced biological aging: A review and guide for research priorities. Brain, Behavior, and Immunity, 104, 97–109. https://doi.org/10.1016/j.bbi.2022.05.016

Stamatakis, E., Gale, J., Bauman, A., Ekelund, U., Hamer, M., & Ding, D. (2019). Sitting time, physical activity, and risk of mortality in adults. Journal of the American College of Cardiology, 73(16), 2062–2072. DOI: 10.1016/j.jacc.2019.02.031

Chen, G. Y., Liu, C., Xia, Y., Wang, P. X., Zhao, Z. Y., Li, A. Y., Zhou, C. Q., Xiang, C., Zhang, J. L., Zeng, Y., Gu, P., & Li, H. (2024). Effects of walking on epigenetic age acceleration: A Mendelian randomization study. Clinical Epigenetics, 16(1), 94. https://doi.org/10.1186/s13148-024-01707-w