Evolutionary considerations suggest aging is caused not by active gene programming but by evolved limitations in somatic maintenance, resulting in a build-up of damage. Ecological factors such as hazard rates and food availability influence the trade-offs between investing in growth, reproduction, and somatic survival, explaining why species evolved different life spans and why aging rate can sometimes be altered, for example, by dietary restriction.

To understand the cell and molecular basis of aging is to unravel the multiplicity of mechanisms causing damage to accumulate and the complex array of systems working to keep damage at bay.

See Also:

“Nutritional ecology and the evolution of aging”
“The metabolic roots of senescence: mechanisms and opportunities for intervention”
“Strategies for targeting senescent cells in human disease”
“Ageing and its implications”
“The Clinical Potential of Senolytic Drugs”
“The reserve-capacity hypothesis: evolutionary origins and modern implications of the trade-off between tumor-suppression and tissue-repair”
“Erosion of the Epigenetic Landscape and Loss of Cellular Identity as a Cause of Aging in Mammals”
“Germline burden of rare damaging variants negatively affects human healthspan and lifespan”
“An aged immune system drives senescence and ageing of solid organs”
“Beneficial and Detrimental Effects of Reactive Oxygen Species on Lifespan: A Comprehensive Review of Comparative and Experimental Studies”
“Current perspectives on the cellular and molecular features of epigenetic ageing”
“The quest to slow ageing through drug discovery”
“Increased somatic mutation burdens in normal human cells due to defective DNA polymerases”
“Somatic mutation rates scale with lifespan across mammals”
“Targeting cellular senescence prevents age-related bone loss in mice”