If I follow the logic correctly, the root cause of aging is that stem cells can irreversibly and invisibly accumulate active transposones, which are then passed on to derived cells, which then become senescent much faster. Also, for some reason this process is supressed in gonads. So, I see these alternatives:
Transposone activation is essentially blocked in gonades, or
There is a barrier which prevents embryos with above-normal number of active transposones from developing, or
Children born from parents of old age will age faster, or
Active transposone accumulation is not a root cause of aging.
On the ‘old parent’ hypothesis : let me point out that if there is not a full ‘reset’ somewhere in the chain, well, we wouldn’t exist, because some of our ancestors were old parents, and the effect would be cumulative, such that none of us would live past childhood due to aging. (there is a disease like that, albeit with a different root cause)
If the suppression of transposons in the gonads is good enough, the reset could be the same as with any other harmful mutation—shuffling by sexual reproduction and natural selection.
Which may suggest a reason why sexual reproduction exists in the first place.
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).
Transposon activity is indeed believed to be repressed in the gonads to a much greater extent than elsewhere. I’ve also seen a few papers talking about health problems in the children of old parents, though I don’t know as much about that.
If I follow the logic correctly, the root cause of aging is that stem cells can irreversibly and invisibly accumulate active transposones, which are then passed on to derived cells, which then become senescent much faster. Also, for some reason this process is supressed in gonads. So, I see these alternatives:
Transposone activation is essentially blocked in gonades, or
There is a barrier which prevents embryos with above-normal number of active transposones from developing, or
Children born from parents of old age will age faster, or
Active transposone accumulation is not a root cause of aging.
On the ‘old parent’ hypothesis : let me point out that if there is not a full ‘reset’ somewhere in the chain, well, we wouldn’t exist, because some of our ancestors were old parents, and the effect would be cumulative, such that none of us would live past childhood due to aging. (there is a disease like that, albeit with a different root cause)
If the suppression of transposons in the gonads is good enough, the reset could be the same as with any other harmful mutation—shuffling by sexual reproduction and natural selection.
Which may suggest a reason why sexual reproduction exists in the first place.
? 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).
Solid reasoning.
Transposon activity is indeed believed to be repressed in the gonads to a much greater extent than elsewhere. I’ve also seen a few papers talking about health problems in the children of old parents, though I don’t know as much about that.