base age = (age of parents at conception) * <a small number>
human bio age = calendar age + base age
With this formula, without anything to subtract base age, it will monotonically increase and eventually extinct the species. Sexual reproduction doesn’t solve the problem because it can only recombine traits that exist, and if all humans in the mating pool have high base age, it won’t work.
Also, pre-human primates would probably increment the ‘base age’.
I am saying that probably there is another piece:
On Human Embryonic development:
base age = 0
This would also suggest how to repair aging:
trigger human embryonic development flags in cells taken from the patient, then trigger flags to differentiate the cells to the target stem cell, then reinject the stem cells where they go into the target tissue. Example, bone marrow.
Tissues that can’t be repaired this way (the brain) you would have to slowly replace with artificial prosthetics, connected by neuro links.
Your assertions about that formula don’t follow; while it is monotonic it converges to a finite value. E.g.for ‘small number’=0.1, ‘calendar age’= 30 at reproduction this converges to a base age at birth of 3.333 repeating and base age of 33.333 repeating. Inverse exponential beats linear (and polynomial) functions.
More directly on topic, germ line damage control doesn’t need to be all that good to keep aging related damage from building up. Anything under unity converges with that model and anything under about half converges to something reasonable.
It’s a stochastic process, not a clock. One person gets an extra transposon copy at location A, another gets one at location B, sexual reproduction drops both 1⁄4 of the time.
It’s possible that natural selection has historically kept the quantity of transposons down to small levels relative to the amount that one gains in non-gonad cells during aging. While this may change now that selection is relaxed, if the transposon suppression in gonads is good enough, it may take a long time. (and selection may not really be relaxed in our case, given our tendencies to late reproduction).
? So the hypothesis here from you is this:
base age = (age of parents at conception) * <a small number>
human bio age = calendar age + base age
With this formula, without anything to subtract base age, it will monotonically increase and eventually extinct the species. Sexual reproduction doesn’t solve the problem because it can only recombine traits that exist, and if all humans in the mating pool have high base age, it won’t work.
Also, pre-human primates would probably increment the ‘base age’.
I am saying that probably there is another piece:
On Human Embryonic development:
base age = 0
This would also suggest how to repair aging:
trigger human embryonic development flags in cells taken from the patient, then trigger flags to differentiate the cells to the target stem cell, then reinject the stem cells where they go into the target tissue. Example, bone marrow.
Tissues that can’t be repaired this way (the brain) you would have to slowly replace with artificial prosthetics, connected by neuro links.
Your assertions about that formula don’t follow; while it is monotonic it converges to a finite value. E.g.for ‘small number’=0.1, ‘calendar age’= 30 at reproduction this converges to a base age at birth of 3.333 repeating and base age of 33.333 repeating. Inverse exponential beats linear (and polynomial) functions.
More directly on topic, germ line damage control doesn’t need to be all that good to keep aging related damage from building up. Anything under unity converges with that model and anything under about half converges to something reasonable.
It’s a stochastic process, not a clock. One person gets an extra transposon copy at location A, another gets one at location B, sexual reproduction drops both 1⁄4 of the time.
That would work. Though why don’t we observe lots of children suffering from aging.
It’s possible that natural selection has historically kept the quantity of transposons down to small levels relative to the amount that one gains in non-gonad cells during aging. While this may change now that selection is relaxed, if the transposon suppression in gonads is good enough, it may take a long time. (and selection may not really be relaxed in our case, given our tendencies to late reproduction).