A new perspective on how to slow aging
By Genomic Press
| Multidimensional nature of aging: phenotypic changes across levels of biological complexity. The figure illustrates time-dependent phenotypic change across molecular, cellular, tissue, and organismal scales in multiple species. Credit: Dan Ehninger |
The analysis, published in Genomic Psychiatry,
calls on researchers to rethink how biological aging is measured and
interpreted. Dr. Dan Ehninger, who leads the Translational Biogerontology
Laboratory at the German Center for Neurodegenerative Diseases, and Dr. Maryam
Keshavarz conducted a systematic review examining widely used indicators of
aging.
Their work argues that common measures such as lifespan
extension, epigenetic clocks, frailty indices, and even the widely cited
hallmarks of aging framework may blur the line between true changes in aging
and general physiological effects that occur regardless of age.
One of the most surprising insights comes from comparing
causes of death across species. In humans, cardiovascular disease is
responsible for roughly 35 to 70 percent of deaths among older adults. Autopsy
studies prove that even centenarians who appeared healthy shortly before death
almost always died from identifiable medical conditions rather than from old
age alone.
Research on people between 97 and 106 years old further supports this pattern, with vascular diseases remaining the leading cause of death. These findings highlight that even exceptional longevity usually ends with a specific disease.









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