Following on the ideas of aging as an adaption that favors evolution, here are some responses to prior comments.
There is no reason for an aging program to exist, because humans did not live long enough for the processes we call aging to come into play until very recently in the evolutionary time scale, so there was no selective pressure to create it. In addition, all the molecular and cellular evidence supports this line of thinking.
Birds, bats, and tortoises are interesting because they all have extremely robust anti-oxidant defense systems which is probably tied to their developmental timescale.
It is not that anything is stopping the increase of lifespans it is just that there is often a great advantage to rapidly get to breeding age, which is tied to shorter lifespans.
The key idea about pressure for increased lifespan is that the pressure isn't on aging itself, but it is on the reproductive period of a species. There definitely is selection for longer time of fertility in species with low environmental stress, but long life after the reproductive period is most likely just a nice side effect (i.e. increased defense mechanisms which continue to function even past their evolutionary usefulness). Evolution just doesn't care about us once we have left successful offspring, and there doesn't seem to be any strong reason to get rid of us either. The pressure against longer lifespans (and for fast breeding times) in humans really is just about nonexistent.
Hmmm... Yet some organisms reproduce at a particular age but do not age until way after, while others age quite rapidly after rerproducing. There are also the negligible senescense species. The existence of species were time of reproduction is decoupled from lifespan, is one that conflicts with this.
Finally, although it's true that reproduction and life span are deeply correlated, there are numerous exceptions (Finch, 1990, 547-550; Le Bourg, 2001).
There are also species were the member of one sex ages and the other seems not to age. How could this be if they've both practically the same genome? Why is one exponentially longer lived, seemingly negligible senescent while the other is not?
How can closely related species, same genus, be one short lived, the other negligible senescent, how can even members of the same species be negligible senescent and some not? How can age of sexual maturity and lifespan be decoupled in some species?
How can the c-elegans enter a dauer like state, while retaining it's reproductive capability, and extreme lifespan extension? How can it be that some females restart menstruation after a short period of CR(which is later discontinued) post menopause?
Over the past few months, Kenyon's team and several other groups of worm researchers have documented an unexpectedly large number of genes controlled by this hormonal system, including genes involved in stress responses and antimicrobial actions.- august, 2003
aging genesLong before Kenyon's work, other researchers linked daf-2 and daf-16 to this arrested form of development. The genes' names derive from "dauer formation." Completely knocking out the activity of daf-2 sends a developing worm right into the dauer state, whether or not nutrients are scarce. Kenyon found something more intriguing: Certain subtle mutations in the gene enabled a developing worm to bypass the dauer state but still have an abnormally long life span.
How can this be?(note an abnormal increase in lifespan by altering regulation/expression of existing mechanisms not by addition of massive novel protective mechanisms)
On the issue of the tortoise, the reason why didn't develop mechanisms for longevity like some more primitive species is because these species never stop growing.
There are species that stop growing yet show negligible senescense, IIRC.
The body knows, as you said, when it is in puberty. It knows when to go through menopause (though that may be simply triggered by the end of Eggs.) It knows when to harden your bones (from the softer, more numerous Baby bones), it knows when to make u grow. It knows when to make u stop growing. It knows when to get hairy.
Women continue to produce eggs throughout their lives, it obviously knows when to stop doing so. Other females after experiencing CR post menopause, and returning to a regular diet start menstruating again. How can this be?
Although I think it is likely that senescence has genetic controls, I think that the death of an individual is a combination of damage and program in a kind of one two punch. It may be that with all the genetic controls that increase senescence turned off that we would still accumulate damage that would eventually cause systems to fail and death. I think it is possible for the two theories to coexist and in fact be linked.
I think the program, if there is one, works by throwing wrenches into the gears, altering genetic expression slowly into a diseased state esque one. If this were taken care of negligible senescense might arise, thus exponential lifespan differences in close species and in members of the same species would be possible, as observed. That is repair/maintainance/etc might actually be downregulated or altered in some controlled way, this would cause deterioration and increased rates of diseases, cancer, etc.
We did see changes that look like the changes that you see in the development of age-related diseases. This has been found by other workers conducting micro-array gene expression studies in other tissues as well. I think our results are very consistent with theirs in showing that gene expression profiles in tissues begin to resemble profiles of tissues that have age related disease processes going on in them. Our tissues looked healthy-we could slice them and look at them under the microscope and see no signs of liver fibrosis for instance. But when we looked at gene expression in these tissues with age, we found changes that more and more resemble those that you see in diseased tissues. So, I think that's part of the development of age-related diseases-a drift towards gene expression that resembles the gene expression of diseased tissues. Calorie restriction reverses much of that, short and long-term.
Also, older organisms with high genetic fitness would still be more desirable for a population than less fit younger ones.
Less fit, non-aging organisms could outcompete fitter but very young organism, causing a detrimental effect to the species, and thus compromising long term survival, fitter ageless ones would monopolize resources, reducing variety by starving young ones who're less fit. Aging begins its effect from early on(some organisms appear to show first signs of it very near, even slightly prior to sexual maturity, this negative effect should be selected out unless it proved beneficial) thus its effect is non-negligible in survival from a young age, it's a negative influence from EARLY ON. Prometheus post, shows examples of how causing negligible senescence might slow evolution itself, compromising species survival.
All the data seems to be pointing to the fact that telomeres are protective, but the enzymes that regenerate them are turned off in an effort by complex organisms to stave off cancer, not as an aging mechanism
Yet negligible senescence species have them always turned on, and they seem to have a low incidence of cancer...
Even telomerase expression, the hallmark of immortal cells, has been found at extraordinary high levels in all the cells of
negligibly aging animals )(Klapper, et al, 1998a, 1998b).
How is that explained?
Edited by apocalypse, 16 August 2004 - 06:13 PM.
