You've proposed that the accumulation of non-cancerous mutations to genes don't contribute to aging in a normal lifespan, because there are tens of trillions of cells in the human body, and a significant fraction of them would have to be damaged to cause trouble. But it only takes a few mutations in a single cell to kill someone through cancer. So we don't have to worry about non-cancerous mutations killing us until a very long time after the average age at which we get cancer (70s or 80s in humans).
As no current technology is capable of repairing DNA damage, this theory is a lynchpin of SENS (and any probably any rejuvenation strategy).
Why is it do you think that this theory is not generally accepted by the scientific community, and what sort of experimental evidence would be needed to help change their minds?
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You've proposed that the accumulation of non-cancerous mutations to genes don't contribute to aging in a normal lifespan, because there are tens of trillions of cells in the human body, and a significant fraction of them would have to be damaged to cause trouble. But it only takes a few mutations in a single cell to kill someone through cancer. So we don't have to worry about non-cancerous mutations killing us until a very long time after the average age at which we get cancer (70s or 80s in humans).
As no current technology is capable of repairing DNA damage, this theory is a lynchpin of SENS (and any probably any rejuvenation strategy).
Why is it do you think that this theory is not generally accepted by the scientific community, and what sort of experimental evidence would be needed to help change their minds?