Theodore C. Goldsmith has written about programmed
aging in the following areas:
See his Aging Theories
Discussion blog.
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
24 Goldsmith T.
Evolvability,
population benefit, and the evolution of programmed aging in mammals Biochemistry
(Mosc) 82:12 2017
25 Goldsmith T.
Externally
Regulated Programmed Aging and the Effects of Population Stress on Mammal
Lifespan Biochemistry (Mosc) 82:12 2017
26
Goldsmith TC. Digital genetics, variation, evolvability, and the
evolution of programmed aging. Biochemistry (Moscow) 84 12 1792-1800
doi:10.1134/S0006297919120046 2019
27 Gu D., DuPre M. (Eds) (2020) Encyclopedia of Gerontology and
Population Aging. Springer Cham ISBN 978-3-319-69892-2.
Biogerontology-General. G. Libertini (Ed)
Goldsmith T. Evolvability Theory of Aging DOI: 10.1007/978-3-
319-69892-2_43-1
Goldsmith T. Timeline of Aging Research DOI: 10.1007/978-3-
319-69892-2_60-1
28 Bouchard D. (Ed).
Exercise and Physical Activity for Older Adults.
Human Kinetics Champaign. ISBN: 9781492572909 2020
Goldsmith T. Aging Theories
29 Goldsmith T.
Anti-Aging Medicine: How We
Can Extend Lifespan and Live Longer and Healthier Lives Azinet
Press ISBN
0978870964 2020
