3 ms·

Not a biologist, but I'm following related research and at this point am fairly convinced that aging is an intentional, pre-programmed process, as opposed to th

Not a biologist, but I'm following related research and at this point am fairly convinced that aging is an intentional, pre-programmed process, as opposed to the popular understanding that it's the consequence of wear and tear. Let's just think logically about it for a bit. Your cells come with all kinds of repair machinery and redundant DNA encoding. All cells do. But there are single-celled creatures that don't age and reproduce by cell division, and they haven't lost their function despite billions of years and millions of generations. Same for humans and whoever else reproduces sexually — there's A LOT that needs to go just right for a new human to be born, including making billions of copies of parents' DNA, yet it does work just fine most of the time. This tells us that the DNA copying process must be very robust, and that with age, it's these mechanisms that keep everything in check that deliberately get weaker or stop working altogether. Recent research proves it. For example, there's evidence that organisms propagate their age throughout all tissues using some kind of signaling in the bloodstream: https://www.nature.com/articles/ncomms13363 https://www.nature.com/articles/ncomms13363 Even more bizarre, the aging clock, as determined by DNA methylation, gets reset to zero at the beginning of embryonal development: https://hplus.club/blog/how-and-when-mother-nature-resets-the-aging-clock-and-why-the-wear-and-tear-theory-of-aging-is-worn-out/ https://hplus.club/blog/how-and-when-mother-nature-resets-th...

ak217 5y ago
You're not wrong, but your models of aging events seem to be too simplistic. Aging is not one process but a complex of interacting processes. There are definitely a number of processes involved in aging that are pre-programmed as you suggest, namely the hormonal clocks involved in puberty and maturation, and then later senescence. It's not particularly useful to compare humans/mammals to single-celled organisms, which operate under way fewer constraints. They don't have to deal with cancer, as just one very basic example. They also don't have to figure out how to clear old junk from their tissues and individual cells. They just start over with a clean slate every time. Signals in the bloodstream - various hormones and immune cells - are obviously involved in aging. But there are many of them, and we are just starting to understand their different interactions. There is no doubt that aging research is going to yield ways to suppress or promote the action of certain hormones, replenish/reactivate certain stem cell populations, etc. but better understanding of intercellular regulatory networks is needed for that. To call DNA methylation the determinant of an "aging clock" is also too narrow or simplistic. DNA methylation is the mechanism of cell differentiation, but it's "metadata" that has to be copied over between cells when they divide, just like the DNA itself. Early in embryogenesis, the DNA methylation pattern is reset and overwritten using the regulatory cascade of master control genes (homeobox, etc.) - so it is expected that the methylation pattern will have lower fidelity with each division cycle before or after that point. This is the golden age of biology - we have just gotten a hold of the tools that will let us solve these problems - but it's messy and complicated. Investing in your understanding of these processes can have a huge payoff - I recommend reading some of the Nature Reviews articles like https://www.nature.com/nrg/ https://www.nature.com/nrg/ - I've always found them to be incredibly helpful in summarizing the state of the art.

ak217 5y ago

You're not wrong, but your models of aging events seem to be too simplistic. Aging is not one process but a complex of interacting processes. There are definitely a number of processes involved in aging that are pre-programmed as you suggest, namely the hormonal clocks involved in puberty and maturation, and then later senescence. It's not particularly useful to compare humans/mammals to single-celled organisms, which operate under way fewer constraints. They don't have to deal with cancer, as just one very basic example. They also don't have to figure out how to clear old junk from their tissues and individual cells. They just start over with a clean slate every time. Signals in the bloodstream - various hormones and immune cells - are obviously involved in aging. But there are many of them, and we are just starting to understand their different interactions. There is no doubt that aging research is going to yield ways to suppress or promote the action of certain hormones, replenish/reactivate certain stem cell populations, etc. but better understanding of intercellular regulatory networks is needed for that. To call DNA methylation the determinant of an "aging clock" is also too narrow or simplistic. DNA methylation is the mechanism of cell differentiation, but it's "metadata" that has to be copied over between cells when they divide, just like the DNA itself. Early in embryogenesis, the DNA methylation pattern is reset and overwritten using the regulatory cascade of master control genes (homeobox, etc.) - so it is expected that the methylation pattern will have lower fidelity with each division cycle before or after that point. This is the golden age of biology - we have just gotten a hold of the tools that will let us solve these problems - but it's messy and complicated. Investing in your understanding of these processes can have a huge payoff - I recommend reading some of the Nature Reviews articles like https://www.nature.com/nrg/ https://www.nature.com/nrg/ - I've always found them to be incredibly helpful in summarizing the state of the art.