I agree my model is very simplified. (Right now I don’t know whether taking a biopsy would or would not age someone, and I’m posting here to find out.)
Interesting point that bigger people don’t die that much earlier.
I think the prediction would be that someone who is twice as big as someone else, so an adult who has say 2^45 cells instead of 2^44, would have had one extra division. Naively this would translate to 80 years / 44 divisions = ~ 2 years earlier death.
(Some short men have told me that tall men actually do die early, but when I googled papers to find out just now, that seemed false? Additionally, people with a lot of fat cells seem to die more from cancer (though the main explanation I have heard for this is that fat cells cause inflammation).)
I am quite interested in how (dangers from) cell division are different in the embryonic stage as compared to at a later stage.
I am quite interested in how (dangers from) cell division are different in the embryonic stage as compared to at a later stage.
I don’t know much about this, but two things (that don’t directly answer your question):
Generally, cells accumulate damage over time.
This happens both genetically and epigenetically. Genetically, damage accumulates (I think the main cause is cosmic rays hitting DNA that’s exposed for transcription and knocking nucleic acids out? Maybe also other copying errors?), so that adult somatic cells have (I think) several hundred new mutations that they weren’t born with. Epigenetically, I imagine that various markers that should be there get lost over time for some reason (I think this is a major hypothesis about the sort of mechanism behind various forms of aging).
This means that generally, ESCs are more healthy than adult somatic cells.
One major function of the reproductive system is to remove various forms of damage.
You can look up gametogenesis (oogenesis, spermatogenesis). Both processes are complicated, in that they involve many distinct steps, various checks of integrity (I think oocytes + their follicles are especially stringently checked?), and a lot of attrition (a fetus has several million oocytes; an adult woman ovulates at most a few hundred oocytes in her lifetime, without exogenous hormones as in IVF).
So, ESCs (from an actual embryo, rather than from some longer-term culture) will be heavily selected for genetic (and epigenetic?) integrity. Mutations that would have been severely damaging to development will have been weeded out. (Though there will also be many miscarriages.)
I agree my model is very simplified. (Right now I don’t know whether taking a biopsy would or would not age someone, and I’m posting here to find out.)
Interesting point that bigger people don’t die that much earlier.
I think the prediction would be that someone who is twice as big as someone else, so an adult who has say 2^45 cells instead of 2^44, would have had one extra division. Naively this would translate to 80 years / 44 divisions = ~ 2 years earlier death.
(Some short men have told me that tall men actually do die early, but when I googled papers to find out just now, that seemed false? Additionally, people with a lot of fat cells seem to die more from cancer (though the main explanation I have heard for this is that fat cells cause inflammation).)
I am quite interested in how (dangers from) cell division are different in the embryonic stage as compared to at a later stage.
I don’t know much about this, but two things (that don’t directly answer your question):
Generally, cells accumulate damage over time.
This happens both genetically and epigenetically. Genetically, damage accumulates (I think the main cause is cosmic rays hitting DNA that’s exposed for transcription and knocking nucleic acids out? Maybe also other copying errors?), so that adult somatic cells have (I think) several hundred new mutations that they weren’t born with. Epigenetically, I imagine that various markers that should be there get lost over time for some reason (I think this is a major hypothesis about the sort of mechanism behind various forms of aging).
This means that generally, ESCs are more healthy than adult somatic cells.
One major function of the reproductive system is to remove various forms of damage.
You can look up gametogenesis (oogenesis, spermatogenesis). Both processes are complicated, in that they involve many distinct steps, various checks of integrity (I think oocytes + their follicles are especially stringently checked?), and a lot of attrition (a fetus has several million oocytes; an adult woman ovulates at most a few hundred oocytes in her lifetime, without exogenous hormones as in IVF).
So, ESCs (from an actual embryo, rather than from some longer-term culture) will be heavily selected for genetic (and epigenetic?) integrity. Mutations that would have been severely damaging to development will have been weeded out. (Though there will also be many miscarriages.)