Aging Theories: is an 'aging program' a treatable common factor?

The big and continuing mystery about aging has been as described by Vit Zemanek in his recent Longecity article [1]
“When Darwin’s theory of evolution by natural selection was established, biologists were puzzled by the existence of senescence and aging among all organisms. 
Why did the evolutionary pressure not produce immortal species?”

A further question might be: why does aging ‘look’ so much like other evolved traits? Why is it that aging (and internally determined lifespan) varies between individual members of a species and varies to a much greater extent between different species?
Unfortunately Zemanek’s account ends prior to the development of modern programmed aging theories, which are emerging as a major force in developing anti-aging medicine. 
Programmed aging theories contend that organisms have developed biological mechanisms (“programs”) that purposely limit individual lifespans in order to obtain an evolutionary benefit for a population of individuals that possess the program. Organisms -including humans- possess what amounts to a biological ‘suicide mechanism’. The drastic increase with age seen in highly age-related diseases and conditions is the result of this ‘aging program’. 

Some theorists have supported the idea that a trait (like programmed aging) can evolve to benefit a population even at the expense of individual members [6]. “Benefit” in this case means increasing the probability that the population will expand, escape extinction, and produce descendant species. 
But does the evolution process operate to benefit a population, or individual members of a population? Many proponents of non-programmed theories such as Tom Kirkwood, (author of the disposable soma theory [4]), dismissed programmed aging theories and other theories based on population benefit because of the conflict with Darwin’s evolutionary mechanics. Some analyses in the 1960’s [10] were also cited as definitively defeating population benefit concepts such as group selection (first proposed in 1962), kin selection, and small-group selection. August Weismann originally considered programmed aging in 1882 [5] but eventually changed his position. A series of aging theories are based on population-oriented evolutionary mechanics concepts originated by Peter Medawar in 1952 [2]. He proposed that the lifespan needed by an organism is highly dependent on species and population-specific circumstances such as age at reproductive maturity and extent of predation. Other authors of the early population benefit theories (e.g. [11) were mainly trying to explain other observed discrepancies with Darwinian mechanics such as animal altruism and were therefore relatively unconcerned with theoretical gerontology. 
However today there are multiple aging theories based on population benefit [6,7,8,9]). Some [6] specifically propose solutions for the evolutionary mechanics issues based on modern genetics discoveries that support population benefit and thereby programmed aging.
One can compare published efforts (e.g. [12] and [13]) to contradict the new programmed theories as well as counter arguments (e.g. [15,16,17,18]). Note that many modern non-programmed aging theories also require population-oriented modifications to Darwin’s mechanics. 

Empirical observations that may favour programmed theories include:
• Explicit suicide mechanisms have been found in some organisms such as octopus [21] and roundworm [22]. 
• Human genetic diseases Hutchinson-Guilford progeria and Werner’s syndrome simultaneously accelerate many or most symptoms of aging including age-related diseases [23] suggesting a defect in a common mechanism that controls the diverse symptoms. 
• Genetic engineering has produced roundworms that live 10 times as long as wild worms [24] suggesting existence of a program. 
• Some species (e.g. Pacific rockfish) have been identified that apparently do not age [25]. This is a problem for non-programmed aging theories that have difficulties explaining why an apparently internally immortal species would exist. Programmed theories suggest these species could be the result of a fault (e.g. mutation) that disabled their program and therefore increased the probability that the population would become extinct [19].

Why is this theoretical question of such crucial relevance? 
The programmed vs. non-programmed issue is critically important to medical efforts toward dealing with aging and age-related diseases precisely because of the “unifying factor” question. 
As described by antagonistic pleiotropy theory author George Williams in 1957 [3], nonprogrammed theories strongly suggest that there is no treatable common cause of the many different age-related diseases and conditions and thus no unifying factor. Western medicine is largely based on the idea that each individual age-related disease or condition has different causes that need different treatments. Non-programmed theories strongly support this view. Programmed theories strongly suggest that there are common factors (elements of the program mechanism) behind the different age-related diseases and conditions. 
I argue that the emergence of modern programmed aging theories provides a sound theoretical basis for new approaches in developing medical treatments for highly age-related diseases and conditions as well as a basis for the idea that human lifespan can be generally increased.



References:

1 Zemanek V. Aging theories: Is there a unifying factor in aging? Longecity 
2 Medawar, P.B, An Unsolved Problem of Biology., 1952. H.K. Lewis & Co., London. 
3 Williams, G Pleiotropy, natural selection and the evolution of senescence,. 1957. Evolution 11, 398-411 
4 Kirkwood T.B.L. & F.R.S. Holliday, The evolution of ageing and longevity, 1979. Proceedings of the Royal Society of London B 205: 531-546 
5 Weismann A. Uber die Dauer des Lebens. 1882 Fischer, Jena 
6 Goldsmith T. (2017) Evolvability, Population Benefit, and the Evolution of Programmed Aging in Mammals. Biochemistry (Moscow), 2017,Vol. 82, No. 12, pp. 14231429 DOI:10.1134/S0006297917120021 
7 Skulachev V. Aging is a Specific Biological Function Rather than the Result of a Disorder in Complex Living Systems: Biochemical Evidence in Support of Weismann's Hypothesis. Biochemistry (Mosc). 1997 Nov;62(11):1191-5. PMID: 9467841 
8 Libertini G (1988) An adaptive theory of increasing mortality with increasing chronological age in populations in the wild. J. Theor. Biol. 132. 145-162. 
9 Mittledorf J. Chaotic Population Dynamics and the Evolution of Ageing. Evolutionary Ecology Research 2006, 8: 561-574 
10 Williams G. Adaptation and Natural Selection: A Critique of Some Current Evolutionary Thought, Princeton UP. ISBN 0-691-02357-3 1966 
11 Wynne-Edwards V. Animal Dispersion in Relation to Social Behaviour, Edinburgh: Oliver & Boyd, 1962 
12 Kowald A, Kirkwood T. Can aging be programmed? A critical literature review Aging Cell 2016 doi: 10.1111/acel.12510 
13 Kirkwood T, Melov S. On the programmed/non-programmed nature of ageing within the life history. Curr Biol. 2011 Sep 27;21(18):R701-7. doi: 10.1016/j.cub.2011.07.020 
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15 Goldsmith T. On the programmed/ non-programmed aging controversy Biochemistry (Moscow) 2012 Vol 77 Nr 7 729-7322012 doi: 10.1134/S00629791207005X PMID: 22817536 
16 Goldsmith T Aging is programmed! (A response to Kowald-Kirkwood “Can aging be programmed? A critical literature review”) DOI: 10.13140/RG.2.2.36205.38883 
17 Skulachev V. Aging as a particular case of phenoptosis, the programmed death of an organism (a response to Kirkwood and Melov "On the programmed/non-programmed nature of ageing within the life history"). Aging (Albany NY). 2011 Nov;3(11):1120-3 
18 Goldsmith T. Arguments against non-programmed aging theories Biochemistry (Moscow) Phenoptosis 78:9 971-978 2013 
19 Goldsmith T. The Evolution of Aging – 3 rd ed. 2014 Azinet Press Annapolis ISBN 9780978870959 
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21 Wodinsky J. 1977. Hormonal inhibition of feeding and death in octopus: control by optic 
gland secretion. Science, 198: 948–951. 
22 Apfeld J, Kenyon C. Regulation of lifespan by sensory perception in Caenorhabditis elegans. Nature 1999. 
23 Gray, Md; Shen, Jc; Kamath-Loeb, As; Blank, A; Sopher, Bl; Martin, Gm; Oshima, J; Loeb, La (Sep 1997). The Werner syndrome protein is a DNA helicase. Nature genetics 17 (1): 100–3. 
doi:10.1038/ng0997-100. PMID 9288107 
24 Kenyon, C. Regulation of Life-Span by Germ-Line Stem Cells in Caenorhabditis elegans, , Science (Vol. 295, 18 January 2002) 
25 Bennett, J.T. et al. Confirmation on longevity in Sebastes diploproa (Pisces: Scorpaenidae) from 210Pb/226Ra measurements in otoliths. 1982. Maritime Biology. 71, 209-215.

further material at http://aging-theories.org