Telomere extension turns back aging clock in cultured human cells, study finds
med.stanford.edu
med.stanford.edu
The Wikipedia articles on telomeres and telomerase have plenty of further resources[2][3].
[0] http://learn.genetics.utah.edu/content/chromosomes/telomeres...
[1] http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3370421/
[2] https://en.wikipedia.org/wiki/Telomere#Cancer
[3] https://en.wikipedia.org/wiki/Telomerase
edit: formatting
Some evolutionary biologists suggest that animals that share wisdom or share childbearing duties with their offspring evolved to survive past fertility because doing so increases the competitiveness of their shared genes.
It might even be testable.
I often wonder if the Upper Paleolithic Revolution (https://en.wikipedia.org/wiki/Upper_Paleolithic_Revolution) could be correlated with genetic changes related to longevity. If the genes responsible for our double-lifetimes (we live about twice as long as you'd expect a mammal of our heart rate to survive) were small in number and had mutations that could be traced back to ~50 ky BP it would be strong evidence for this idea.
Even Aristotle knew about menopause. And Plato lived to be 80.
Staying fertile till we drop dead would be sub-optimal because germline stem cells (the "factories" that produce sperm and eggs) accumulate mutations as we age. Those mutations are useful as one of many mechanisms of evolution, but they must only occur in reasonable amounts, as they also increase the probability of nonviable offspring.
In short, protecting genetic information while still allowing evolution is a hard problem. This problem is not solved in exactly the same way by different organisms, and occurs on different time-scales.
"Best of all possible worlds" suggests a global maximum to me. Evolution can get stuck in local maxima.
In some ways, it seems like this is all that life on Earth is about. A planet-size computer running for billions of years to try and come up with a good solution to this problem.
Fertility is the main thing it optimizes. To think you know the way this should work better than evolution is like betting you know adwords better than Google.
In general it would be extremely safe to assume that human fertility is the best optimized part of the human genome and that in 1000 years we'll still be discovering factors that evolution took into account "designing" human fertility. There is (or will turn out to be) a very good reason for every single tiny detail about how our bodies procreate. If you can't see the reason, the fault is likely with you, and assuming otherwise is effectively betting against an algorithm that has had 3 billion years to ponder this question. It thinks slower than you, of course, but you're still quite unlikely to have the upper hand in that bet.
> does all kinds of glitchy seemingly suboptimal things so aging is not perfect and divine because it's evolution
This is how evolution works. It's called "mutation". And you're right. Species are a big fan of it, as it massively improves them. For the large, large majority of individuals, mutation is a small or large disaster.
Every human is an experiment meant to improve the human species as a whole. This is great if you're a successful experiment, but the extremely large majority of individuals in any species will be a failed experiment that don't get to propagate their genes (meaning the genes that are different in that particular individual). The vast majority of individuals will turn out to have a (usually small) weakness that will get filtered out. Usually that will be something like a toe that's a few millimeters shorter than most, sometimes it's ALS.
The key here is that evolution very likely won't decide any particular human is a success or failure until the human species gets into trouble again. When that happens, something like 98% or more of all lineages will go extinct, and until that happens, even evolution itself won't know or care what fitness even means.
Unless you know what is going to cause the human species to lose >90% of it's population at some point, you have no point of comparison.
This is more hedged than it really needs to be. In an infinite-integral-across-time sense, fertility is the only thing evolution optimizes.
That this formula works would seem to indicate that you are right. Death is natural, but it's "planned". The easiest way for such a formula to work would be that your genes somehow contain a death clock.
But there are multiple death clocks. One limits number of cell divisions. There is another one known that limits the amount of energy that can pass through a cell, after which it will kill itself. There are various others, one that kills the cell if it isn't deactivated on a regular basis (presumably meant as a check on DNA integrity), one that is triggered from the outside of the cell, ... the list goes on.
That's my uneducated but logical sounding assumption.
Average telomere length in tissue is a measure of health in general: since telomere length decreases with each cell division it is a proxy for some combination of cell division rates and rate of influx of fresh new cells with long telomeres provided by the stem cell population maintaining a tissue. Since average telomere length is often measured in white blood cells it goes up and down with health and generally downward with age. Stem cell activity declines with age, so this shouldn't be surprising.
Lengthening telomeres via telomerase may extend life in mice for any number of reasons, some of which actually have nothing to do with telomeres. Telomerase, like all biomolecules, has a lot of roles, not all of which are fully understood. Alternative and more controllable methods of lengthening telomeres should help narrow down what is going on in those studies. Is it greater stem cell activity, something to do with telomerase influencing mitochondrial function, something completely different?
In general if you're thinking of aging as accumulated molecular damage, telomere shortening looks like a consequence not a root cause. It may cause further issues itself, but targeting it is probably not as effective as going for the actual root causes that lead to it. The interesting question is why telomerase therapy does do comparatively well in extending life in mice.
When the telomere is in bad condition, your cells divide slower or even not divide itself.
When this happens your tissues do not repair fast enough, and everything gets a worse condition, your skin, your hair, your brain, your heart.
Restoring telomeres means your cells could start dividing again. At 75 your body will go back to "young adult" 20 years old, without the hair, teeth and whatever you have lost in your life, and the scars, and broken bones soldering, or damaged ligaments that you already have got in your life.
However, lots of animals could grow hair and teeth again so they will probably find a way to make that too.
People will continue dying, but young in their 100s, or in their 20s like today, in things like accidents, wars, terrorist attacks and so on.
People won't die from old age, like most people do today.
Of course this will change the world and will have terrible social consequences.
We will need a better (bigger and cheaper) energy source(fusion) that what we have today to sustain a population that mostly never dies, population and social controls(because old-now young people will have a terrible advantage, experience while being young, and all their accumulated compound wealth) and a way to start exploring other planets and living there.
Not for long. Years from now living without a backup of yourself will be as abhorrent as currently operating a database with no backup.
Amazing how many people forget this simple fact.
You'd then have all the time in the world for them to find improvements.
I guess if you could compare many strands you could find the spots that are the same in all.
But then to somehow repair them all?