or are they programmed to get old and in fact there is nothing wrong with chemical processes that occur in organisms that would prohibit them from living forever?
Not sure but this is my simplied understanding. It has something to do with the DNA and chromosomes not being able to replicate properly after having been replicated countless times over many years. Much like making copies of copies of copies; at some point you get to far off the original and errors occur. This is why stem cell research holds so much promise because it brings in fresh unreplicated cells into the mix.
I don’t think that there’s any truely insurmountable biochemical barrier to living forever – any truly irreversible DNA decay would happen in the gametes, too, leading to the extinction of the entire line. After all, stem cells aren’t new cells created ex nihilo; they divided from prior cells just like all others in your body.
But immortality, (in the never dying of old age sense,) isn’t that great a strategy for passing on your genes. At a certain lifespan you’re probably going to be eaten or killed by disease anyway, so there’s no real point in evolving a body that would stay alive on its own past that point. Better to re-purpose those resources towards making your body stronger and hornier while it’s young.
The telomeres on the ends of their chromosomes are lost over time.
Immortality is actually counterproductive on a species level. A species of immortals that just keep living and reproducing will eventually grow too numerous for the environment to support it. The basic idea is that if you live long enough, you’ll eventually run out of things to eat.
While it is true that there are organisms that seem immortal like the amoeba that reproduces by binary fission, most organisms do indeed age. Cell damage accumulates, including damage to DNA. That damage could be repaired, but as has been said before, there is a disadvantage to immortality, at least to the species if not the individual.
You may recall that there are strains of cancer cells that have been through thousands if not millions of cell generations; the mother cell having lost the normal process of aging and dying. These cell cultures have been maintained in lab cultures and are used to study both cancer and cell aging.
As a bit of a side comment to the main thread (immortality is possible, but in the biological world most often undesired.
In fact, during embryological development, cells are programmed to die - the brain is a good example of cycles of cell growth and die off; this is in fact required to develop what in humans is called a mature brain, and the process doesn’t end until we are in early adulthood, having started during early embryonic neural development.
This. As far as I’ve been able to gather, once the caps at the end of your chromosomes have been shorten to a certain number of repeats (these repeats define the telomere), a cell enters senescence. It’s called the Hayflick limit.
I believe almost all cancer cell manufacture their own telomerase to replenish these caps and at one time I think was the focus of anti-cancer therapies but I haven’t read anything about that in a long time so I’m guessing that was a dead end.
edit - BTW, every person is born with their telomeres being a different length and the length of one’s telomeres are now being shown to have health consequences beyond aging.
While this is true, there is no clear mechanism by which teleomeres themselves regulate cell reproduction or why they shorten. Telomeres shortening after replication may well be an effect of aging rather than a cause.
There are a large number of hypotheses on the mechanisms that cause aging and necrosis, but few even rise to the level of being potentially falsified. (The entire “Organisms must die so that the species can perpetuate itself,” falls under this category, and is nothing more than an ad hoc attempt at rationalizing, usually invoking some combination of gene mixing and competition for scarce resources. There are, in fact, highly successful species with very long lived organisms with no indication of being compromised by their longevity.)
One of the more interesting areas of hypothesis likes in intracellular competition, and particularly with mitochondria, organelles which, among other functions, provide energy to the cell and are passed directly down one line (the female for animals) without meiosis. They are also known or hypothesized to be involved with a number of different chronic syndromes involving cellular aging and replication dysfunction. However, the really interesting thing about mitochondria is that, according to the now well-accepted endosymbiosis theory, they were once separate bacterial organisms which joined with single celled bacteria to form eukayrotic cells, the essential building block for all complex life forms, including virtually all that reproduce sexually. The theory for this is that mitochondria, specializing in certain energy-rich functions, allowed other types of bacteria to enclose themselves for better protection, and ultimately to form symbiotic relationships with yet other types of bacteria without having to compete for raw resources, thereby giving rise to multicellular life. (In the interests of brevity I have skipped a large amount of mostly speculative interventing steps, but this is the gist of the theory.)
However, being totally isolated other than via transfer during reproduction and some limited amount of horizontal gene transfer, mitochondrial organelles have no direct way to compete or propogate DNA. But by controlling the phenotypical and epigenetic behavior of the host organism including development, maturity, and necrosis on the cellular and organism level, they can influence propagation of their own genese and ensure that their genes are spread as widely as possible, providing maximal assurence of success. Unlike the host organism–which is motivated not only to spread its genes but also achieve maximal longevity during peak sexual fertility (and perhaps after, depending on post-fertility selection theories) the mitochondrion only “cares” (purely in the game theory sense of maximal distribution–it of course has no actual volition of itself) about creating as many different organisms as possible and ensuring that each lives long enough to reproduce successfully and then stops consuming valuable resources.
So, from the mitochondrial point of view, aging and death of the organism after a period of fertiility is highly desireable in perpetuating its own form, and it happens to be in exactly the functional role to control aging, especially in the epigenetic (controlling gene experession) influences. You’ve heard the (now) old joke that “A human is a computer’s way of making another computer”? Well, it may be that, quite aside from being slaves to our own genes, we are actually just a medium for mitochondria to perpetuating mitochondria.
Stranger
The hayflick limit on cell replication and senescence is virtually dogma in the world molecular biology.
edit: also where did you get this from
epigenetic changes are far more complex than the behavior of mitochondria as is the process of necrosis.
Yes, as I said, shortening of telomeres is correlated with limits to cell reproduction, and ultimately, the lifespan of the organism. However, the reason that telomeres get shorter with replication and why this limit exsits on cell division is not well understood.
I don’t understand the question or statement you are attempting to make here. One of the functions of mitochondria which is currently only poorly understood is regulation of gene expression and in particular its role in DNA methylation.
Stranger
The limit exist because as teleomeres get shorter, you encroach on the encoding regions of the chromosome - this is pretty elementary stuff. It’s why cancer cells turn on the gene for telomerase.
Mitochondria do not regulate gene expression in any material way of which I am aware but I would love for you to enlighten me on this topic.
The same is true for methylation, phosphorylation as well as the myriad other types of epigenetic markers. But again, if you can educate us in this area, it would be welcomed.
Isn’t the answer to this question Nobel-prize winning material? I don’t think people are just going to post the answer here.
The answer to aging? Sure. Even a full understanding of epigenetics - sure. But we’re hardly at that level with these topics. Understanding that changes to the the DNA require mechanisms that infiltrate the nucleus and that mitochondria exist in the cytoplasm is really, as I said before, pretty basic stuff.
But whether aging is deliberate and programmed, or just accumulated errors that genetics didn’t see a need to correct is still under debate, and that seems, to me, to be what the OP is asking.
Some recent work points towards some trade-off between tumor suppression and aging: some of the molecular mechanisms that have to be inactivated in order for a cell to escape control and develop into a cancer cell have been found to influence the speed of aging. p53, a gene regulatory protein, seems to be a key player in this process, and inactivation of this protein in cancer cells may be one of the reasons why cancer cells, in contrast to normal cells, are not restricted by the Hayflick limit.
Mitochondria play a role in this process because they are involved in the regulation of programmed cell death (apoptosis) - intrinsic triggering of apoptosis, e.g. in response to DNA damage or metabolic stress, involves the release of proteins normally sequestered between the mitochondrial membranes into the cytoplasm, where they trigger the activation of the apoptotic cascade.
If you google for “aging”, “cancer” and “p53”, you’ll find many articles on the unravelling of this complex regulatory network.
It seems that aging is the price complex multicellular organisms have to pay for keeping cellular propagation under tight control.
Telomeres are often thrown out in these discussions in a way that make them seem like The Answer. They’re not. They are one factor - possibly even an important factor - in aging, but there’s a whole hell of a lot more going on than just that.
One massively important factor that doesn’t seem to have been mentioned is oxidative damage. Reactive oxygen species (ROS) are molecules that arise as a normal byproduct of metabolism. As the name implies, they contain oxygen (hence oxidative damage) and are very reactive. They can do lots and lots of damage in the cell. We do have proteins whose job it is to protect us from them, but for reasons that aren’t fully understood, we all accumulate oxidative damage as we age. This has been shown to contribute to all sorts of aging phenotypes.
That’s certainly true but the limit imposed by telomere length is a hard one. That was the point I wanted to make personally.
In addition to oxidative damage, don’t forget to add transcription errors, especially for mitochondria which do not have the same error checking machinery as nuclear DNA.
But telomere length is not a hard limit at all. There is a process to regrow telemeres that is used in germ lines. If there was a really great benefit to having immortal non-germ cell lines, it could be used there as well (and as is noted, this happens in cancer cell lines). Non-germ cell lines obey the Hayflick limit because it is convenient as part of the process of forming a functional body, not because they intrinsically have to.
Again, these transcription errors are not a problem for germ-line cells, so why would they be an insurmountable problem for non-germ-line cells?
I like to think of humans as basically single-celled organisms with immortal cell lines that periodically spawn off a colony of division-limited cells to form structures to carry the immoral cells around. 
I’m confident that the answer is “both”, as shown by the answers above.
Another way to look at it is, while there may be possible mechanisms to heal better from damage and live (even) longer, there’s no strong evolutionary pressure to do so. We’re a quite long-lived species as it is, uness compared with certain trees or turtles. What would favor devoting more energy and complexity to avoiding the damage of aging?
A couple fascinating books that have some insights in this area:
Cancer, the Evolutionary Legacy - Mel Greaves
Power, Sex, Suicide - Mitochondria and the Meaning of Life - David Lane
But of course, you’re totally wrong. Instead, we’re colonies of genes, each gene having the goal of making the most copies of itself among all the gene colonies. But yes, there is that pesky phenotypic form. 