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Author
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Topic: Programmed for death?
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Jules
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Member # 181
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posted 16. January 2003 20:52
Joy made a comment at the Nature of Protein topic that I thought was interesting:
"And as I said, neither the dynamic data-processors we call “life” nor the phenomenon of life called “evolution” could occur in the absence of programmed obsolescence... death, universal in all generations. It’s quite the efficient system."
I heard somewhere that someone had discovered a gene (or something in the cell) that actually causes the death of the organism. I was wondering if this is true. And I was wondering if it is true, if it fits best into a teleological or non-teleological perspective.
[ 16. January 2003, 21:27: Message edited by: Jules ]
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Frances
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Member # 169
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posted 17. January 2003 01:14
An interesting topic indeed and while I am hardly an expert I may be able to provide for some initial links.
Cell death and apoptosis
The other form of 'programmed death' seems to be through telomeres which over time get shorter and shorter. As I understand them in simple terms, they are a buffer that protects the coding DNA but over time they become shorter and shorter and once they are really short...
Apoptosis or programmed cell death seems to be a response by the body to deal with instances in which cells need to be replaced since they have become damaged. Apoptosis seems to be a way for the cell to commit suicide so to speak without causing an inflammation response.
Apoptosis
and A german site in English
Seems that there may be some good survival reasons for programmed cell death.
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Rex Kerr
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Member # 632
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posted 17. January 2003 07:32
Studies in the nematode worm Caenorhabditis elegans have implicated a number of pathways that are involved in aging, including the daf-2 pathway. daf-2 is homologous to the human insulin/IGF-1 receptor, and while loss of this gene is fatal, reductions in activity (recently achieved in mice in a heterozygous background) seem to cause increased lifespan. It is unclear whether modulating the insulin/IGF-1 receptor can alter lifespan in humans.
In C. elegans, the lifespan extension is apparently without cost in terms of quality of life or reproductive capacity, although it does shift the distribution of progeny later. This is potentially maladaptive in the wild where reproducing quickly to consume all available food (a local bacterial bloom) is a good competitive strategy.
Regardless, you don't need programmed obsolescence to have death. Starvation, getting eaten/diseased, freezing, burning, falling, etc., all can do the job.
As far as I know, apoptosis (programmed cell death) is a hallmark of multicellular organisms, and thus isn't directly involved in programmed obsolescence at the organismal level. It is organismal obsolescence that is relevant here.
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Jules
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Member # 181
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posted 18. January 2003 19:36
Thanks, Frances, for the apoptosis info. But I think Rex was better at getting what I was looking for: obsolesence at the organismal level. But he doesn't seem to think that programmed death is necessary:
""Regardless, you don't need programmed obsolescence to have death. Starvation, getting eaten/diseased, freezing, burning, falling, etc., all can do the job."
Which raises the question: Why is death programmed at the organismal level, if indeed it is? What would be the selective benefit? What would be the design benefit?
[ 18. January 2003, 19:37: Message edited by: Jules ]
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charlie d.
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Member # 159
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posted 18. January 2003 20:27
I think the prediction is, either aging is simply unavoidable (a consequence of basic chemical/physical properties of living organisms), and/or, as in the case of the daf-2 pathway, it is the result of mechanisms that affect other necessary organismal functions, and whose aging-causing effects cannot be modified without negatively affecting reproductive success (and therefore being counterselected).
Most likely, it's a little bit of both: aging is unavoidable, but its rate is likely determined by the interaction of multiple physiologic pathways affecting metabolism, development, reproduction, cell division, etc, that have reached an adaptive equilibrium as a result of the evolutionary history of each organism. Significant changes of these pathways are therefore likely to be non-adaptive in natural conditions (as in the daf-2 pathway), though in principle artificial manipulations could be possible in humans (after all, we wouldn't care much if we reached sexual maturity at age 30, if that would add 50 healthy years at the other end of our lives, would we?).
[EDIT: Thinking about it, that would mean we'd have sexually immature, prepubescent children around until age 30, and probably they'd be like teen-agers until what - 50 or so? Yikes! ![[Eek!]](eek.gif) )
[ 18. January 2003, 20:31: Message edited by: charlie d. ]
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Rex Kerr
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posted 19. January 2003 01:17
There are a variety of classes of age-related damage.
Some of it seems unavoidable--buildup of mutations over time.
Some of it is due to genes with beneficial effects during reproductive life that cause problems after reproductive age.
Some of it is due to genes that fail to be maintained at post-reproductive ages.
It is hypothesized by some that the daf-2 pathway is none of these, but rather is a mechanism by which reproductively inviable animals are removed from competition with their progeny. But the jury is still out; the genetics of aging is a young field, and people haven't yet figured out how to distinguish different classes (or, possibly, even figured out the relevant classes) of mutations.
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Jules
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posted 20. January 2003 11:45
So it's too soon to conclude that organisms are programmed for death. Should it turn out that they are, would this be a fairly difficult obstacle for non-teleological theories to overcome?
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Rex Kerr
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posted 21. January 2003 05:57
There is no inherent difficulty in an organism being programmed for death per se; all that is important is that fitness be maintained. So introduction of suicidal mechanisms to prevent an organism who is past its prime (or damaged) reproductively from competing with its offspring for resources is certainly a possibility.
Likewise, there is no problem with single celled organisms dying as part of a genetically related colony, or single genetically identical cells dying in an organism.
What would present a problem for a non-teleological theory is if either the death did not benefit the genes that resulted in death (i.e. favored members of the species that did not die), or if the capability arose and was maintained before the advantageousness of programmed death became apparent.
In any case, it is too soon to tell to what degree, if any, multicellular organisms are specifically programmed for death due to aging.
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nobody
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Member # 145
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posted 23. January 2003 21:48
quote:
introduction of suicidal mechanisms to prevent an organism who is past its prime (or damaged) reproductively from competing with its offspring for resources is certainly a possibility.
Are you saying early life did not have these mechanisms?
Who would introduce suicidal mechanisms into the programming of life? That kind of programming is beyond current human ability. In fact, humans are trying to figure out a way to defeat these mechanisms, without success.
I imagine someone will disagree with me and point to longer lifetimes for humans. However that has been achieved through better nutrition, better medical care, less dangerous jobs, plus cleaner water and air, and other factors. We have not extended human life by overcoming our programming.
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