A study from the University of Minnesota Medical School links social stress to accelerated aging, finding that stress damages DNA and induces cellular senescence in the brain. Future research will explore mechanisms behind these effects and potential protective strategies.
A study published in Nature Aging by researchers from the University of Minnesota Medical School explores the connection between stress and aging, focusing on shared biological mechanisms. The research investigates how exposure to social and psychological stressors may speed up aging and impact health, using preclinical models.
The team discovered that social stress triggers neurons in the hippocampus and cortex to exhibit signs of senescence and DNA damage—hallmarks of accelerated aging. This finding provides evidence that stress in social environments can directly contribute to the aging process.
The Inspiration Behind the Study
“This research was inspired by a significant amount of work proving that life stress, social determinants, and low socioeconomic status, in particular, adversely affect health and aging in humans. However, the causal mechanisms are almost impossible to identify in humans,” said Alessandro Bartolomucci, PhD, a professor at the U of M Medical School and senior author of the study. “Our study represents the first step in the quest to identify how life stress can impact aging. The observation that social stressors increase markers of cellular senescence in the brain and other organs, which appears to be driven by DNA damage, among other factors, was a major finding.”
Future research will focus on understanding how stress influences several interconnected biological mechanisms known as hallmarks of aging, and whether targeting these mechanisms could help protect against the adverse health impact of life stress on the aging process.
Reference: “Chronic social stress induces p16-mediated senescent cell accumulation in mice” by Carey E. Lyons, Jean Pierre Pallais, Seth McGonigle, Rachel P. Mansk, Charles W. Collinge, Matthew J. Yousefzadeh, Darren J. Baker, Patricia R. Schrank, Jesse W. Williams, Laura J. Niedernhofer, Jan M. van Deursen, Maria Razzoli and Alessandro Bartolomucci, 11 November 2024, Nature Aging.
DOI: 10.1038/s43587-024-00743-8
Funding was provided primarily by the National Institute on Aging, and the MN Partnership for Biotechnology and Molecular Genomics.
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3 Comments
“As a lay investigator researching chronic diseases online, early-on years ago I found that stress of any kind can stimulate the release of xanthine oxidase which breaks down to uric acid and free radicals. All they have to do, I believe, is to follow the greatest flow of acidic blood to see how various systems, organs, glands, tissues and cells will begin to age prematurely.”
Isn’t that, like, common knowledge already? People who’ve been through a really traumatic event (like war, for instance) often look older for their age.
Social stress is systemic because it incorporates our emotions which throws off the entire endocrine system eventually disrupting the Katp channels.
Add in the environmental stress caused by social activity and you get mitochondrial depletion, disrupting ATP production that further affects the activity of Katp channels.