Does the accumulation of stochastic nuclear DNA damage over time contribute to all aspects of degenerative aging, or only contribute to cancer risk? That is an interesting question, and the answers lack strong proof in one direction or another. The current consensus is that mutational damage to nuclear DNA does indeed contribute to aging, most likely through expansion of such mutations into sizable fractions of a tissue when they occur in stem and progenitor cells. Thus there is some interest in the research community in finding ways to enhance the stability of the genome: better repair, or lower levels of damaging incidents. Given an efficient enough approach that only affects DNA damage and no other aging-related mechanism, it should be possible to use that to obtain strong proof or disproof of the role of nuclear DNA damage in aspects of aging other than cancer risk.
When does the aging process begin? How long can we live? Why do we age? These questions are highly debated with no distinct, definitive answers. Does aging begin when our skin starts to wrinkle, or when our hair commences to turn grey? Or perhaps aging begins after the completion of
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