The standard explanation by evolutionists is that aging results from a tradeoff. All else equal, natural selection favors early reproduction over later reproduction. Genes that favor healthy, vigorous individuals in the prime reproductive period at some cost to vigor at later ages will be favored by selection. "Life history theory " is the branch of evolutionary biology concerned with working out the details of how this and other life history tradeoffs play out in different circumstances. The Wikipedia article on life history theory is an adequate short primer on the subject.

The standard explanation by evolutionists is that aging results from a tradeoff. All else equal, natural selection favors early reproduction over later reproduction. Genes that favor healthy, vigorous individuals in the prime reproductive period at some cost to vigor at later ages will be favored by selection. "Life history theory " is the branch of evolutionary biology concerned with working out the details of how this and other life history tradeoffs play out in different circumstances. The Wikipedia article on life history theory is an adequate short primer on the subject.

Yes that senescence is adaptive follow lifehistory theory too, if it has à function in development. Before, it has just not been considered possible for it to have à function only to be à malfunction that appaers in the selektion shadow. There are diskussions on this matter in the recent numbers of Cell and Embo J, for those interested.

Helen, I disagree that it has always been viewed as a malfunction during aging. But maybe I do not see the point here? Could you link to a few papers? Antagonistic pleiotropy is a clear example of this no? Genes involved in development were key to this reasoning. However I think all can be viewed as a life-history optimization problem and single gene effects are unlikely to be large. Even the increase usually seen in performance with age (in the wild) can be explained by such an optimization approach. See:

McNamara J, Houston AI, Barta Z, Scheuerlein A, Fromhage L (2009) Deterioration, death and the evolution of reproductive restraint in late life. Proc R Soc B 276, 4061–4066.

I refer to last lines in http://dx.doi.org/10.1016/j.cell.2013.10.019

"Conceptually, we add cellular senescence to the collection of

processes that contribute to embryonic development, together

with proliferation, differentiation, migration, and cell death. This

opens up the possibility that cellular senescence originated in

evolution as a tissue-remodeling mechanism during embryonic

development, and it was subsequently adapted to orchestrate

tissue regeneration and healing upon damage in adult organisms."

It has been thought that there can be no death genes, although there are, and this new evidence from recent papers in Cell provide one explanation why they may exist.

Hi Helen. One could also easily argue the other way round.. senescence repair mechanisms etc were recruited to be used in embryonic tissue-remodelling. One can detect senescence in single celled organisms, so this should at least in part falsify this hypothesis, or not?

That is a point. To know that, data from more and diverse species are needed.

Senescence appears to be behind the mortality distributions observed in nature. The Penna mutation accumulation model cannot reproduce these distributions. See http://pre.aps.org/abstract/PRE/v88/i5/e052702.

A recent paper in Nature overviews changes in mortality and fecundity as function of organisms' age. The surprising (?) result is that not all species age (get old in the human sense of decreased fecundity and increased mortality).

Jones, O. R., Scheuerlein, A., Salguero-Gomez, R., Camarda, C. G., Schaible, R., Casper, B. B., Dahlgren, J. P., Ehrlen, J., Garcia, M. B., Menges, E. S., Quintana-Ascencio, P. F., Caswell, H., Baudisch, A. & Vaupel, J. W. 2014 .Diversity of ageing across the tree of life. Nature 505: 169-173.

I have seen that, but I would also like to see in that ageing markers. Some of these seemingly non ageing and very longlived may hold secrets with potential. That is where I go.

I think the paper actually states some of "secrets" of non-aging. Modular and indeterminate growth being among them. We, humans, cannot copy the first, and maybe hardly the second (known in some reptiles, but not in mammals)

I study clonal species for this reason, but I am after the mechanisms they use at molecular levels at the phases of rejuvenation. We cannot start budding for sure.

Adam, the only point the paper can make is that some species do not seem to age demographically. Although this is potentially very interesting, it cannot tell you that there is no physiological aging going on, especially in a comparative setting. It may just be a reflection of the flexibility of the trade-offs shaping longevity. For example in some fish predation reduces with size and therefore you see negative senescence, mortality decrease with age through growth, but this does not tell you that there is no physiological aging going on. Note that for quite a few studies included in the study, they are collected in wild populations, this is a good thing when you are interested in evolution. Less interesting when you are interested in deterring physiological aging, because this will not necessarily be fully represented in the wild environment (due to things like predation etc.).

In my view the key evolutionary insight is that senescence is not itself adaptive but is the price paid for adaptive aspects of development. The most cited and original source is Williams 1957 EVOLUTION Volume: 11: 398-411.

Right exactly, but exactly that was tested and shown by the Cell papers where senecence was shown by using markers to have a function in development (thus have a function, a trait, adaptive). That it then leads to organismal death is too bad. I think we have solved this now. Thanks for you interest!

I like both freeing resources for offspring and of course Williams 1957 Evol:11 398-411. Additionally, we have to kill off cells when we differentiate cell types, Cell papers. However, there is the good ol desert tortoise, who not only are long lived, but lives with high natural radiation background in Thorium and Uranium. Additionally, some other reptiles have very good repair enzymes. There are reptile with long lifespans as will as much shorter. In mammals we have humans and the short lived shrew! Again in plants there are annuals, bi-annuals, and long-lived trees. Hence aging and senescence can be very varied., both among reptiles, mammals and even plants. I think given the variation in life-spans with-in Class, indicates that the life span, reproductive strategy, and genetic variability will have selections by the environment.

As August Weissman originally thought (but later rejected). From a selfish gene perspective, an adaptive somatic lifespan is not controversial. But it is from selection on the level of individual only.