Are there checkpoints regulating the transition of organisms into different distinct lifespan intervals?

Also I feel that the cycle of life of an individual shares similarities with the cell cycle, i.e. it is controlled by checkpoints that must be passed to enter into the next lifespan interval.

Especially the changes observed during childhood development must be caused by changes in the overall transcriptome and proteome because they must be responsible for the phenotypic changes we observe during development.

How for example is the growth of girls stopped shortly after they got their first period?  The expression of genes, which allowed them to grow, must be suppressed.  This observation supports the hypothesis of a slowly but mercilessly ticking suicide clock that ensures that we pass through the different stages of our lives eventually leading to death.  But what if we could prevent that an individual can pass through the checkpoints needed to enter a new stage of life.  The worm would be a good model to study the effects of checkpoints between different its stages of life because their phenotypes are very distinct.  But other species may also have even though more fuzzy and phentotypically less distinct phases of its lifespan intervals but nevertheless it must pass from the previous to the next somehow.  As people age, heir muscle mass declines and eventually their degenerative exceed the regenerative processes.  But the transcription of these processes is controlled and hence could be manipulated.  If we could prevent the degeneration to exceed regeneration we could live forever.  The physiology of old people differs from that of young adult but I believe that each single individual change can only occur in concurrence of other accompanying changes.  Hence, one could assume checkpoints regulating the transition from the preceding transcriptional unique lifespan interval into the subsequent lifespan interval.  I found that certain drugs stopped working as I grew older whereas others, which had no effect when I was younger, suddenly started working when I tried them again 10 years later.  One of my major questions is whether these transcriptional and proteomically unique lifespan intervals are the driver of the aging process or only an adaptation to it or a combination of both.  For example, as we age, increasingly advanced glycosylation end products (AGE) accumulate thus compromising the flexibility of our cardiovascular system.  Maybe the observed decline in our resting metabolic rate by about 1% per year has evolved is the only way to prevent our increasingly less resilient and less flexible vessels from bursting instead of driving the aging process.

Aging could be regulated by the interplay between many different kinds of data-dimensions, all of which provide a fraction of information and dependencies, which must be manipulated in such a way that our evolved internal suicide clock, which is most likely driven by our developmental genes, can not only be stopped but also reversed, because our lives should no longer depend on a kind of evolution, which selects for mechanisms that cause our lifespan to be finite.

Long time ago, back in the RNA world, evolution could not select against an individual RNA strand without adversely affecting its replication rate. Because back then, everything, which helped the RNA strand to withstand degradation and stressors, also helped its replication. Hence, there was no distinction between the individual and the replication-relevant material, since both were exactly identical and therefore, they could not be separated. 

 But now evolution can select against individual parents without adversely affecting any relevant aspect of replication. As long as the entire individual was completely composed of exactly the same matter, which was essential for replication, e.g. an individual RNA strand, there was - by default - no aging at all - but instead - only replication. 

 Aging could only evolve in the protein world because then not all the physical matter, of which the parents consisted, was essential for replication anymore. Only this distinction allowed evolution to select for active killing programs, which are most likely driven either directly by actively programmed destruction mechanisms, e.g. apoptosis, or indirectly by neglecting to maintain, repair and restore essential functions, e.g. chaperone-aided protein-folding, peroxisome degradation, or maintaining the steepness of the needed proton-, salinity-, ion- and nutrient-gradients across membranes because our evolved in-built suicide clock killed faster than those life-essential processes declined enough for posing a threat on life.  

 The life-cycle, i.e. the time span from birth to death, seems to be very similar to the cell cycle because it appears to consist of long phases of relative stability and little change interrupted by short periods of rapid changes, which can be as drastic as metamorphosis in species, like worms or frogs, but which nevertheless can be found to a lesser extend in all species. The periodic interval pattern of changes is too similar across members of the same species to be solely the result of the much more randomly acting wear and tear process alone.  

Women, for example, lose their ability to have children between 50 and 60 years of age. This low variation makes it impossible for this loss of function being caused by wear and tear alone. The same applies to the lifespan. Its variation between members of the same species is way too small for claiming that its length is determined by wear and tear alone. Therefore, I believe that it is likely that there is actually an actively regulated and well timed transition mechanism, which works similar to cell cycle checkpoints, from old age into death. 

Such kind of questions are of interest to me and they keep crossing my mind when analyzing time series datasets because they could help to elucidate the mechanisms of aging. And we must understand them before we can effectively disrupt them.  

We need to start thinking about initiating mechanisms similar to targeted and directed, i.e. intelligently designed and goal-driven evolution, which is aimed at maintaining and restoring all life-essential processes or substituting them accordingly, if they cannot be maintained in the way they have initially evolved. We need to become fast enough that - if we see a particular approach to fail - we'll still have enough time for quickly developing much better alternatives for preventing the otherwise unavoidable -seeming aging-induced decline, which would inevitably kill us. 

Any suggestions are welcome! Please email suggestions directly to Hahn5Thomas@gmail.com because my text to speech software, which I must use because I am legally blind, has trouble reading this platform properly.