| > ... the implication meant here is that there has not been an optimisation towards perfection on the cellular ... This is why I'm limiting what I mean by death. Specifically to organism-wide senescence, loss of energy, and the death that follows. That senescence is very much programmed into our cells and is something that can be disabled (but as I pointed out, a lot of "downstream" inventions depend on it, so disabling it using current methods has disastrous consequences in practice) We are also far short of the limits of human lifespan through damage. Old people die from "natural causes". What that is, exactly, is: Step 1. the level of energy your metabolism produces within an entire cycle goes negative (ie. a 24 hour cycle, so there can be energy shortage during the day fixed during sleep, that doesn't cause this feedback loop to start) When you're very young at this point homeostasis intervenes and refills your energy stores and go back to stage 1. However, that stops. Step 2. In order to keep functioning your body effectively disables a system (there's dozens of ways this happens, from lowering blood suger to cutting blood flow entirely), reducing it's energy use. This starts with repair functions, then goes to immune response, and goes from there. Mostly, at this point, we go back to step 1, and of course you stay alive while the energy level is dropping. But step 2 fixes less and less. Step 3. Eventually your body has to cut critical functions. Digestion is not the first critical system to get cut, but let's say it is and keep things simple. You can disable digestion. Even just food intake itself (ie. keep water intake going). This will buy you weeks of energy, maybe months. But of course, this eventually causes more energy loss than energy gain. Step 4. Your energy level drops to zero. Very disconcerting is that I very much get the impression that moving from step 2 to step 3 is at least a semi-conscious decision. People decide, to an extent, when they die. Or should I say, people can consciously choose to delay it by a few months, at a cost. And certainly, they know pretty accurately when it will happen. I guess I'll find out sometime. But this is not "damage". This is a combination of feedback loops, the way all "DNA programming" works. DNA has this death programmed in, and certainly in individuals you can achieve better outcomes by intervening externally. The time it takes for the mechanism to fire is also a parameter in our DNA, and obviously, the only way to implement this is with some sort of clock. Telomeres are thought to be part of the clock mechanism that does this, but they can't be the full answer. Now you can say this is not "causing death". If anything, this is preventing it. And except for one major detail you're kind of right. That major detail is that increasing energy output is trivial, yet the system stops doing it (permanently increasing energy output is what happens during growth and temporarily increasing energy output is what happens during early aging). Your body restricts itself from that solution to the point that average energy use systematically decreases during your life after a certain point and that is what finally leads to a natural death, what finally fires off steps 2 and 3. I don't claim that if you fix this there wouldn't be other problems, such as DNA damage, which would require their own solutions (even though we have that too. Crispr-CAS is restricted to short changes. But you can write an algorithm that, by combining literally tens of thousands of little Crispr-CAS cuts, repair essentially any DNA damage. And while that is probably not good enough a solution, you can easily demonstrate it works. Not working well enough, but working) However, finding ways to do large scale fixing of DNA damage makes little sense until we can reset or disable the death clock. > No, it is not. What should that be? Describe that mysterious word "death". Which genes are related here? There are a great many genes involved, and many more regulatory factors. That's the problem. If it was one, "fixing" it would be easy. A famous example is p54, which puts a sort of absolute limit on cell age (when it fires, it activates other proteins that destroy the DNA, it fires off the self destruct mechanism of mitochondria and it rips open the cell membrane). There are also highly regulated genes that delay death under specific circumstances, like TERT changing the time at which such mechanisms will fire during cell division, for example. |