Programmed Aging Theory Information Goldsmith - Evolvability Theory of Aging

 

Theodore Goldsmith has written about programmed aging in the following areas:

 

Feasibility and Mechanics of Evolvability

 

Followers of traditional evolutionary mechanics theory contend that an evolvability benefit (no matter how large) cannot override an individual fitness disadvantage (no matter how small) because of propagation considerations. Propagation of evolvability characteristics would be "slow" and "late" relative to fitness characteristics. Goldsmith provides extensive arguments to the effect that propagation of evolvability characteristics should be no slower than that of fitness characteristics so that an evolvability benefit can trade off with a fitness disadvantage.[1][2]

 

Evolvability Benefits of Programmed Aging and Other Life-Span-Limiting Design Characteristics

 

Goldsmith suggests that a design-limited life span provides evolvability benefit in several ways:[1][2][4]

 

Because of genetic recombination, the life of each individual in a population of complex organisms is essentially a test or trial of the particular combination of traits possessed by that individual. The rate at which evolution can proceed is therefore proportional to the rate at which trials are performed. Death rate is a measure of trials per unit time. By decreasing generation time, design-limited life span increases death rate. It is the relative differences in the lengths of the lives and other factors governing reproductive success that power the evolution process.

 

Further, it is generally accepted that natural selection can not act on characteristics that are not expressed in such a way as to affect the competitive performance of an organism. Adult characteristics are not fully expressed in juveniles. Therefore evolution of adult characteristics in any organism requires participation of adults. Organisms that die prior to becoming adults therefore generally do not contribute to the evolution of adult characteristics.  Adult death rate is therefore a measure of the rate at which evolution could proceed. Characteristics that tend to enhance adult death rate enhance evolvability.

 

The total population of any organism is generally limited by external forces (habitat, food supply). However the relative mix of juveniles and adults (and therefore adult death rate and participation of adults in the evolution process) is more controlled by organism characteristics. For example, a population of non-aging animals would tend to have a relatively larger proportion of juveniles and therefore a low adult death rate. Life span interacts with other organism internal and external characteristics in this regard. If, for example, age of sexual maturity were lower or higher, the effect on adult death rate could be similar to a change in life span. Very long-lived organisms also tend to have very late sexual maturity. Mating rituals that tend to generally delay mating would have a similar effect.  Note that mating rituals that generally delay mating and excess age of sexual maturity are both incompatible with traditional evolutionary mechanics theory but have evolvability properties. This sort of logic suggests that age of sexual maturity and life span have a special relationship beyond the Medawar hypothesis. This in turn suggests that a programmed aging mechanism could be similar to the mechanism that determines age of sexual maturity. An aging mechanism and the sexual maturity mechanism could even share common elements.

 

Predation of adults would also tend to affect the optimum life span for the population. Under predation, the population could increase its nominal life span to compensate. This is an explanation for stress-related increases in observed life span.

 

Intelligence and immunity are examples of traits whose usefulness is dependent on acquisition of some non-genetic property that accumulates for the life of the organism. Intelligence and immunity are useless without acquiring knowledge (experience) and exposure to pathogens respectively. These traits represent a problem for the evolution process because, in the absence of limited life span, the acquired, non-genetic property is competing with the inherited property. An older, more experienced but less intelligent animal would have an advantage over a younger, more intelligent but less experienced animal, therefore interfering with the evolution of intelligence. A design-limited life span offsets this problem. Common characteristics of complex organisms such as pecking order would lead to similar issues.

 

In a non-aging population, given intelligence, pecking order, and other animal characteristics, a few older individuals would tend to dominate the gene-pool, reducing genetic diversity and variation and effectively reducing adult participation.

 

Goldsmith, like Skulachev, believes that gradual aging provides additional evolvability benefit over biological suicide by providing a "challenge effect" that acts to increase the effective difference between a more fit and less fit individual and thereby enhance natural selection.

 

Social and Psychological Factors Surrounding Aging Theory and Underlying Evolution Theory

 

How is it possible that even the fundamental nature of aging (programmed vs. non-programmed) is still unresolved in 2014? One would think that the 75 percent of Americans that can expect to die of age-related diseases would have more than a passing interest in the aging process and that there would therefore have been major efforts to resolve the question of aging. Instead, Americans spend more on chewing gum than on basic research into aging. Goldsmith points out that aging and underlying evolutionary mechanics theory are surrounded by a host of non-science factors that tend to inhibit inquiry.[1][5][6][9][20]

 

Experimental Evidence Favoring Programmed Aging

 

Goldsmith has cataloged extensive observational evidence favoring programmed aging as opposed to non-programmed aging.[1]

 

Goldsmith was educated as an electronics engineer (MIT) and has extensive experience in developing and analyzing digital data systems for NASA and the aerospace industry. The reason this is germane to aging is that biological inheritance is accomplished by means of a digital communication in the form of the genetic "code" possessed by an organism. Goldsmith's main scientific interest is in the digital nature of genetic information, and the implications this nature has for evolutionary mechanics theory and therefore aging theory.

 

References

 

1. Goldsmith T. The Evolution of Aging 3rd ed. 2014. ISBN: 0978879856  paperback  Kindle ebook

2. Goldsmith T. Aging, evolvability, and the individual benefit requirement. 2008. Journal of Theoretical Biology. doi.10.1016/j.jtbi.2008.02.235 PubMed

3. Goldsmith T. Mammal aging: active and passive mechanisms and their medical implications. Journal of Bioscience Hypotheses. doi: 10.1016/j.bihy.2008.12.002

4. Goldsmith T. Aging as an evolved characteristic - Weismann's theory reconsidered. 2004. Journal of Medical Hypotheses. 62 (2)304-308 PubMed

5. Goldsmith T. Evolvability and programmed aging: a reply to de Grey. 2008. Rejuvenation Research.11(4) 847-8 PubMed

6. Goldsmith T. Evolution controversies and the theory of aging. 2009

7. Goldsmith T. The case for programmed mammal aging. 2009. Mendeleev Russian Chemical Journal. DOI: 10.1134/S107036321007039X. Invited paper.

8. Goldsmith T. Rationale for complex programmed life span regulation in mammals. 2010. Invited paper Homo Sapiens Liberatus Workshop, Moscow May 2010

9.   Goldsmith T. An Introduction to Biological Aging Theory 2nd ed. 2014. ISBN: 0-9788709-1-3.  Apple ibook  Kindle ebook  Nook ebook   

10. Goldsmith T. Aging by Design. 2011. ISBN: 0-9788709-3-X. Kindle ebook  Apple ibook  Nook ebook 

11. Goldsmith T. New Truth to the Fountain of Youth 2nd ed. 2014 ISBN: 0-9788709-4-8. Nook ebook  Kindle ebook  Apple ibook

12. Goldsmith T. On the programmed/ non-programmed aging controversy. Biochemistry (Moscow) Phenoptosis 77-7 2012

13 

14  Goldsmith T. Arguments Against Non-Programmed Aging Theories. 2013. Biochemistry (Moscow) Phenoptosis 78-9 PMID: 24228918

15  Goldsmith T. Aging Theories and the Zero-Sum Game. 2014 Guest Editorial Rejuvenation Research 17(1):1-2  PMID: 24438180

16  Goldsmith T. Modern evolutionary mechanics and resolving the programmed/ non-programmed aging controversy. 2014. Biochemistry (Moscow) 79-10.

17  Goldsmith T. Solving the programmed/ non-programmed aging conundrum. 2015 Current Aging Science. 8-1, PMID: 26054346.

18  Goldsmith T. Is the Evolutionary Programmed/ Non-Programmed Aging Argument Moot? Current Aging Science. 8-1,  PMID: 26054347.

19  Goldsmith T. Emerging Programmed Aging Mechanisms and their Medical Implications. Medical Hypotheses 2015 doi: 10.1016/j.mehy.2015.10.015. PMID: 26547271

20  Goldsmith T. Programmed Aging and the Intelligent Design Effect. 2015

21 Goldsmith T. Anti-Aging Medicine in 2016

22 Goldsmith T. The evolution of aging theories: why modern programmed aging concepts are transforming medical research. Biochemistry (Moscow) 81:12 2016

23 Goldsmith T. Aging is programmed! (A response to Kowald-Kirkwood "Can aging be programmed? A critical literature review") 2016

 

 

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