Sexual Selection and Diseconomies of Scale

Theory of Aging


Kevin L. Brown

 Version 7.25

 Updated Feb. 7, 2017


Copyright: Kevin L. Brown, All rights reserved.

First Published Version August 11, 2009


A theory of aging is proposed presenting an alternative to the concept that economic trade-offs between body repair and reproduction are the primary drivers of senescence.  It is proposed that aging is a downstream evolutionary adaptation in response to the activity of  growth termination mechanisms which have evolved and persist as the last major act of the developmental process.  In many species these growth termination mechanisms have evolved because they mitigate diseconomies of scale which results in loss of vigor if the individual does not terminate its growth.   Deprived of growth as a primary method of continually increasing fitness, the individual is unable to fully compensate for the loss of fitness caused by extrinsic factors such as, predation, parasitism, famine and natural disasters.   The inability to maintain ever increasing fitness over time, through continuous growth, drives sexual selection processes to more strongly favor young adult progeny by discounting the fitness of older adult progeny.  

It is proposed that aging constitutes this process by which fitness is discounted in chronologically older adult progeny.  Aging evolves and persists via preferences for mates that are maturing and senescing at rates relative to their own rate of senescence.  When predation rates are increasing the individual is more reproductively successful when it is chooses a mate that is aging faster than itself because this indicates that the prospective mate has a faster running developmental clock than their own and as a result will produce offspring that will mature faster and become reproductive quicker.   On the other hand, when predation rates are decreasing the individual is reproductively more successful if it selects a mate that is aging more slowly than itself and as a result produce offspring that have a longer reproductive period of life in which to have more offspring over their lifetime.    

Individuals sexual selection preference for senescing mates is also adaptive to the  individual because it results in the conservation of a broad spectrum of resources which are advantageous to its progeny.  One important resource, that improves the transgenerational reproductive success of the individual is the establishment and maintenance of habitats in which the predation rate on young breeding adults is attenuated because the ease of preying on aging progeny de-selects for predator competence reducing the probability of predation on the younger,  more vigorous, reproductive adults.


Since the publication of the Origin of the Species,  many people have attempted to identify the fundamental causes of aging.   Prominent theories have proposed that aging is caused by one or more of three basic processes:

In spite of the fact that the high degree of variability in lifespan across species strongly supports the concept that aging is under genetic control, all three of these theories  essentially define senescence as beyond direct regulation by natural selection.  The continuing support of these theories by evolutionary biologists is in some part due to their inability to square the genetic control of senescence with the idea that selection operates to increase the fitness of the individual and not the group.  Relative to aging theory this has remained problematic because It has not been intuitively obvious how senescence can function as a trait that favors the fitness of the individual. 

Aging theories built on the foundational logic described above have persisted due to the lack of  acceptable explanations as to how aging can be favored across such a wide spectrum of species.     Specifically, the question persists, what prevents all species from evolving toward negligible senescence?   Stated another way, what stop the proliferation of individuals that cheat the natural order by living too long?  Over the last fifty years the dearth of adequate answers to this question has lent indirect support to disposable soma theory which proposes that economic cost to reproduction disfavors body-repair, resulting in senescence.   However, in recent years, many experimental results that contradict this concept by demonstrating increased life-span with increased reproductive capacity leaves this question in aging theory unresolved.  This paper proposes a solution to this question which is consistent with the experimental evidence while remaining based the individual as the object of selection.   This paper presents straightforward mechanisms that overcome the problem of explaining how senescence benefits the individual, and how sexual selection functions as the primary driver of the evolution and persistence of aging.  

In a variety of animal models, manipulations of mechanisms involving TOR and Daf-2 / Daf-16 - FOXO genes and their protein products have demonstrated increases in lifespan that  range from 15 percent to 75 percent or more.  Though impressive, none of these life extending interventions have transformed senescent species into negligibly senescent species to date.    It is reasonable that important additional mechanisms are involved in the regulation of aging.  

The Purposes of Aging

This paper,  "Sexual Selection and Diseconomies of Scale Theory of Aging “ or (SSDS) Theory of Aging describes significant effects of aging and provides the rationale for the specific rates of senescence that we see across species, from the very short lived to the negligibly senescent.    

The following introduces the adaptive value of aging and describes the sexual selection forces that drove the evolution and persistence of aging across such a large spectrum of animal species.  

Aging is nearly ubiquitous in terrestrial iteroparous animals and it shares many of the same  characteristics across species.  The ubiquity of aging obligates the need for very impactful and broadly beneficial effects to explain its evolution and persistence.  

The Theory

Aging has primarily evolved as a method of implementing growth termination which mitigates diseconomies of scale, and secondarily aging is, in a sense, self-reinforcing in that aging is also an adaptive response to the consequences of growth termination.  

The Adaptative Value of Senescence

  1. Limits Diseconomies of Scale -  In iteroparous terrestrial animal species, when growth exceeds a size threshold for a given species, diseconomies of scale greatly reduces the vigor and “reproductive” fitness of the individual.  In such species it is advantageous for individuals to choose mates that can definitively demonstrate that they will remain vigorous at the largest body size that they will ever attain as reproductive adults.  The way the individual can ensure that prospective mates will remain vigorous when they reach their largest size is to exclusively mate with individuals that can be accurately assess to be both vigorous and to have already terminated their growth and as a result already reached their maximum size.  Aging is sexually selected because it functions as a highly efficient growth termination mechanism by simply down-regulating body repair and growth.  Therefore senescence also functions as an honest indicator that a prospective mate is growth terminated.

By  observing indicators of senescence in prospective mates the individual is able to choose only mates that are growth terminated allowing them to avoid passing genes to offspring that will render them reproductively capable and competitive when small and still growing, but leaves their offspring less vigorous, less fit, and as a result unable to successfully compete for mates as they grow larger.  

Establishes The Juvenile Developmental Period:  A strong preference for mates that are growth terminated can also account for the evolution and persistence of the infertile “juvenile period” exhibited by most animal species.   The logic here is, why be fertile while you are still growing if you are not going to be chosen for mating.  Better to defer sexual maturity so as to dedicate your energies exclusively to growth and repair until you reach maximum size and have your best chance to compete for mates.

  1. Optimizes Rates of Reproduction - I propose that, the degree or extent of aging in combination with the rate of aging functions as a “Tell” in mate selection, enabling the individual to determine how fast a potential mate’s developmental clock is running.  Mate selecting individuals can use this information to infer how long a prospective mate took to mature without actually having been present in the past to actually witness the how long it took a prospective mate to mature.   During changing rates of predation or as famines come and go,   by choosing mates whose developmental clock runs at a rate that produces a maturation time that is optimized to the present conditions, the mate selecting individual improves the survival rate and or number of its progeny.  This mechanism accounts for the evolutionary plasticity we see in aging rates both across species and within discrete populations within species when populations are isolated in areas subject to dramatically different rates of predation.

  1. Protects Young Adults Against Predation - I propose that prey species that terminate their growth around the time of maturation regulate rates of aging in their own population to prevent their predator species from evolving into “super-predators” capable of efficiently preying on their progeny when they are fertile young adults.  Prey species accomplish this manipulation of its predator species by reducing the selective pressure on the young adults of its predator species which drives them to evolve into more effective predators in order to capture sufficient food to reproduce.  Prey species reduce selective pressures that drives predation effectiveness by presenting individuals of the predator species with prey individuals that are progressively aging and thus easy to identify and easier to kill than the young adults of their species.  By preferring mates that are aging the individuals of prey species preserves the aging phenotype in its progeny.  Aging adults in the prey population progressively decline in their ability to evade predation.   As long as the predator species is also an aging species, the young reproductive adults in the predator population should be the most successful at hunting aging prey as they will be high in any pecking orders as a result of being the most vigorous individuals in the predator population.  Easy identification and capture of aging prey by the young reproductive adults in the predator species greatly reduces the selective pressure on this reproductive population to become effective predator of the vigorous young adult population of the prey species.   In summation, through mate selection preferences for the aging phenotypes the young adults of the prey species improve the survival rate of young reproductive adult progeny by limiting the effectiveness of its predators.

  1. Suppresses  Predator Overpopulation:  Animals species exist both as a predator and a prey species at the same time. In growth terminating species, mate selection preferences for an aging phenotype also has positive effects on species in its role as a predator.  As already described aging predators will not compete well against the more vigorous young adults of their species for the limited number of aging prey.  Also, aging predators are even less of a threat to be able to successfully prey on the vigorous fertile young adults of the prey species.  The inability of the aging predator to reliably procure high quality food shortens or ends their reproductive success.  In contrast, in non-growth terminating, non-senescing species,  selective pressure to evolve into a “super predator” is not attenuated by this mechanism.   In the case of a species that does not terminate its growth and as a result evolving into a super predator, the young adults in the predator population do not have an advantage in being able to consume the less vigorous and easier to capture aging prey animals because the older adults will out compete younger adults as they are more experienced hunters and are more vigorous and larger than the young adults.        

Each of these four mechanisms and others drive and explain the persistence of aging.  I propose that standard selection and group selection processes are not capable to evolving and sustaining aging as a dominant trait as is exhibited by many species, only sexual selection processes are sufficient to drive the evolution and persistence of aging.    

Aging & Negligible Senescence

Theories of Aging And Negligible Senescence

Two decades have past since Caleb Finch in Longevity Senescence and the Genome exhaustively exposed the persistence of negligible senescence in nature and yet the dominant theories of aging continue to lack viable mechanisms or explanations for negligible senescence within their models.   This paper presents a mechanism as to how and why negligible senescence persists in select species that is contiguous with the  mechanisms I propose for senescence.  

Negligible Senescence Across Taxa

Negligible senescence is exhibited by a fraction of animal species found spread throughout the phylogenetic tree as specific species of hydroids, corals, clams, lobsters, turtles, fish, amphibians, lizards, and probably whales.   A large percentage of these genetically diverse animals grow continuously and are aquatic.   It should be noted that the concept of continuous growth, as used in this paper, represents a fully expressed implementation of a genotype, however the phenotype of the animal may not reflect continuous growth due to external factors acting against growth, such as nutritional limitations and parasitism.  The paper "The case for negative senescence" provides evidence of these relationships between continuous growth and negligible senescence.  

Negligibly Senescent Animals

Some specific examples of negligibly senescent animal species are, the American lobster, the rougheye rockfish, quahog (Arctica islandica) clams, all of which grow continuously throughout life.  The only mammal known to exhibit minimal or negligible senescence is the Arctic Bowhead Whale which also appear to grow throughout life.  

Hydra exhibit negligible senescence, in some sense without continuous growth.  However the somatic cells of the hydra migrate from the center of the body to the periphery where they are sloughed off, preventing growth.  Additionally, hydra reproduce asexually via budding.  Asexual reproduction applies radically different selective pressure on the evolution of senescence, as I discuss in the section titled "The evolution of Death Mechanisms".   Asexual reproduction effectively allows hydra to continue to increase their reproductive capability by increasing the total size of the clone, while terminating the growth of all individuals in the clone.  A hydra clone consisting of many individuals can be thought of as a single animal consisting of clusters of autonomous differentiated cells that have simply lost direct physical contact with other differentiated clusters, we call individuals, but the number of clusters continues to increase increasing the size of the entire clone of individuals and therefore the clones fitness.

Blanding's Turtles  also appear to exhibit negligible senescence without continuous growth, this seeming anomaly is discussed in the supplementary materials at the end of the paper.  

The Logic of Negligible Senescence

In sexual species which cannot rely on the increasing size of the clone, larger size in the individual often provides a fitness advantage by improving the ability of animals to produce more gametes,and produce larger and more numerous offspring.  Larger size improves animals ability to acquire more food and protect self and offspring from predation.   These fitness advantages, drive natural selection to favor mechanisms that facilitate non-terminated or continuous growth so as to attain larger size in the individual.  

One essential facilitator of continuous growth is negligible senescence because it sustains the vitality of the organism providing more time for growth to take place.   The relationship between continuous growth and negligible senescence creates a self-reinforcing process in which fitness and size is always greater in the future than it is in the present, further favoring the future.  

This self-reinforcing process drives natural selection to continuously discount some portion of present fitness in favor of the combination of growth, negligible senescence, and future reproductive capability.   

In support of this concept,  David Reznick et al . (2002) proposed in an article titled: "The evolution of senescence in Fish", "indeterminate growth (non-terminated-growth) is a primary driver to delayed senescence in fish because increased size leads to increases in fecundity."   In summation, natural selection favors the evolution of mechanisms that facilitate negligible senescence in species that possess a combination of three attributes consisting of, a low mortality rate in young adults, unlimited iteroparity and non-terminating growth.

The relationship between continuous growth and negligible senescence will be made clearer through the following examination of the relationships between terminated-growth and senescence.


Why Senescence Is Common

Senescence is a common phenotype because few species are able to grow throughout adult life due to limitations of body plan and environmental constraints.  Without continued growth producing ever increasing fitness, extrinsic risks to fitness of the individual drive the sacrifice of vigor (senescence) in the adult in favor of the fitness of progeny.

Senescence And The Cessation of Growth

This is not the first theory of Aging to recognize that the cessation of growth was involved in senescence.   G. P. Bidder (1932)  in a paper titled Senescence, reviewed by Caleb Finch in Longevity, Senescence, and the Genome,  proposed that senescence is linked to the cessation of growth.  He stated that "weakness inherent in protoplasm of nucleated cells; is the unimportant by-product of regulating mechanisms."  He proposed senescence resulted "from the continued action of the regulator after growth was ceased,".  

Example of Growth-Termination And Senescence

One particularly instructive example, discussed by Bidder,  that reinforces the theory that continuous growth is linked to negligible senescence and the corollary that  the cessation of growth is the attribute linked to senescence is found in a species of flatfish Pleuronectes platessa which exhibits continuous growth without signs of senescence in the female.  While the males stop growing and experience senescence.  

It has long been understood that there is a general positive correlation between size and lifespan.  The paradox is that within mammalian species dwarf individuals live significantly longer than non-dwarf individuals.  I propose that the understanding of this paradox lies in understanding the effects of scaling on fitness, and more specifically on the secondary effects of the mechanisms that mitigate the negative effects of scale on the individual.  I will lay the groundwork for this topic next.

Dis-Economies-of-Scale Drive Growth-Termination

Mammals and many non-mammalian species terminate growth in the individual at some point in the life cycle as a way to mitigate the fitness reducing effects resulting from increasing size as described by the square-cube law.   See the paper titled "Growth Termination and Scale" for a detailed description of the role of the square-cube law in the evolution of growth deceleration and growth-termination.    

Though growth-termination mitigates against a reductions in fitness caused by dis-economies-of-scale (DES's), I propose that second order effects that derive from a state of terminated-growth drive the evolution of senescence.   Here I propose answers to the questions of how do these second order effects function and how do they culminate in the near ubiquity of senescence in terrestrial animals.

Growth-Termination Caps Fitness

In many species, growth constitutes the last process operating within the individual that provides continual incremental increases in vigor and fitness.  Other than senescence itself, growth-termination is the last act of morphological and phenotypic development in most animals and in many species of plants.   As a result, growth-termination brings to an end the reasonable probability of  additional intrinsically produced increases in the vigor of the individual.   Across many species, growth-termination constitutes a cap on the vigor and fitness of the individual.  

Extrinsic Risks To Fitness Also Modulates Growth-Termination

Many species terminate growth at sizes that are below the body size necessary to produce a loss of fitness caused by DES.   For example, species experiencing increasing mortality rates that are due to predation or parasitism can adapt to the threatened loss of future fitness by initiating reproduction earlier in their life cycle.   In many species early growth deceleration drives early sexual maturation and early reproduction.    

After defining some terms, I will next describe how the capping of fitness in the adult drives the evolution of mechanisms that favor the fitness of offspring at the expense of the adult.

Definition of Key Terms


"Mate-Selection” and “Sexual Selection" are defined here as:  "Any process implemented by an individual that discriminate between potential mates on the basis of phenotype which influences the success or failure of combining a haploid complement of it's own genes with the haploid complement of another individual's genes in the production of diploid offspring.”  

The term  "Mate-Selection" has been introduced in order to distinguish a concept that is broader in scope than the conventional meaning ascribed to the term "Sexual Selection" which has come to be associated with the production of sexually dimorphic traits.  Mate-Selection on the other hand drives the production of both dimorphic and non-dimorphic traits.  However these two terms can be used interchangeably if the reader ascribes the broader meaning to the term Sexual Selection. In this paper I use the term Sexual Selection to carry the broader meaning I have ascribed to the term Mate-Selection.

“Non-Sexual Selection”  Forces or effects in nature other than those encompassed by the term Mate-selection or sexual selection as defined above that selectively reduce or increase the reproductive success of the individual.   Most frequently Non-Sexual Selection is implemented as negative selection or culling selection because it often eliminates or reduces an individual's success at reproduction.  Typical examples are, predation, starvation, disease, accident, and natural disaster.

This term can be described as :

Non-Sexual Selection = Natural Selection - ( Mate Selection + Group Selection).  

Within this definition framework “Natural Selection” is the all encompassing term defined as:

Natural Selection = ( Mate Selection + Group Selection + Non-Sexual Selection )

 "Trans-Generational Selection" is defined as:  "Selection acting on the individual that results from forces that directly or indirectly favor the fitness of young adults while directly or indirectly disfavoring the fitness of the older adult individual."  

"Trans-Generational Fitness" is defined as:  "The survival and developmental fitness experienced through the young adult period of life of successive generations of an individual's descendants " .

Trans-Generational Fitness VS. Individual Fitness

Trans-Generational Fitness is distinguished from other concepts of fitness that are also focused on the individual as the object of selection, in that  trans-generational fitness is an expression of the effectiveness of genes to survive over multiple generations of progeny.  Trans-Generational Fitness is an orientation and focus on the survival of genes through generational time rather than a focus on the increase or decrease in the relative numbers of copies of genes in the next generation.  Trans-generational fitness reflects the fact that in nature specific genes and the phenotypes they manifest can in some instances persist for long periods of generational time, avoiding extinction, while the populations of the genes fluctuate in both absolute and relative numbers.  

Trans-generational fitness can be visualized as one end of what I would call a  fitness continuum in which forces that favor the fitness of young adult progeny are highly influential, while the other end of the fitness continuum represents individuals which are relativistically more influenced by selection forces that favor the fitness of adult individuals without a any preference for young adults.    Viewed across the spectrum of mate selecting animal species, the summation of all selection forces that act on the individual define where on the fitness continuum the individual and as a result the species exists, and depicts how strongly the collective effects of all selection forces favors the adult individual and alternatively favors the individual's current and future progeny through young adulthood. 

A more complete description of the implications of trans-generational selection and trans-generational fitness can be found is sister paper titled: The Evolution of Selection.

Favoring The Fitness of Progeny At the Expense Of Adults

Across all organisms time inherently harbors the risk of loss of fitness that results from accidental injury, illness or any cause of death.   In many species the inability of the individual to compensate for loss of fitness through continuous growth or through successive bouts of morphological change, favors genes that discount the fitness of parents when the results of this action favors the fitness of existing and future descendants.   In other words, extrinsic risks of fitness-loss sometimes favors Trans-Generational fitness by disfavoring the fitness of the adult individual.  This concept is expressed more fully in the sister paper titled:Growth Termination and Scale.

The  Paradigm of Trans-Generational Selection

Though sexual reproduction is fundamentally an altruistic act, it is generally considered settled that natural selection acts primarily on the individual to maximize its fitness and not to maximize the fitness of the group and the concepts I express here are in agreement with this conclusion.   However, different elements of natural selection impact different aspects of fitness.   To extend our understanding of the evolution of senescence it is helpful to distinguish the selection drivers that positively affect the survival of the individual from the Trans-Generational Selection drivers that favor the fitness of progeny.  

I propose that relative to senescence and other altruistic traits Natural Selection should be seen as fundamentally bifurcated into the group of drivers that favor individual fitness and the group of drivers that favor Trans-Generational Fitness.  I propose that the failure to recognize the primacy of this bifurcation of Natural Selection drivers has been one of the main conceptual obstacles to developing a clearer understanding of senescence and other altruistic traits.

Given the altruistic nature of traits that favor Trans-Generational Fitness, how do we account for the evolution and persistence of these traits across taxa?  I propose that the explanation can be found in the effects of Mate-Selection processes.  

Mating Options

With the exception of some species of social insects, sperm and eggs contain only half of the chromosomes required to produce a fully functioning reproductive adult.   Therefore the production of gametes via meiotic division enforces the need to reconstitute diploidy in offspring via the union of haploid gametes which in turn obligates most animal species to in some way, select mates.  The typical existence of a pool of prospective mates provides the common individual with multiple reproductive options.  Even when there are equal numbers of both sexes and both sexes are selecting equally, the individual typically has a choice of more than one potential mate, this constitutes a fundamental one-to-many asymmetry of Mate-Selection.  The relative number of options available to the selecting individual produces a divergence of interest between the selecting individual and its potential mates and binds the self-interest of the individual to mate discrimination processes enabling greater exploitation of the mating resources and thus improving the individual's ability to compete with other individuals more successfully.  

Selection Across Multi-generational Time  

Because some mate-selection mechanisms can be implemented with very little effort, very little risk, and very little reduction in future reproductive opportunity, mate-selection can extract a very low cost to the mate-selecting individual.  When these low costs to the mate-selecting individual are combined with the asymmetry of mating opportunity this summation affords and enables mate discrimination processes the ability to drive the individual to choose mates with behaviors and genes that improve the fitness of descendants not just in the next generation but also genes that favor the fitness of descendants multiple generations into the future.  

Trans-generational Selection

Processes and forces that favor mate-selection processes that favor descendants beyond just the next generation I have termed "Trans-generational Selection."  It is this attribute of sexual species, in which the individual is influenced by selection forces that favor multi-generational time, that plays a major role in the evolution and persistence of senescence.

Mate-Selection Or Sexual Selection

Many processes of Mate-Selection affords the individual opportunities to discriminate on the quality of genes as they are expressed in the phenotypes of prospective mates.   Predation, competition among individuals of a species, and other conditions, drive the individual to select for altruistic traits in their mates because such traits favor the fitness of their mutual descendants.  The flexibility of the processes of Mate-Selection that derives from the effects of diploidy enables and drives the selection of altruistic traits while exacting little cost to the fitness of the selecting individual.  The fitness cost that is born by the selecting individual comes in the form of the energy and time required to execute the processes used to discriminate between prospective mates, and this cost is relatively low in the sense that it is not prohibitively high so as to preclude such selection criteria on the part of the selecting individual.  

Genes and Self-Interest

Though Trans-Generational Selection favors generations of progeny at the expense of the older  adult, this is an external or retrospective view of the process.  In actuality, both the selecting and selected individuals are acting in their own best-interest.   For example, a prospective mate that is being selected by an individual for its complement of altruistic traits, already possesses the altruistic traits and behaviors at the time of mating.   Behaviors such as feeding and defending offspring are essentially beyond the individual's control.  These traits are largely dictates of genes which resulted from the Mate-Selection processes of its ancestors.  From this perspective an animal's own phenotype, including all of its altruistic traits, represents part of the total environmental context within which the animal determines, optimizes and executes it self-interest.

Sustaining Reproductive Agendas Trans-Generationally

The active selection of mates that express altruistic, offspring-favoring, phenotypes is one of the most effective mechanisms, available to the individual by which it is capable of preserving traits and behaviors that favor the survival of its genes for generations beyond its own lifespan.   Said another way, active Mate-Selection may be the best mechanism available to the individual that has the capacity to compel successive generations of descendants to autonomously act in ways that favor its reproductive agendas after it has died.  I must emphasize that trans-generational selection represents the action of those forces that favor the persistence of an individual's genes over multi-generational time, not the traditional focus on the number of copies of an individual's genes simply survive to the next generation.  The details of the role Mate-Selection plays in the emergence of Trans-Generational Selection and the fitness of progeny are beyond the intended scope of this paper,  these mechanisms and processes are elaborated in a sister paper titled: The Evolution of Selection.  

Before leaving this topic it should be noted that in species in which both males and females engage in mate selection processes it is in the interest of individuals of both sexes to add another element to its selection criteria of favoring mates with traits that enhance trans-generational fitness.   If the individual is to be successful in maintaining  its reproductive agendas for an indefinite number of generations into the future the individual must also select mates that show the same behavior of selecting mates that exhibit trans-generationally fitness enhancing traits.   Put simply, the selecting individual needs to select mates that also choose mates that  use the same selection criteria.  Only in this way can the selecting individual maximize the probability of producing descendants that will persist in expressing the trans-generational fitness enhancing trait but also execute this same selection criteria and stabilize these traits and  behaviors over generational time.   This just constitutes conventional evolutionary logic, to stabilize a sexually selected trait there is often needed an additional trait that drives the individual to select for the primary trait in in its mate.

Resource Conservation Increases Trans-Generational Fitness

Given that Mate-Selection both drives and enables the individual to execute reproductive agendas that favor the fitness of descendants for successive  generations beyond its lifetime the question must be asked, specifically what behaviors can an individual engage in that will improve the fitness of its progeny over many generations into the deep future?  I propose that to endow progeny with genes for traits and behaviors that preserve future environmental resources, such as food, habitat, and protection from predators, is one of the most effective thing the individual can do to accomplish it reproductive agendas and ensure the fitness of it's future descendants.  Since failing to maximally exploit environmental resources to enhance one's own fitness is fundamentally altruistic, these traits and behaviors constitute Trans-Generational Fitness enhancing traits.   As previously described DES and other extrinsic risks to fitness provide the selective pressure that drive Mate-Selection processes to favor the evolution of Trans-Generational Fitness enhancing mechanisms that conserve environmental resources.    

This paper proposes that two fundamental mechanisms operate in the adult that result in the conservation of environmental resources.   Both of these mechanisms conserve a broad spectrum of environmental resources by reducing their use or negatively impacting older adults.  These mechanisms operates as optimized processes that extracts real costs from the vitality of the adult by manifesting their effects as senescence.  

Why Resource Conservation Mechanisms Are Broad Spectrum

Here I propose that generalized resource conservation mechanisms evolved to dominance because any one of many possible environmental factors and circumstances can establish any one of a multitude of environmental resources as a specific and unique fitness limiting resource at a given point in time.   Any conservation mechanism that preserves a specific resource will simply shift the fitness limiting resource to the next most scarce resource in line.  Any mechanism that evolved to conserve a specific resource or a set of specific resources would over time not compete successfully across multiple generations against a generalized "broad spectrum" resource conservation strategy.  Additionally it is easier for evolutionary processes to construct and maintain strong selection for a single mechanism of conservation than to maintain strong selection for a large number of mechanisms most of which are conserving a resource that is non-limiting at any given point in time.  

Evidence That  Mate-Selection Drives Senescence

Corals, sponges, hydra, and clams, which do not appear to senesce in the conventional sense of the term, are sessile during reproductive stages of life.    While reproducing sexually, these sessile animals simply release egg and sperm into the water where fertilization takes place.  This method of sexual reproduction precludes the individual from being able to use Mate-Selection mechanisms to discriminate the phenotypes of potential mates.   Specifically, without Mate-Selection the individual is not able to differentiate and choose mates that are senescing.  As a result, over evolutionary time,  individuals are not able to sustain sufficient selective pressure to maintain competence in the genes that are responsible for the senescent phenotype.  This erosion of the senescent phenotype is further reinforced as lengthening lifespans directly favor the fitness of the individual over the trans-generational fitness of decedents.

Sea urchins though not truly sessile also reproduce by releasing sperm into the water precluding Mate-Selection, some of these species such as the Red Sea Urchin live over 100 years and do not show signs of senescence.  At this time I have not seen data to indicate if shorter lived species of sea urchins  senesce or simple die due to high predation rate or due to loss of fitness resulting from dis-economies of scale etc.

Factors Regulating The Strength of Resource Conservation Mechanisms

The existence of non-sessile negligibly senescent animals demonstrates that even though diploidy and Mate-Selection favors Trans-Generational Fitness at the expense of the adult individual, this cost does not have to be so high as to senesce the individual across the spectrum of all animal species.   In many species, it appears that a growth-terminating phenotype is required to tip the balance toward strong resource conservation and away from the fitness of the individual far enough to produce the senescent phenotype.


The Linkage of Growth Termination, Maturation and Aging


In this paper I propose that, aging, growth termination, and the rate of sexual maturation remain linked as highly dominant  traits in terrestrial animals because it would require multiple fitness lowering, simultaneous adaptations, which I elaborate, to enable the divergence from such linkage and the creation of  independent persistent mechanisms th

as total lifespan increases, supports  the conclusion that these traits are linked, and could be implemented as part of  the same mechanisms.  This paper presents my ideas as to why these processes are linked in nature and, therefore, are appropriate as a foundational attribute of my computer simulation model of aging.

An Aging Clock or More Aptly A Developmental Clock 

The length of gestation, the length of the juvenile period, and the length of reproductive life is population specific within a species and m

uch evidence supports the conclusion that the processes that result in these life stages and their duration are controlled by developmental clocking.   Even gastrulation of the blastula, menopause and the onset and patterning of graying fur and hair appear to be species specific and controlled by developmental clocking.  The question can be asked, are all these processes controlled by the same clock or are they controlled by multiple independent developmental clocks?  

Non-Deleterious Indicators of Age

As speciation has occurred in animals, some species have evolved toward very long life spans and to negligible senescence, in these species it is still adaptive for a mate selecting individual to look for mates that have proven that they can and have survived for multiple reproductive periods, for this reason I believe that non-deleterious markers of age have evolved that can be used to quantify the age of a prospective mate.  Graying fur and hair is an example of this type of non-deleterious trait.   Non-deleterious traits are also valuable for species that are aging and select for mates that are aging because they function as a corroboration that the senescent traits are accumulating at the rate that they should.  A mismatch in the degree of senescence and the non-deleterious traits will indicate that the individual might have genetically or epigenetically “opted out of aging” and is a poor mate choice.  

Secondary Sexual Traits are Sexually Selected to Quantify the Degree of Fitness

Sexual maturation itself, as it is manifested as primary and secondary sexual characteristics such as display ornaments, are used to indicate the degree of fitness of the individual. These characteristics, as described by Sir Harvey the israeli professor, decrease the survivability of the individual possessing them.  It is noteworthy that these traits occur at sexual maturation, as growth deceleration is underway and resources are diverted to the sexual maturation process.   As these traits are under the control of the sex hormones that vary in concentration, these sexual ornaments diminish when the animal is under stress and increase when they are not.   Thus, they can function as an indicator of how well adapted the individual is their environment, but there are limitations to the honesty of this mechanism relative to mate selection.

The Burden of Sexual Traits

Secondary sexual characteristics can be seen as being driven by the preferences of mates.  Traits such as the size of peacock tails and the color of male guppies and vivid plumage of the males of many bird species reduce the survival probability of the individuals possessing them.  However these traits do represent “tells” as to the fitness of the individual as the prominence of these traits are associated with increased levels of stress.  For example, male secondary sexual traits often increase predation rates by making males more prominent.  Greater demand for food to support exaggerated male size can also increase stress. Thirdly, competition such as fighting for mates can also increase stress.   These sexual traits indicate how much surplus physiological resources the individual has to dedicate to these traits while at the same time dedicating sufficient resources and time to growth are repair necessary to  remaining vigorous.

It can be expected that, in general, individuals with secondary sex characteristics upon which its prospective mates will choose, will through various diverse competitions for mates,  drive selection in the species to favor individuals that will sacrifice some small degree of vigor and to present a more desirable level of secondary sexual characteristics. However, exceptional individuals that are more highly optimized for their environment should be able to sustain secondary sexual characteristics sufficient to win mates while at the same time avoiding any  compromise of vigor.  

Physiological Control of Resource Allocation

Decades of calorie restriction studies had demonstrated that animals from protists to primates  have the ability to control the allocation of physiological resources to such an extent that they can down regulate reproductive capacity, shifting resources to the maintenance of the body when food is scarce and or other stressors are high.   This makes sense since it is pointless to dedicate resources to reproduction when the probability of producing offspring that can survive to maturity is low.  It is more adaptive at these time to maintain the vigor of  the body and wait for the environment to improve.  

The ability of the individual to balance the maintenance of vigor and the expression of sexual traits demonstrates that the apportionment of  resources between these two demands is under genetic and epigenetic control.   I propose and demonstrate in simulation that contrary to conventional thought, regulatory genetic and epigenetic controls favor the vigor of the individual over fertility and the expression of sexual characteristics.  When physiological resources are no longer sufficient to maintain both vigor and the fertility, fertility is shut down to fund vigor.

 I further propose that this is this regulatory control that shuts down fertility during time of famine and this same  control system also accounts for the phenomenon of menopause.  

Because the expression of  sexual traits are under genetic regulation the resource apportionment described above points out that the individual cannot rely on secondary sexual characteristics as an always-honest indicator of aging in prospective mates, nor as an always-honest indicator of growth termination in prospective mates.  

Mating is often a competition among prospective mates and is contested on the basis of both vigor and the prominence of sexual characteristics, as describe above, it is in the interest of the individual to allocate resources to vigor and then use remaining resources to sustaining the greatest degree of sexual characteristics as it can manage.  An animal that is not growth terminated will attain a size at some point that is optimal for the production of vigor and at this point such an individual is able to present strong secondary sexual characteristics and high state of fertility while not being growth terminated.  Therefore this resource allocation strategy precludes the use of sexual maturation as an honest indicator of growth termination.  

Note: Dedicating resources to the vigor of the individual before resources are dedicated to sexuality contradicts the Hobbesian notion that the living world is a continuous brutal struggle for the majority of animals, it is not.   The allocation to resources to vigor before reproduction down regulates populations in such a way as to keep the population small and vigorous instead of large and on the verge of starvation.    

Evolution of Growth Termination

It appears that  complex organisms first evolved in the water and as animals became multicellular growth termination became common, but how and why did it evolve?   The fossil record up to the time just before the cambrian explosion documents the lack of large multicellular animals for over 2 billion years. It is consensus opinion that low oxygen concentrations in the early oceans limited the size of animals because these early animals had not evolved organs to efficiently absorb and concentrate and transport oxygen.   Without gills or other organs to absorb oxygen and a circulatory system to transport the oxygen to internal tissues animals possessed had to remain small to maintain a sufficient surface area to body mass ratio to meet oxygen demand.  

Once the oxygen concentrations of the oceans increased and oxygen collection and transport evolved many animals began to grow what seems to be arbitrarily larger.  Growth termination in larger complex aquatic animals seems to have evolved to mitigate diseconomies of scale related to food capture and habitat when and if such diseconomies apply sufficiently to any given species.  Even in water, which removes the diseconomies of scale associated with the effects of gravity found in terrestrial environments, other diseconomies of scale still exist such as being able to dissipate heat sufficiently at very large body size, or out growing your prey species limiting prey species, or becoming prey to other larger species because you can no longer hide in the way you had before, such as a hermit crab no longer being able to find shells large enough to accommodate their larger body size.  So it would seem that all animals would have a mechanism to terminate growth, however this is not required if the individual has a high probability of death from predation or other causes long before it reach a size that greatly reduces its vigor due to diseconomies of scale.   In these cases growth termination need not evolve and if evolved it need not persist in the species.  This condition appears to be the case in many aquatic species.

Growth Termination and Bony Skeletons

When Animals without a bony skeleton, grow too large diseconomies of scale reduces fitness, however they have the capacity to utilize body tissues as a food source and in essence grow smaller reducing the diseconomies of scale and reestablishing vigor.  In contrast animals with bony skeletons, do not seem to have the ability to ‘scale down” their basic skeletal frame size, and for this reason they have to commit to a basic size and permanently commit to it in a growth termination process.  Terrestrial animals with a rigid endoskeleton seem to be required to commit to a finite size range while the individual is still vigorous, before its skeleton gets so large as to incur significant diseconomy of scale.  So growth termination can be executed as simply a further turning down of the growth processes across all body tissues such that the cells producing bone growth and tissue growth are not given sufficient resources and sufficient signaling substances necessary to continue making existing structures larger.  

Aging Is An Honest Indicator of Growth Termination.    hhhhhhhere

If the resources saved by growth termination are utilized to produce primary  and secondary sexual characteristics in the individual and as a result indicate both vigor and reproductive capability, what is aging needed for and what drives the persistence of  aging in the population?  I propose that aging is used in mate selection as an honest signal that prospective mates are growth terminated.   Here is the supporting logic.  

As described above, in any environment some individuals will be more highly optimized than other individuals to the point at which these individuals support stronger indicators of sexual maturity and stronger secondary sexual characteristics than other competing individuals in the population while still having the capacity to continue to grow at some slow rate within a window of time.  For this reason, it is reasonable to conclude that signals of sexual maturation cannot be interpreted as honest signals that  growth termination has occurred in prospective mates.  

Growth termination directly results when physiological resources and signaling allocated to growth drop below a threshold required to fully maintain and grow critical body tissues.  Below this point of resource allocation to tissue maintenance and growth, senescence ensues.  An animal with the ability to detect systemic senescence in prospective mates possess accurate, reliable information that a prospective mate is growth terminated.  

When an individual has the ability to accurately assess the accumulation of senescence or “age” in prospective mates it has  the second vital element required to fully assess mates on the basis of growth termination.  The ability to detect age and not just a rate of aging informs the individual whether a prospective mate has remained fit enough to sustain a significant rate of senescence over time and still be sufficiently vigorous to be a viable mating prospect, all the while being growth terminated. In iteroparous animals it is in the interest of animals to pass the ability to remain reproductive over multiple breeding seasons, aging is the attribute that informs the individual that it is selecting mates with this capability.  

The combination of detecting the current rate of senescence along with the ability to detect the accumulation of senescence “aging” enables the individual to reject potential mates that can exhibit a spike in its rate of senescence during a breeding season and then return to a growth mode and negligible senescence the rest of the time.  Along with the rate of senescence, the accumulation of systemic senescent traits over time, aging, is required to construct an “honest” indicator that a prospective mate has decelerated its growth to the point of growth termination and that they are maintaining this growth terminated state.  

Aging as an indicator of Juvenile and Gestational Duration   


Since the infertile periods of life are positively correlated with the length of the fertile period it is  advantageous  for an animal to be able to discern how fast a potential mate's developmental clock is running.   This is an important selection criteria for the individual for the following reason. When predation rates are high the individual will leave more offspring over multiple generations by choosing mates that pass genes to its offspring that result in shorter gestation period and shorter juvenile periods in their offspring.  This choice results in offspring that start reproducing earlier, reducing the effects of a high predation rate.  Alternatively, when predation rates are low, the individual will leave more genes in the gene pool over multiple generations if it selects mates with a developmental clock that is running slower because this results in longer reproductive life spans even though the gestation and juvenile periods are extended as well.   My aging computer model demonstrate this logic.  

When the predation rate increases in a population it is in the interest of the individual to produce offspring that can reach sexual maturity sooner and begin reproducing sooner.  When the predation rate in a population is low, producing offspring that reach maturity and start reproducing later reduces population pressure on food supply and helps prevent a spike in the population of animals that prey on the species.  These population stabilizing effects help prevent the onset of prey and predator population boom and bust cycles that can result in the extinction of populations of both prey and predators.    Therefore the linkage of the length of the developmental periods and the length of the juvenile period to the rate of aging enables the mate selecting individual to use the rate of aging of mates to optimize the rate at which its offspring will sexually mature thus increasing the probability that its genes will persist longer over multi-generational  time.   In essence the rate of aging informs the the mate selecting individual of how fast the developmental clock is running in its prospective mates.    

How Aging Functions as an Indicator of the Length of Gestational and Juvenile Lifespan

With the rate of aging is controlled by the same developmental_clock as is utilized by the developmental processes,  then, there must be one or more processes that manifest or signal this rate of aging which is utilizing the same developmental_clock as is used to time the length of gestation and the length of the  juvenile period.  So an individual can now accurately assess how fast a prospective mates developmental clock is running and as a result “tell” how a prospective mate will influence not just how large their potential shared offspring will grow, but also how long it will take the offspring to reach sexual maturity and become reproductive.  

Senescence, constituting a state of accumulating damage to the organism, across organ systems, tells the individual that a prospective mate has terminated growth.   Additionally, the rate of senescence informs the same individual of the rate of development, a prospective mate, will potentially  genetically or epigenetically pass to its offspring .

Adaptations Required to De-link Growth Termination, Maturation, and Aging

1. Growth termination mechanisms are needed by terrestrial animals and many non-terrestrial animals to prevent a loss of fitness which is caused by diseconomies of scale that results as the size of the individual increases.  For this fundamental reason, iteroparous terrestrial animals possess highly conserved  mechanisms of growth termination.  

One or more epigenetic or mutational changes must occur to deactivate these long established growth termination mechanisms in order to allow growth to continue.   By itself, non-terminating growth will, over time, decrease the fitness of the iteroparous individual and be de-selected.  

2. Across nearly all terrestrial animal species, sexual maturation is delayed until growth decelerates nearly to the point of growth termination.   It is conjectured that this is the norm across animals because mates often select for size, strength and vigor.   Individuals reaching sexual maturity before attaining full size would often not result in successful matings and therefore wastes time and energy that could be dedicated to attaining near maximum size, at that point allowing the diversion of resources to supporting faster sexual maturation and more successful matings.  

One or more mutations or epigenetic changes should be necessary to enable sexual maturation without near terminal growth deceleration.  By itself sexual maturation without strong growth deceleration will not persist as a trait in terrestrial animals species because it will be out competed by animals of the species that delay maturation.

3. In many species in which matings cannot be forced on the individual by potential mates, an individual already possessing the other two adaptations above must possess a third adaptation, that being, its mate selection preferences must no longer wait for its own growth to nearly terminate before selecting mates.  Again, by itself, this adaptation is maladaptive to the individual when it is not accompanied by the adaptations described in items 1 and 2 above and will be quickly deselected from the gene pool.  

4.  Because there is an optimal size for most terrestrial animals, in iteroparous species terminated growth is an important mate selection criteria because it plays such a critical role in an individual's  ability to accurately asses how fit a prospective mate is in its environment.   For example if an animal selects a mate that is still growing, the selecting individual cannot tell how "fit" its mate will be in the future, once it does stop growing, if its potential mate ever does stops growing.  Because size is heritable it is important for the individual to pass optimal size onto its offspring.

For most non-aquatic species growth termination is essential for the animal to avoid becoming less fit over time due to diseconomies of scale that increase as an animal gets larger.    Therefore one attribute that individuals should look for in prospective mates is that they possesses a genotype that will eventually result in a phenotype that is growth terminated before the animal reaches a size that starts making it less fit that it would be if it had remained smaller.  As a result  it is both in the interest of the individual to terminate it growth and to honestly advertise that it has terminated it growth to prospective mates.    

A growth terminated phenotype is a critical attribute that animals of most terrestrial species should strongly select for.   Animals of these species should select mates that are growth terminated at the time of mating because if the selected mate is not growth terminated they do not know if the selected mate is done growing and therefore they do not know if the mate they have selected will be more or less fit than other potential mates when all other potential mates have finally terminate growth.  So in effect, in animals that reproduce more than once, selecting mates that have reached sexual maturation without growth termination denies this individual the ability to select on the basis of an attribute that is a very important element in its selection criteria.  In terrestrial iteroparous species, an individual’s preference system  that does not

de-select for mates that are still growing will not leave as many descendants over multigenerational time as will individuals that select for mates that are both sexually mature and growth terminated.  


In iteroparous terrestrial animals it is important to mate with an individual that is very fit across the entirety of its reproductive time as this is an important trait is to pass on to offspring.   The only way the individual can determine this is to select mates that are growth terminated at the time of mating.

By itself sexual maturation without growth termination will be strongly selected against in the population and should not persist in significant quantity.  However to drive the fixation of the adaptations of continuous non-terminating growth with sexual maturation and without growth termination, these traits will also have to be available in the population at the same time so as to provide a selection preference for such mates.

Calorie Restriction - The Effects of Famine

CR should within the Mate Selection Theory of Aging cause the individual to cut its production of sexual hormones and fertility, and then begin go into preservation mode, and cut the rate of the developmental clock so as to preserve the animal for a time when the the famine is over.  Additionally there should be epigenetic changes that occur to increase the lifespan of the individual which can be able to be passed onto offspring.   This effect should be different than the result of increased predation rate which shortens life span and with it shortens time to maturation making it possible to reproduce sooner to counter the increased predation rate effect.  Starvation or “CR” and increased predation both increase the death rate on a population but the effect on aging rate within the affected species population should be the opposite relative to aging.   It has been demonstrated that a near starvation event early in life provides greater longevity in humans that persists to some extent for the rest of their lives.  

When a species experiences a greater predation rate, the food supply for the remaining individuals should be more abundant and should drive a shorter lifespan via epigenetic changes caused by increases in IGF signaling.   Also this should be coupled with greater stress hormones in surviving individuals caused by near predation events in many species, though this is probable the lesser of the two drivers.  

Population Boom and Bust 

When a species exploits a new habitat in which it has no predators the following thing should happen.   First the species should boom as its life span shortens driven by the availability of resources and food, low population density, and a low predation rate.  Then as the population overruns the food supply, the population will experience starvation, the surviving individuals will have experienced extreme CR causing them to undergo an epigenetic change to a longer life span and as a result smaller litter sizes, a longer juvenile period slowing the birth rate of the population.  This can repeat over multiple cycles but in the end the population should stabilize with longer life spans, until the predation rate increases.

It should be noted here that the choices being made by a mate selecting individual are consistent with their selfish interest of producing offspring that have the best chance to preserve their genes over many generations into the future.

Increasing the Duration of the Juvenile period as lifespan Increases.

Famine is a reality for all species of animals, one mechanism that sexual selection has devised to mitigate the effects of famine is to delay reproduction,  and  to reduce  population.  Famine produces a state of CR in the population, so species that keep the length of the juvenile period linked to the rate of senescence can use the rate of senescence to select mates that are aging slower which also brings with it,  delayed reproduction in its offspring and extended lifespan.   Species that delinked aging from the length of the Juvenile period cannot mitigate the effects of  future famine by reducing its population through the  down regulation of the fertility of its offspring and as a result are unable to use this mechanism to mitigate the risk that population boom and bust cycles will increase the probability of  extinction.   By delaying maturity and at the same time extending the lifespan of its offspring the selecting individual effectively  stretches out the fertile period of its offspring helping to  maintain fertility of its offspring long enough to outlive the famine and its action to delay the maturity of its offspring at the same time reduces the rate of growth of the population, mitigating the severity of the famine as well.  By stretching out the length of the Juvenile period offspring delay the energy expenditure of reproduction providing more time for the famine to end.  

Stem Cell Populations

Evidence now points to the conclusion that all body tissues are replenished by stem cells not by the division of standard fully differentiated cells residing in the tissues.  It seems that keeping antioxidants low in differentiated tissues allow apoptosis to eliminate these cells and then for the stem cell populations to replace the eliminated cells.   It seems that the body does maintain high concentrations of antioxidants in the stem cell populations. (find citation? )  

Selection for a Trait in Mates that can not be observed because it no longer exists

When selecting a mate from a variety of options, it will benefit the individual to select a mate that had a juvenile period that was the length that is best optimised to the current environment.  In other words, if a famine is underway the individual optimally will select a mate that matured later and has a longer fertile life span than the average potential mate.  The problem is the individual has no direct way of determining how long it took any given prospective mate took to reach sexual maturity.  So how can an individual select for a trait that cannot be observed since it no longer exists because it occurred completely in the past?  This is one of the functions of the rate of aging and the total age of the potential mates addresses. The combination of these traits exists as indicators or proxies of the length of the juvenile period and the total fertile lifespan of the animal.  

The Value of Selecting Mates with Proven Long Lifespan.

In very long lived species such as primates, whales, humans, Blandings turtles, species that repetitively reproduce over many years, it is important for the individual be able to select a mate that has been mature and has survived for multiple reproductive time periods.  This ability to survive and reproduce over many reproductive periods is an important attribute to pass to offspring and therefore should be of interest when the individual is choosing mates.    Individuals that are capable of discerning the rate of aging and discerning the accumulation of senescent traits in prospective mates has the ability to differentiate individuals on the basis of how good a prospective mate is at surviving has been successful at mating over multiple reproductive time periods.

The Evolution of Negligible Senescence in Growth Attenuated Animals

Blandings turtles stop growing but do not appear to age in the conventional sense.  This could mean that in these turtles the aging phenotype is not sexually selected for.  However this species does have a relatively long juvenile period before it becomes fertile.  This all points to the idea that separate mechanisms one involved in the production of sexual maturation and another that produces the senescent phenotype, but both traits are fundamentally driven by the developmental aging clock.   I think that it is likely that species that no longer select for senescence in their mates can still decellerate growth to the point that it is effectively terminated while at the same time avoiding senescence by maintaining youthful PPS (pluripotent  stem cell)  

Reproductive Frequency and Litter Size Control

In general in related species the populations of animals that mature more slowly also produce fewer offspring per reproductive event  and the frequency of reproductive events is also longer in long lived species and populations.   This makes sense in the case of famine, in that not only does it make sense for the animals to delay sexual maturity and fertility of its offspring but it also makes sense to reduce the frequency of reproductive events.  Taked together these three elements can greatly reduce population pressure on food supply and it also makes sense because it enables the offspring to conserve resources so as to focus scarce resources on the nurturing of the offspring that are produced.  

This logic implies that the frequency of reproduction, the rate of aging, and the number of offspring produced per reproductive event should be linked as part of the same epigenetic control mechanism.

High predation rates should have the opposite effect of increasing the rate of aging , shortening the juvenile period, and increasing frequency of reproduction and increasing the clutch size.   Again the point of linkage here is that the same events affect all of these parameters in the same direction, toward increasing rates of reproduction when predation rates increase and reducing the rate of reproduction in times of famine.

Predation and Aging

Predator Prey Population Dynamics and Aging

One way an individual can succeed at having its genes survive over many generations is to ensure that the population of predators that prey on them does grow so large as to risk bringing  its progeny to extinction.  It can accomplish this by not becoming a reliable, consistent food source that is easy to procure. When a prey species becomes a reliable food source for a predator population the predator population can overpopulate placing even more demand on the prey species which can quickly lead to population extinction.  A high fertility rate, coupled with a short juvenile period and a short lifespan makes a prey species capable of having its population  diminished to a  small size in a region and then recover via its high reproductive rate when the predator population has collapsed in the area due to famine.  

Once both the predator and prey species has had their populations reduced, the increased food supply that went under exploited due to the population drop of the prey species now fuels the recovery of the prey species.  

Since most animals are in essence both prey and predator species, it is important to look at the same dynamic from the perspective of the predator species.  As the prey species collapses the predator species will experience famine, which will induce CR effects in its populations.  The CR effect will lengthen the juvenile period of the prey species, it will reduce the number of offspring produced per breeding season.  The effect will be to reduce the pressure on the remaining population of prey animals also facilitating the recovery of the prey species over generational time.   Over many generations the reproduction rate of the prey species and the reproduction rate of the predator species will oscillate but also converge over multiple generational time on an optimum for each species such that the length of juvenile time, litter size and aging rate will be optimized to stabilize both populations.  

Aging In Prey Species Attenuates the Predator Prey Arms Race

The primary predator species are caught in an arms race with their primary prey species.  The predator is attempting to evolve the ability to eat all the prey and the prey are attempting to evolve the ability to avoid ever being eaten.  In prey species that do not age, the predator will be driven to evolve the ability to consume even the most vigorous individuals in the population since all the adults are essentially vigorous. If the predator species does happen get lucky and gain the advantage and evolve the ability to consume even the most vigorous prey efficiently, then both predator and prey populations can be driven to extinction.  Contrast this to a population in which the prey species is aging, now the predator population need only evolve the efficiency to prey on individuals that are less than maximally vigorous.  

Aging in the prey species reduced the selective pressure on the predator species eliminating the need for the predators to evolve the capability to easily prey on the most vigorous reproductive prey individuals since the predator can meet its dietary needs by consuming the older individuals, infants and juveniles.  It can be seen in many predators, even the most vigorous among them single out the easiest kills, avoiding the most vigorous of the prey which happen to be the young mature individuals.  Aging increases the vulnerability of the prey individual to predation by increasing probability of disease, injury, reduced agility, reduced acuity of the senses, etc.  

Aging in the prey species provides a period of time for the vigorous mature fertile animals to have a good probability to evade predation until after they have  successfully reproduced.   In a nutshell aging on the part of prey species dampens the arms race between predator and prey preventing the the development of selective pressure on the predator species that would result in the evolution of a super-predator that can prey on even the most vigorous members of its primary prey species.  Aging provides prey species with a window of time in which to successfully reproduce.  

Rational Predators Seek the Easiest Kills

Predators are rational in their hunting strategies and focus on the easiest kills because they offer the highest probability of success and also because an injury incurred by hunting the more vigorous animals can prevent further hunting resulting in death by starvation.  With the most vigorous of the predator focusing and potentially monopolizing the hunting of the less vigorous aging prey individuals deprives the aging and infirm predators of adequate food supply since they are unable to very successfully prey on the most vigorous in the prey species.  This effect  hasten the demise of aging predators eliminating them from the breeding population more quickly, helping to hold the predator population in check.    

Aging and Death Mechanisms

Naked Mole Rats and Senescence

Naked Mole Rats do not show conventional aging in the sense that they maintain a high fertility rate with age, however their tissues do show significant aging in the form of large amounts of oxidative damage.  This supports my conclusion that Aging is not a direct death mechanism, but aging does increase the chances that overt death mechanisms are triggered.  This is consistent with the realization that across all causes of death aging is the most significant factor.  


This is expressed by one web site

Naked mole rates are exceptions to several theories of aging. For example, the free radical theory states that aging happens, because of the extensive cellular damage from reactive oxygen species. However, naked mole rats show very high levels of oxidative damage from these free radicals and still their cells are perfectly functioning for years and years. Another hypothesis claims that aging is due to shortening of telomeres – DNA molecules caps, that shorten every time a cells undergoes division. Yet the naked mole rat has relatively short telomeres. Also the telomerase, protein that lengthens telomeres, is not really active in naked mole rats’ cells. So telomere maintenance is unlikely to explain the outstanding longevity in these animals.


Naked Mole Rats also demonstrate that the body can override general senescence to maintain the functioning of specific organ systems, even though general systemic damage is being carried by the cells constituting the tissues.   This points out that aging tissues can function as an indicator in mate selection of the speed of the developmental clock even in species that have not terminated growth but have decelerated their growth rate to almost zero.   These species from the standpoint of reproductive rate are not senescencing, this seems to apply to naked mole rates and for example blandings turtles etc.

Rate of Aging is a Sufficient Tell in Non-Senescing Apex Predators

In apex species the rate of tissue senescence alone is sufficient as an indicator in mate selection informing the individual of how fast or slow a prospective mates developmental clock is running.  The accumulation of senescence in tissues that we call aging does not need to continue to rise with age but can instead plato at some non-deleterious level and the individual does not need to select mates on the basis of signs of accumulated age itself.  In non-apex species, the continued accumulation of aging with time is needed and used in mate selection to provide their predators with progressively more feeble adults for their predators to consume easily  preventing their predators from evolving into super-predators as previously described.

Famine Its Cascading Effects on Species In Predation Hierarchies

When famine is caused by significant drought conditions for a long period of time for example, the herbivores at the bottom of the food chain suffer a loss of population due to starvation, with death occurring mostly in the very old and the very young.  Additionally the populations converts to a CR metabolism, including the currently surviving aging animals.  Reproduction in this herbivorous prey species is greatly reduced, making new born nearly unavailable to the predator species.  The CR metabolism, due to famine, also  invigorates even the remaining aging animals.  The effect of these changes is to make it more difficult for the predator species to locate prey and when located to make it more difficult to successfully kill and consume the prey species even the prey animal is aged.  Very quickly, this results in a state of famine in the predator species as well where the events just described now occur to this species as well effecting the next predator up the food chain similarly.   AS a result the predation rate will fall across the entire predator hierarchy, but the populations will remain small as long as the famine continues in the foundation predator.

The effect of this cascade of effects over multiple generations is to slow the rate of reproduction by extending the juvenile period and extending the lifespan of the species of all predatory species from the bottom of the food chain to the highest apex predator.

When famine ends the foundation herbivore-predator now enjoys lots of food ending the CR effects.  This causes fertility to rise, and since the predator population is greatly reduced in size the foundation predators population booms, ending the famine in its predator species as more young are available and the older prey animals are again aging and becoming feeble and easier to hunt.

Invasion by a Super-Predator

When a species is introduced to a new environment in which it has no established predators preying on it, the following series of events can happen.

The species may be incapable of developing the ability to efficiently prey on any species that it encounters in its environment, in these case the species will fail to successfully invade the new environment and will die off.   Or, at the other extreme, it may find that it is capable of preying on one or more species which have no evolved defense against it and it becomes, in effect, a super-predator in this new environment. In these cases, even the young adults are vulnerable to predation by this species.  

Effect on the Prey Species

The population size of the prey species declines at an accelerating rate as the population size of the super-predator begins to increase.  As the density of the prey species drops the demands on its food supply drops.  So the prey species now experiences a larger than normal food supply and low population density both of which causes the species to select mate with a faster running developmental clock.  With this, the length of gestation and the length of the juvenile period are reduced and the prey start to reproduce at a younger age. Additionally litter size increases as females have no trouble finding enough food to support large litter size.  

As the prey population continues to decrease fertile individuals that escape predation are reproducing quickly.

Selection Effects on Super-Predators

As the prey population drops famine sets in with the predator species.  A CR metabolism is invoked by the famine, this reduces reproduction in the species and causes the young and the aged to die.  Reproduction is essentially shut down, as the reproductive individuals also begin to die.  With very few prey animals left, the predator species may decline to an extremely small number if they do not become extinct in the area altogether.  The predator animals that do survive will be evolving toward greater lifespan and a longer non-reproductive period and smaller litter sizes as famine selects for those animals that thrive under the effects of CR, which is one that have smaller litter sizes leaving more food for the young produced and the individuals that extend the juvenile period and the total reproductive life span allowing them to potentially outlive the famine.

Population Rebound of Prey Species

With very few predators left in the environment the prey species now equipped with larger litter sizes and faster maturation and reproduction, the population of the prey species begins to rebound.  In contrast the legacy of the famine state in the predator population over multiple generation has caused it to mature more slowly and to have smaller litter sizes.

At this point the prey population begins to grow rapidly, with a population that grows old more quickly than it did before the introduction of the super-predator.  Now the super-predator population can prey on old and young prey avoiding the harder work of preying on young adults.  Selective pressure required to maintain the traits required to be able to prey on young adults will be gone and the Prey population will incrementally evolve away from being able to efficiently consume the young adults in the prey species.

Slowly the super-predator species population will recover, and since they are still able to somewhat efficiently  prey on young adults in the prey species the cycle will begin again with the crash in the population of the prey species and all the steps will repeat.  However now the prey species will begin the process again from a somewhat more optimal genetic and-or epigenetic starting point allowing them to evolve still faster reproduction times and still larger litter sizes, and the predator starts the new cycle at as somewhat less of a super-predator on the prey species and therefore impacts the size of the prey species less with each repeat of the cycle.  

These cycles will continue until the maturation, aging rate, and average litter size of the prey species is in balance with the ability or inability of the predator species to prey on young adults in the prey species.  

Biological Clocks and Aging

At this writing I know of no natural or experimental intervention that transforms an individual of a senescing species into a non-senescing individual, instead anti-aging interventions only extend lifespan some percentage beyond an average within a species specific genetically defined range of lifespans.  So it seems very likely that one or more aging biological clocks exist which define the range of lifespans individuals of a given species experience.   Recent research by Steve Horvath has pointed to the possibility that a highly accurate epigenetic clock which consists of DNA methylation at specific sites exists in most cells of the body which tracks and determines age of the cell.  This research has been described in a Nature News article and the research paper reported in Genome Biology, opens potentially significant new vistas for aging research.  

Recently, supercentenarian research points to the possibility that  exhaustion of blood stem cell reserves may play a significant role in aging pointing to another potential example of a significant clock of aging.  

The Nature of the Clock

So, we are left with a significant set of unanswered questions.  If aging is fundamentally driven by a clock, is this clock defined genetically, recording time epigenetically as possibly exemplified by the work of M Horvath and acting neurologically via the hypothalamus?  How do we tell the difference between the clock with its actual cogs and gears and the closest downstream effects of the clock where it simply logs time?  And finally is the fundamental clock we are seeking systemic or highly localized in the body?   There are still more significant questions, for example, in animals is there fundamentally one systemic clock and only one way this clock logs the passage of time, and are all systems that have a temporal element to them, utilized this time log to initiate and terminate actions in the body?  If this is the case we may not want to change the intrinsic rate at which this clock logs time or for that matter we may not want to zero the time log due to its effect on other aspects of body regulation.  Clearly if there is a fundamentally independent clock of aging then this would not be the case and it might be possible to intercede at the level of the clocks initial logging or even change the rate the clock "ticks" later in life.  

As a result of this characterization of the nature of the clock I think it is useful to differentiate the "aging-clock" from other biological clocks or a fundamental systemic clock even if the aging-clock utilizes the time log of a more fundamental clock as its temporal cadence to initiate and regulate the rate of senescence and the activation of death mechanisms.  

 The Aging-Clock & the Rate of Senescence

Because the rate of aging is so species specific and has proved only incrementally malleable over generational time I propose that the fundamental aging clock is genetically defined.  However I have attempted to make the case in this paper for the idea that epigenetic and neuro-hormonal mechanisms exist that  allow the individual to up or down regulate their rate of senescence to more fully optimize their rate of development, maturation and senescence.  I have propose that individuals select for mates that attempt to optimize their rate of senescence to make it consistent with changes in the relative strength of individual selection pressure to trans-generational selection pressure to which they are exposed in real time.

The Hypothalamic Clock and Senescence as developmental stage

Thyrotropin Releasing hormone which is produced by the hypothalamus has been shown to have a role in growth and development and in senescence.  via its  regulation of the production of Thyroid Stimulating Hormone (TSH).    


I wish to note that we have come full circle in our conception of the logic of aging, Alfred Russel Wallace , one of the first to speak on the evolution of aging, proposed that aging and subsequent dying occurs to the benefit of the species namely because of the death of old individuals would free up resources for subsequent generations.  This idea though well thought of in the past has declined in popularity because it seemed to require a mechanism based on group selection.   It is now clear that group selection is not necessary, Mate-Selection or Sexual Selection in conjunction with dis-economies of scale is sufficient to drive the evolution and persistence of aging via mechanisms that generally conserve resources and specifically bequeath progeny with habitats that attenuate predation rates on young adults, providing them with time to successfully reproduce.  

It gives us pause to accept that aging is a direct result of the selfish interest of the individual as expressed through our Mate-Selection or sexual selection biases.  The evolutionary pressure to senesce the individual must be viewed as high considering that this is a trait that we share with a vast number of divergent species through evolutionary time.  Fortunately it may not have to be this way as we are now poised at the moment in time when it becomes feasible to forestall and possibly reverse senescence in humans through resetting the developmental clock.  


It is plausible that Negligible Senescence can be achieved  in growth-terminating vertebrates through interventions that up-regulate the rates of autophagy in such a manner as to maintain static size while maintaining the rate of intracellular repair above the threshold of senescence. ( See Appendix A. )  This component of negligible senescence should be feasible as there are many methods such as CR, rapamycin, protein restriction, etc, that can be employed to up-regulate autophagy and intracellular repair in general.  

It will also be necessary to supplement the  production of parenchymal replacement cells in great enough numbers to compensate for programmed cell death so as to sustain tissue functions at youthful levels throughout the body.  Blanding's turtles may be an example of this strategy, implemented in nature. ( See Appendix B. )  Once this result has been achieved it may be necessary to address potential deleterious genetic conditions that result from the effects of antagonistic pleiotropy or other presently unknown mechanisms.  

It is reasonably probable that we will soon identify and synthesize the regulatory factors of stem and progenitor cell proliferation and differentiation, if researchers have not already done so by the time of this writing.  As described earlier, recent studies utilizing heterochronic parabiotic pairings seem to be making great strides in closing on the mechanism and structure of these factors, giving us reason for optimism.  

The End


Finch, Caleb E.; "Senescence, Longevity, and the Genome" (1990). The University of Chicago Press, Chicago and London.

Adamson L, Walum E,  (2007).   Insulin and IGF-1 mediated inhibition of apoptosis in CHO cells grown in suspension in a protein-free medium.  Altern Lab Anim. 2007 Jun;35(3):349-52.

Rick Lane, Bill Martin, (2010).  Why Complex life probably evolved only once; NEW SCIENTIST 12:52 21 October 2010 by Michael Le PageGabriela P. Finkielstain, Patricia Forcinito, Julian C. K. Lui, Kevin M. Barnes, Rose Marino, Sami Makaroun, Vina Nguyen, Jacob E. Lazarus, Ola Nilsson, and Jeffrey Baron, (2009).  An Extensive Genetic Program Occurring during Postnatal Growth in Multiple Tissues.

Endocrinology. 2009 April; 150(4): 1791–1800. Published online 2008 November 26. doi: 10.1210/en.2008-0868.

Irina M. Conboy, Michael J. Conboy, Amy J. Wagers, Eric R. Girma, Irving L. Weissman & Thomas A. Rando (2005), Rejuvenation of aged progenitor cells by exposure to a young systemic environment.  Nature 433, 760-764

Andrew S. Brack,  Michael J. Conboy,  Sudeep Roy,  Mark Lee,  Calvin J. Kuo,  Charles Keller, Thomas A. Rando, (2007).  Increased Wnt Signaling During Aging Alters Muscle Stem Cell Fate and Increases Fibrosis. Science 317 (5839): 807-810

Reznick, D., C. Ghalambor, and L. Nunney.  The evolution of senescence in fish.  Mechanisms of Aging and development. 123: 773-789.

Jicun Wang, Thomas Michelitsch, Arne Wunderlin & Ravi Mahadeva (2009), Aging as a consequence of misrepair - A novel theory of aging. Nature Precedings, hdl:10101/npre.2009.2988.3

BERGAMINI, E., CAVALLINI, G., DONATI, A. and GORI, Z. (2007), The Role of Autophagy in Aging. Annals of the New York Academy of Sciences, 1114: 69–78. doi: 10.1196/annals.1396.020Finch, Caleb E.; "Senescence, Longevity, and the Genome" (1990). The University of Chicago Press, Chicago and London.  Page 240 4.5.2Mitteldorf, J. (2004). "Ageing selected for its own sake" (PDF). Evol. Ecol. Res. 6: 937–53. On the tension between experimental data and evolutionary theory. Bredesen DE (October 2004). "The non-existent aging program: how does it work?". Aging Cell 3 (5): 255–9. doi:10.1111/j.1474-9728.2004.00121.x. PMID 15379848. More on the tension between experiment and theory.  Speaks to evolution of delayed reproduction in snapping turtles. 

20. Norman E. Sharpless1 and Ronald A. DePinho2 Telomeres, stem cells, senescence, and cancer J Clin Invest. 2004;113(2):160–168. doi:10.1172/JCI20761.

Who-Seung Lee, Pat Monaghan and Neil B. Metcalfe, Experimental demonstration of the growth rate–lifespan trade-off,Proceedings of the Royal Society B, 2012, DOI: 10.1098/rspb.2012.2370 (open access)


Authors Note:  

I elected to self publish this paper and its two sister papers, Growth Termination and Scale, and The Evolution of Selection , for several reasons.   Firstly I wanted the ability to update and refine the paper and its concepts frequently within a medium that can document all of the changes that have occurred over time.  Secondly I wanted a medium in which I could utilized hyperlinks as a way to provide references that are more convenient to the reader than traditional references.   Thirdly I published on the internet because I wanted a medium in which search engines can be leveraged to provide ever improving indexing and search capabilities over time as the concepts expressed in the papers evolve.   Google and other search engines are employing ever more effective artificial intelligence technologies to improve their search results.  So, it is my expectation that the concepts expressed in these three papers will be continually more differentiated from the corpus of evolution and aging theory papers as search technology advance.  Search technologies in the near future I expect will go substantially beyond basic keyword indexing and begin to map and contrast the conceptual meaning of content even when different papers are using dispirit language and different metaphor with which to describe similar concepts,   As this technological change occurs I am confident, that individuals looking for new or different conceptions of evolution and aging theory will be served these papers.    And lastly because the concepts presented in this paper deviate greatly from conventional evolutionary thought at this time, I have elected to self publish  to be free myself of editorial review that can and often results in considerable publication delay and sometimes de facto censorship.  I am prepared instead to allow the reader and the passage of time to judge the merits of the ideas I have presented.      


Supplementary Material

Note: Supplementary Material is still in draft and under active edit.

The Evolution of Death Mechanisms

Asexual Reproduction and Death Mechanisms

It has been proposed by Nick Lane in his book titled "Life Ascending" and others that cellular death mechanisms are required in the creation of complex life forms for the production of differentiated tissue types.  But why would this be the case, since cells show great capacity to de-differentiate, re-differentiate and migrate to needed locations to build and grow the complex body form.  However,  I do agree with Nick  that death mechanisms at the cellular level and at the level of the multicellular individual evolved as a way to deal with parasites.   Here I go further to propose that death mechanisms evolved specifically in organisms as a direct consequence of the asexual reproduction strategy and as a result, mechanisms of death, senescence and negligible senescence have all been profoundly molded by asexuality.  

Many obligately asexual species today are recently derived from sexual species and utilize remnants of the remaining sexual apparatus to accomplish asexual reproduction.  These species are not the ones under discussion as they are not the precursors to the evolution of sexual species and do not account for the evolution of mechanisms described here.  

It has been proposed that the cellular death mechanisms employed by single cellular life as a defense against viral and bacteriological parasitism were simply modified for use by the very first multicellular organisms to accomplish death of the multicellular individual as there should have been strong selective pressure due to the likelihood that all of the cells constituting the individual were likely infected as well.  

Asexual Clones and Death

From the perspective of the selfish gene metaphor, since all member of a clone of asexual individual can stand in for any and all other individuals in in the clone relative to reproduction, the death of any subset of individuals in the clone that prevents the extinction of the entire clone is adaptive and should be selected for.  Therefore it is adaptive for any individual in a clone that becomes infected by a parasite to kill itself to stop further spread of the parasite.   This I propose is the driving logic behind the evolution and persistence of death mechanisms.  Since obligately sexual organisms are not capable of employing this kind of selection logic, I propose that death mechanisms predate evolution of sexual reproduction and that sexually reproducing species have co-oped and modified preexisting death mechanisms for their use and in the production of mechanisms of senescence.  

Asexual Clones and Negligible Senescence 

Individuals of a obligately asexual clone that reproduce by budding for instance can only effectively employee death mechanisms as an effective strategy if other members of the clone do not utilize death mechanisms and do not have finite life spans thus ensuring the continued reproduction of the clone.  Therefore I propose that death mechanisms and negligible senescence  co-evolved as complementary mechanisms in the same asexual species, as both capabilities must exist in the shared genotype across all the individuals to ensure the rationality of death mechanisms as a way to counter parasitism.  

I propose that the initial complementary co-evolution of death mechanisms and unlimited life span or negligible senescence has persisted to this day within the same species and accounts for the high degree of plasticity of lifespan as has been demonstrated over short periods of evolutionary time in nature.  

Sexual Species and Death Mechanisms

Within clonal species from cyanobacteria to much more complex forms mass dyings of individuals within the clone are well known and the logic of this can be understood as an effective strategy against predation or parasitism, etc, however In obligately sexual species no individual can represent the complete reproductive interest of the entire phenotype of another individual unless they happen to be an identical twin.  For this reason the  selection pressure for the maintenance of viable death mechanisms for the purposes of protecting other individuals that can reproductively stand in for the sexual individual does not exist.  Therefor other sources of selection pressure must be employed to account for the specific form and  persistence of death mechanisms, senescence and negligible senescence exhibited by sexual species and is the next topic considered.              

Death Mechanisms as Implementation of Trans-Generational Fitness Algorithms

Just as the individual is employing mate-selection to obtain the  appropriate balance of altruistic traits in prospective mates which enhance the fitness of progeny  against the selfish traits that favor the adult survival of prospective mate and progeny,    

This strategy also dependent on the selected mate and shared future progeny actually manifests these traits and behavior, whether they be care of the young or the implementation of death mechanisms at the appropriate time and place.  

If, as I propose, the implementation of these death mechanisms in modulated neurologically, is there a opportunity to modulate the action of these death mechanisms and senescence in general at the neurological level or must intercession occur at the level of neuro-hormonal interface or is one of these loci of control layered on top of the other?

Death Mechanisms And Their Modulation

Just as semelparous animals harbor death mechanisms, once iteroparous animals have senesced to a threshold level,  Trans-Generational Selection favors total resource conservation or complete termination of resource consumption.   Said another way, I propose that trans-generational selection favors the evolution of death mechanisms  that  are activated once the individual reaches a threshold level of senescence.  For example once senescence has compromised the immune system to a major degree disease in a very old animal can threaten other individuals, death mechanisms are adaptive to efficiently remove these individuals at this time.

Diseases of Aging As Death Mechanisms

It appears clear that fundamental actions of the IDM and TDM are at the root of many diseases of aging such as cardiovascular disease, immune competence  diseases such as cancer, and skeleto-muscular diseases.  It has been demonstrated actuarially that senescence is the most important risk factor in the manifestation of these causes of death. Therefore, within the paradigm in which senescence is at its root senescence is genetic and selected for, all of the major causes of death in humans can be seen to be overt death mechanisms.

Digestive System Senescence as Death Mechanism

Consistent with concept that the goal of transgenerational selection constitutes resource conservation by the adult, many animals path to death is mediated by failures of some aspect of the digestive system.   Elephants lose the ability to feed after they wear out their last set of molars, pelicans lose the ability to feed when their stomachs fill with fish bones, and  octopus are hormonally driven to stop feeding.  Now new research reported by Michael Rera, Rebecca I. Clark, and David W. Walker in an article titled Why old flies die, published In the online journal Impact Aging, report that the cells lining the intestinal tract of Drosophila melanogaster senesce reducing intestinal permeability and therefore reduce the assimilation of nutrients from food.  

Neurological Modulation of Senescence and Death Mechanisms

Though the death mechanisms that I have just described can act to some extent autonomously. I propose that the IDM and TDM based mechanisms of death have evolved under, and in most instances remain under neurological control.  The rationale for this is that sexually selected traits such as these lifespan modulating death mechanisms evolved as a consequence of trans-generational selection pressures and as a result emerge from the processes of mate-selection.   At a fundamental level locomotion, the moving toward a selected mate and away from deselected mating options is essential to mate-selection   Even though it can be argued that mate-selection can result from following chemical gradients diffused in the environment this system must inform some aspect of the neurological system which is required to integrate the sensing of the chemical gradient with complex muscular actions which are required to bring the individual into proximity with its source.   Based on this logic all mate-selection processes including trans-generational selection processes are mediated by neurological processes.

Selfish, Virally Derived Genes and Aging

It seems plausible to me that genes that are derived from viruses such as elements of the vertebrate immune system, even those originating deep in the evolutionary past will be selected for based on their ability to recognise (in some fashion) that the host cell is dying.  In this event it seems reasonable that these genes will attempt to initiate processes that will lead to their expression as phage particle so that they can escape the dying cell.  This process should occur even if they no longer have a complete and intact genetic apparatus with which to implement and complete the process successfully as many genes “decay” very slowly in evolutionary time.   If correct, this could explain why we see such unusual patterns of exaggerated gene expression is aged tissues.  One way to examine this potentiality is to compare expression rates in aging cells of genes that do not have viral origin with those that do.  

If this idea is correct, then these aberrant  gene expression patterns that are characteristic of aging are not causes of aging as some recent theories propose such as the Transposon Theory of Aging suggest.   Rather they are a response to a more fundamental aging process that is already proceeding in the cell.  Considering that VCAM-1 proteins are immunoglobulins and as a result have a viral origin, their over expression in aging animals may not be a foundational cause of aging in vertebrates but simply be an expression of the action of selfish genes to an already aging environment.

Optimism and Longevity

 Centenarian studies demonstrate that populations of very old humans are unusually rich in people with a high degree of optimism, a sense of abundance and other physiological traits that collectively can be viewed as the opposite or at least inconsistent with the modalities of depression.  This correlation is further supported by the failure of these same studies to find a strong set of  physiological reasons for long life span in humans that is common across the population of individuals in these studies.  Additionally, centenarian studies have demonstrated that these individuals share life style habits such as smoking, drinking alcohol, and the consumption of what is believed to be unhealthy diets that is similar in scope and magnitude with the rest of the population of people that experience much shorter lives.  

If optimism is a driver of extended life-span, what actually constitutes this attribute, as a physiological phenomenon?   For clarification,  it has been defined at the conviction of the individual  that events will unfold in the future in a favorable or "optimal" way for the same individual.  From this it can be seen that an individual that concludes that the adversity it may presently be experiencing will be short lived and that the current circumstances will result in positive events in the future.  So when an individual is optimistic and as a result arrives at such a conclusion it is then rational that the individual  takes actions to preserve itself for the future.  However if an organism is more pessimistic in the same situation it may rationally conclude that adversity will continue and that it makes sense to invoke death mechanisms as part of its trans-generational fitness strategy.   I propose that the action taken by an organism that has determined that they cannot be optimistic about the future is to invoke a state of mental depression.  I propose that mental depression when left unchecked is the mental state that initiates a cascade events that invoke death mechanisms.  

Depression Driven Death Mechanisms

The up-regulation of the IDM and TDM is not the only type of death mechanisms that can evolve under trans-generational selection pressure, the increase in mental depression can both driven by the action of the IDM and TDM but can possibly be driven independently of these mechanism, such as by infectious disease or heavy metals for example.  In either case, increasing rates of mental depression which undergoes an initial spike at sexual maturity, seems to have the ability to precipitate a cascade of events that culminates in death in mammals, via a variety of modalities, at a rate that is much faster than would happen in a senescing animal that is not experiencing mental depression.   Many in the biomedical community has speculated on the how mental depression could be an adaptive or beneficial trait in the individual.  If depression is as I propose, a trans-generationally selected trait, this line of reasoning is misguided in that this adaptation favors progeny and disfavors the adult individual.  The biomedical community needs to rethink the causal foundation of the diseases of aging, including all diseases that increase at sexual maturity, and rethink how these diseases as a result may be most effectively treated.  


End of Chapter on Death Mechanisms



Modeling Aging via Computer Simulation


Justification For Modeling Aging Using a Specific Set of Controls and Attributes

The computer program for modeling aging that I have been developing over the past two years is founded primarily on the common condition in nature that the adult-lifespan of a species is positively correlated with the length of gestation period and the length of the juvenile period. I feel that this approach is strongly supported by the evidence I have presented above.   The correlation between these three life periods in my model of aging have proved pivotal to the persistence of aging in  modeling iteroparous animal species and helps to explain the relationships of these life periods in natural populations .   A strong linkage among these three life periods have proved critical in my computer model in the demonstration of  a downregulation of the aging rate when predation rates fall and an upregulation when predation rates rise.  This dynamic relationship among these three life periods is consistent with what is observed in nature.

End of Computer Modeling Chapter


The Thymus and Aging

The thymus development in the fetus of all jawed vertebrate animals is controlled by FoXN1 type proteins.  At puberty or sexual development FOXN1 drops and as a result the thymus starts to involute or shrink.   This fits my model of down regulation of growth, as this protein drops in production as well.  This must be under the control of the hypothalamus in some way.  

So with the deceleration  of growth to the point of growth termination can bring with it a general reduction in the production of all signaling factors in the body.  

Telomere Length and Aging

Considering that naked Mole Rats do not possess long telomeres, it seems less than likely that this is a foundational cause of aging in mammals.  

Aging in Fish

Fishes show three types of senescence. Lampreys, eels and pacific salmon exhibit rapid senescence and sudden death at first spawning. The guppy, red panchax, medaka, platyfish, Indian murrel and many other teleosts undergo gradual senescence, as observed in most of the vertebrates. A number of fishes (e.g. sturgeons, paddlefish, female plaice, flatfish, rockfish) show indeterminate growth, the occurrence of senescence in them is supposed to be very slow or negligible.

Patnaik BK, N Mahapatro, and BS Jena. 1994. 'Ageing in fishes' Gerontology 40:113-32

Senescence Modulation, A Network Or Hierarchy

As described, there are overt death mechanisms which can be invoked by extrinsic factors or by senescence.  So the question remains in the quest for the complete understanding and remediation of aging, is there a single foundational cause or physiological driver of aging or is there a network of multiple causes which can not be separated and  redefined as a hierarchy?  I propose that the malleability of rates of aging as has been demonstrated in breeding experiments across the phylogenetic landscape points to a hierarchy.   I would argue that a true network of controls would not allow the flexibility and rapidity of change in length of lifespan as has been demonstrated in worms, flies, fish and possums and dogs etc.

If we are dealing with a true hierarchy then I feel we should be looking for a single mediator that communicates information from a mechanism that integrates, time, animal vigor and transgenerational fitness, in its modulation of the rate of senescence.  As I have previously expressed, experimental evidence  supports the idea that this mediator is a soluble evolutionarily highly conserved morphogenic type substance that when expressed at high concentrations prevents senescence.

Chronic Stress and Aging

What does the individual use to accurately assess the rate of aging of prospective mates,?  I propose that across animal species, stress hormones that are produced as a response to chronic stress constitute a good proxy for rate of aging as these substances seem to mediate the aging process.  Therefore the mate selecting individual should be able to assess the relative aging rate of prospective mates by determining  the concentration of stress hormones externally expressed by prospective mates and compare these concentrations to their own.  

So what does this accomplish?  It can be assumed that stress response and rates of aging vary to some degree in a population in a given environment, so if an individual selects for mates that exhibit  hormone concentrations that are indicative of chronic stress that is  somewhat higher than it's own levels of the same hormones it will have the effect of producing progeny that terminate growth sooner,  mature faster, and age quicker in the next generation.  if the individual selects mates that exhibit stress hormone concentrations that are less than its own when environmental stress is low, and hormone concentrations greater than its own when the environmental stress it is experiencing is high then it will be using a simple algorithm to produce offspring that are better adapted to a life that likely to be more or less stress filled at the time the individual executed its mate-selection strategy.

It should be noted that this strategy/algorithm of mate-selection is an evolutionarily stable strategy (ESS) as it invests both the selecting mate and the selected mate to select-on and display these attributes explicitly and honestly as their expression and detection both favor the survival of offspring.    

The Island Rule

So lets consider how this applies as an explanation of the Island Rule, which is the phenomena in which small animals grow much larger and live longer on isolated islands and large animals grow much smaller, over generational time.    Small animals that are isolated on islands that are devoid of predators experience lower stress through the elimination of threat of predation and as a result have lower stress hormones.  So applying my stressed based mate-selecting algorithm the mate selecting individuals will be selecting individual with even lower stress hormone levels , these offspring should on average mature more slowly and as a result grow larger and live longer.    For large animals isolated on relatively small islands, food and habitat limitations will leave the population in a chronically stressed state which will drive mate selection toward mates that exhibit higher levels of hormones indicative of chronic stress than the selecting mate and drive the evolution of the population toward faster maturation,  smaller size and faster aging.    

Mate-Selection And Dimorphism

Sexual Selection has been seen as processes that drive sexually dimorphic traits, I have used the term Mate-Selection in this paper in part to draw the distinction that Mate-Selection is not so constrained.  When a female animal selects for senescing mates it is in her interest to pass this trait on to both her male and female progeny.    A female that can discern whether a prospective mate's senescence is sex linked will be more successful than a female that does not make such a distinction and as a result selects mates with sex linked senescent traits which will fail to be expressed in the phenotype of it's female offspring leading to negligibly senescent females in the species.  

Juvenile Growth - An Echo of Negligible Senescence

Why do the majority of animals species fail to become reproductive immediately after birth, or put another way, how do we account for the evolution of delayed reproduction in senescent and non-senescent species alike?  For example, some whale species produce offspring that are far larger at birth than the size attained by other closely related species over their entire lifetime, yet the majority of species defer reproduction during much of the growth period?   The answer to this question is that the period of growth up until sexual maturity is a strong example of the negligibly senescent continuous growth phenotype described earlier.  

The mechanisms that determine and favor the reproductive behavior of negligibly senescent growth-non-terminating animals also disfavors immediate reproduction during growth in the juvenile phase of senescent species.  As growth decelerates during puberty, reproductive capacity then begins as it is no longer beneficial to defer reproduction.  Additionally, delayed reproduction facilitates the ability of individuals to select mates on the merits of fully mature phenotypes which constitutes a less speculative strategy for mate selection.  

Lastly, as individuals of most species select for a senescing phenotype as one of the selection criteria when choosing mates, as this is an indicator of transgenerational fitness enhancing traits, the individual generally need to wait until the end of the growth phase to accurately assess if a potential mate possesses a senescing phenotype.  This mate selection process renders early reproductive capability detrimental to the individual as it diverts resources away from growth and its incumbent fitness advantages.  

Maturation Signaling Driving Senescence

Just as juvenile growth is an echo of negligible senescence I propose that sexual maturation drives the production of the signaling that drives senescence of both the TDM and IDM types.   I propose that at sexual maturity the neural-endocrine system reduces the production of soluble growth/differentiation factors that drives senescence through epigenetic processes.  This hypothesis is supported by two animal models a jellyfish and a beetle that have the ability to avoid senescence by repeatedly returning to the juvenile morphology and then back to the mature sexual morphology.  It seems reasonable that just as stress is the element in the environment that triggers conversion from asexual reproduction to sexual reproduction in some species that are capable of doing both, physical and physiological stressors seem to play a pivotal role in triggering sexual maturation and senescence in obligately sexual animal species.

Mate-Selection And The Rate-of-Aging

With aging, as I propose, a mate selected trait then such selection cannot be a binary choice made by mate-selecting individuals on the basis of prospective mates exhibiting markers of senescence or not.  Instead I propose that individuals select mates on the basis of the rate of aging that is optimal for the selecting individuals reproductive goals.  It seems unlikely that individuals are selecting mates on the basis of the degree of senescence or on the basis of the number of senescent traits as this would not inform the individual as to the expected life span being passed on to its offspring.  The rate of aging is the attribute that the selecting individual needs to be selecting on if it is to optimize the life span of its progeny and if it is to pass the same ability to discriminate rate of aging onto its progeny.  

Indicators of Aging Rate

So what can an individual use to determine the rate of aging of prospective mates if the accumulation of senescent traits is not indicative of rate of senescence and lifespan?    I propose that one possibility is that the selecting individual is determining the rate of aging by evaluating the concentration of one or  more hormones or hormone like substances which are  outwardly expressed and are readily discernible by prospective mates.  

It is clear that a  life span that is totally determined by genetics is not fully optimal because the environment can change significantly in single a generation dramatically changing the optimal life span of the affected population.  Therefore it seem likely that the factors that are determining the rate of aging across species should be subject to some degree of up and down regulation as a result of environmental and epigenetic factors.   This conclusion speaks for regulation of aging rates by neurological processes which are the processes most able of aggregating all of the factors that are capable of computing the optimal life span of a species in a given environment.  

Plants And Senescence

Most perennial plants species do not employ growth-termination as a strategy to avoid a reduction in fitness.  As a result many plants appear to express negligible senescence until they exceed a specific size.  Perennial plants tend to grow until they die and unlike animals many plants die as a direct consequence of growing past their optimal size.  Tree core rotting, uprooting, lightning strikes, desiccation of the upper-most branches etc, are examples where large size can negatively effect fitness.   In support of this observation, it has been demonstrated in a paper found in Exp Gerontol. 2001 Apr;36(4-6):651-73. titled "The paradox of great longevity in a short-lived tree species."  that even in species considered to be short lived individual trees can live to extraordinary ages of more than 1600 years when their growth rate is slowed and their size remains smaller than that of standard trees of the species.  

The prevalence of negligible senescence in plants also supports the primacy of the role of Mate-Selection in senescence.  As with sessile animals, the sessile nature of plants limit interaction with mates to contact and selection of gametes.    As a result, plants are unable to employ Mate-Selection mechanisms in the evaluation of  the phenotype of their prospective mates to determine if they are senescing,  however  mate-selection is to some extent provided indirectly via insect and animal pollinators though they do not share the same evolutionary agendas for the plant species.   As a result, sufficient selective pressure is not brought to bare on iteroparous plants leaving them unable to evolve or maintain the genes capable of producing a senescing phenotype.  

Appendix A.

Depicting  Metabolism And Senescence

Figures A, B, C, E, F, and H, found here in the supplementary material are used to diagrammatically represent my speculations on the relationships between the anabolic processes of biosynthesis and growth the catabolic processes of autophagy and senescence across various conditions and life histories.  

Figure A.   The Meaning of Cell Repair

Figure A, depicts the mutually exclusive relationship between anabolic cell growth and the catabolic processes of autophagy and apoptosis.  When a cell is engaged in the anabolic process of protein synthesis it is being primarily driven by the insulin/IGF-1 axis, when insulin/IGF-1 concentration is low the cell will be experiencing a greater amount of autophagic activity.   Point A. in the figure above represents the average metabolic state when the cell is involved in anabolic operations, and point C. represent the Cell in its average catabolic state of autophagy.  

Point B above represents the combination of the two states and illustrates the average state of the cell by combining the anabolic and catabolic processes of one complete cycle.  The location of the point relative to the boarder of constant size indicates whether the cell is, growing, shrinking or remaining the same size.  In this specific case point B. depicts a cell that is growing.  

Figure B.         Biosynthesis Autophagy & Senescence

The blue line that bisects Figure B. designates the Boarder of Constant Cell Size, this line depicts the plot of possible equilibrium points that represent a balance between the various levels of anabolic and catabolic activity associated with autophagy and biosynthesis that results in no change in size of the cell over time.  This blue line also depicts increasing metabolism and increasing resource utilization as you move away from the origin.

The red asymptotic line defines the upper boundary  of the "Zone of Senescence" which is the various ratios of anabolic to catabolic activity that defines the threshold or boarder for the accumulation of senescent traits.  The Zone of Senescence reflects the fitness discounting activity of the IDM, where as  above and to the right of this line represents cell that will not be accumulating senescent intracellular components.  

Located as shown, the red dot illustrates an average state in which metabolic resources are being conserved by reducing the catabolic and anabolic functions that constitute intracellular repair, driving metabolism into the zone of senescence.  The location of the red dot within the graph also illustrates a state of "metabolically discounting the future".  Shown below the blue line, the Red Dot also depicts a state in which a slight reduction in cell size is occurring over time.

B. Optimized Senescence

Figure B. above also makes clear that if the sexually mature growth-terminated organism is not senescing while maintaining a near static size then fitness of the individual is likely not being discounted optimally and fitness of progeny is not being favored optimally as well.   This state in a hypothetical species could be an indication that natural selection has not yet had enough time to drive the optimization of the IDMs resource conservation mechanisms, in the species.   This condition could arise when a growth-terminating species has recently evolved from a negligibly senescent continuously growing species.   The Blanding's Turtle could be such a species.  

The Discount Rate of Senescence

The "Discount Rate of Senescence" is a term intended to connote that a mechanism exists within the IDM and TDM that establishes a species specific rate of accumulation of senescent traits or generally this concept can be thought of as  the species specific rate of aging.   Experimental verification will be required to determine the complete list  of parameters that control the rate that natural selection and more directly Trans-Generational Selection discounts future fitness of the individual.  Until such time here is a short list of items that potentially could calibrate the Discount Rate of Senescence:   This list consists of, mortality rate of young adults, the length of the reproductive cycle, and the productivity of the average individuals reproductive cycle.  

Figure C.  illustrates graphically the effects on intracellular repair as the organisms growth phase is terminated and replaced by an equilibrium of the anabolic (biosynthetic) and the catabolic (autophagic) rate of cellular repair which results from the action of an IDM that is insufficient to prevent the accumulation of senescent traits.  

Figure C.   Example of Senescent Iteroparous Animals

Figure C. above provides an example of the metabolic shift undertaken by a growth terminating iteroparous animal.  The upper red dot depicts the growth phase of the animal and the lower red dot represents  the process of growth-termination within the Zone of Senescence.  The distance the red dot moves down into the zone of senescence, relative to its position during growth defines the quantity of resources that are being conserved for potential use to support the Trans-Generational Fitness or the present and future fitness of progeny.  The (x,y) distance that the metabolism of the animal resides below the boundary of the zone of senescence along the blue line  indicates how strongly a species discounts individual fitness in favor of Trans-Generational Fitness, as growth decelerates to the point of growth-termination.  

Figure H.    Negligible Senescence And The Allocation of Resources

Figure H.    Continuously Growing Negligibly Senescent Animals

The two yellow points in Figure H above represent the metabolic growth and repair characteristics exhibited by a negligibly senescent continuously growing animal that is iteroparous.  The point labeled POIR is the point of optimal iteroparous reproduction.   In this example, the animal will, during a reproductive period, exist physiologically just above the zone of senescence on the line of equilibrium between growth and repair processes in order to optimize reproductive capacity as this is the point that maintains negligible senescence while exploiting a  minimum of resources.   During non-reproductive times the animal will exist at the higher point favoring anabolic processes driving growth through the utilization of the stem cell derived parenchymal cell proliferation.   Growth and repair position cycling depicted by the double headed arrow above the Zone of Senescence optimizes current reproductive capability while preserving future reproductive capability.

Figure F.  Simultaneous Growth And Senescence

Figure F.   The movement of the Red Dot over evolutionary time towards the upper left position depicts natural selection favoring a mechanism by which a species evolves toward  faster growth and early sexual maturation by lowering the rate of autophagy and up-regulating biosynthesis.  Note that faster growth is achieved without any increase in energy demand, however the animal is subjected to faster rates of senescence.   It has been reported that this does occur in guppies and it could occur in other short lived fast growing vertebrates such as opossums.    Under different conditions, when the mortality rate of young adults is lower, nature selection can favor mechanisms the drive the ratio of biosynthesis to autophagy towards the ratio expressed by the lower Red dot, which in this example produces slow growth without accumulation of senescent cellular constituents.  

The concepts illustrated in Figure F are also supported by the research of

Who-Seung Lee,

Pat Monaghan and

Neil B. Metcalfe at

University of Glasgow in a paper titled, "Experimental demonstration of the growth rate-lifespan trade-off" suggests that lifespan is affected by the rate at which body's grow early in life: manipulating growth rates in stickleback fish can extend their lifespan by nearly a third or reduce it by 15 percent.  The team from the University’s Institute of Biodiversity, Animal Health and Comparative Medicine altered the growth rate of 240 fish by exposing the fish to brief cold or warm spells, which put them behind or ahead their normal growth schedule.

Appendix B.  General Considerations  

Programmed Cell Death and Negligible Senescence  

It is conventional thought that apoptotic and autophagic based forms of Programmed Cell Death (PCD) play a significant role in the generation of senescence.  However, evidence is often overlooked that PCD can be both positively and negatively modulated through a broad variety of initiating events, some of these initiating events has the effect of applying PCD as a critically important component in anti-senescence mechanisms as proposed in this paper. In support of this idea, it has been demonstrated that IGF-1 levels are inversely correlated with life span in many organisms, while it has also been demonstrated that  IGF-1 inhibits autophagic and apoptotic activity. 

Negligible Senescence cannot be achieved in complex organisms through growth alone because the "mutational ratchet" will incrementally compromise the fitness of the individual with the continuous cell division that is required for non-terminating growth .   The elimination of genetically defective cells is required to maintain the integrity of the organism over extended periods of time.   Random mutational events, free radical damage, viral infection and other assaults, drives the tissues of organisms to perform PCD to eliminate cells with altered DNA.  Apoptosis and some forms of autophagy provide this function.  The cells eliminated through PCD are replaced by the same feed-stocks of cells that are used in tissue growth as described previously.  

Evidence For Stem Cell Regulation Via Systemic Factors

Stem Cell Differentiation in Growth-Terminated Animals


Once the growth period in animals is terminated, populations of stem cells have been shown to differentiate into fibroblasts at a higher rate than normal,  which is consistent with our lifelong anecdotal observations of senescence.  Due to the body's attempt to maintain tissue size, the continuing intrinsic apoptotic activity sustains the demand for new functional cells within tissues.   However, even a slight reallocation of stem cells away from the functional tissue-specific cell types and toward the fibroblast differentiation pathways results in a progressive fibrosis of tissues.

This concept is supported by the laboratory of Edden Heber-Katz which as demonstrated  that p21 gene knockout enables tissue regeneration is mammals such as the MRL mouse.   Blood factors that result from the elimination of the functioning of this gene have been shown to elicit the same regenerative capability in non-p21-knockout mice.

Why A Non-Senescing GTM Is Rare

Why isn't  it common to find that a non-senescing GTM has evolved in growth-terminating species which experience a very low mortality rate in young adults?   Ultimately the answer to this question comes down to the need to mitigate the trans-generational selective advantage of discounting the fitness of the individual.    The only way to marginally dis-favor Trans-Generational Fitness is to ensure that future fitness of the individual is greater than present fitness of the individual, or said another way, that the fitness of the individual increases with time.  

Since all genomes are finite morphological change within the individual cannot be relied on for continued increases in fitness over time, the only obvious way for growth-terminating species to tip the balance in favor of future fitness is through building up resources that can be used to produce continued incremental improvement in fitness over time.  The organisms that might possibly be performing this increase in fitness of the individual over time, via the accumulation of resources and without continued growth, are humans and some social insects.  

Social insects have achieved significant extensions of life-span within the constraints of  growth-termination, however this may have been achieved through very slow non-terminated-growth as the long lived reproductive individuals are much larger than the shorter lived non-reproductive individuals.  With respect to humans, sufficient time may not have passed since the beginning of, the agricultural revolution, education, and culture, to have facilitated the accumulation of resources sufficient to drive a mechanism that discounts present fitness and as a result favor the evolution of a non-senescing GTM.   Few if any other animal species accumulate enough resources over time sufficient to demonstrate continued improvement in individual fitness.   This is what we would expect based on the rarity of negligibly senescent growth-terminating species.    Growth-termination is a high evolutionary barrier  to the achievement of negligible senescence.  

The Persistence And Regulation of Senescence

To describe the role of the IDM and the TDM as the primary mechanisms of senescence does not provide a complete explanation of the phenomena.  This section provides possible additional mechanisms for the persistence of senescence and describes factors and potential mechanisms for the species specific regulation of the rate of senescence.

Cheating Senescence

Theories of Aging have long struggled in their attempt to provide a viable explanation as to how and why individuals do not "cheat" by evolving life-spans that significantly exceed the species specific life span.  This has been a persistent problem in aging theory given that it has been shown repeatedly that point mutations in single genes that render some specific proteins ineffective results in significant increases in life span in many species.    

This paper makes clear that this problem is based on the false assumption that the self interest of the individual is the controlling metric.   It is the self interest of the individual  to ensure that future generations of its species continue to senesce.   Toward this end  the individual applies mate selection criteria to select for longevity traits in mates that do not exceed their own longevity.  When point mutations occur that increase lifespan in the individual, the trait is breed out of the population through the application of Mate-Selection criteria that favor Trans-Generational Fitness and as a result select against greater longevity.

Overtly Senescent Traits Are Indicators of Trans-Generational Fitness  

In support of the concept that Mate-Selection effectively removes point mutations that increase longevity, it is proposed that overt markers such as graying hair have evolved to act as accurate indicators of the existence, rate and strength of senescence, and as such act as a metric that guides Mate-Selection processes to efficiently select mates with traits that favor Trans-Generational Fitness.  In support of this it has been demonstrated that skin stem cell lines associated with hair follicle are know to senesce while other skin stem cell lines do not show replicative senescence.  

Self Reinforcing Longevity Phenotypes

The Sensibility Of The IDM And The TDM As The Cause of Senescence

Why is it not obvious that growth-termination is a primary cause of senescence and why has it taken so long to arrive at this conclusion?   One reason could be the coexistence of similar species some which demonstrate negligible senescence while others demonstrate senescence and still others demonstrate semelparity, seemingly within similar niche.  This picture is confused further by the variability of lifespan in similar species, and by the observation that many closely related species can differ greatly in size.  

Though it is not possible to define the conditions under which each species evolved, this paper provides an explanation as to why convergent evolution has not eliminated the diversity of these, persistent, yet seemingly opposite phenotypes.  MSSA proposes that convergent evolution does not occur among these species because these phenotypes are composed of synergistic trait pairs which endow the species with the capability to resist selective pressure to change.  

Persistence of Senescent and Negligibly Senescent Phenotypes

Synergistic trait pairs illustrated in Figure F. below, provides an explanation for the persistence of these disparate phenotypes to resist selective pressure for convergence.  For a species to convert it's phenotype from the trait pair consisting of continuous growth and negligible senescence to one that exhibits the trait pair of terminated growth and senescence, the species has to assume a trait pair of continuous growth and senescence as a transitional phenotype.  This trait pair effectively dedicates excess resources to vegetative growth without increasing the fitness of the individual.  This phenotype disfavors Trans-Generational Fitness without greatly improving individual fitness.   Therefore, this transitional trait pair confers less fitness than either of the other two trait pairs and as a result it is negatively selected for.  

The same logic applies to the transitioning of a species from a growth-terminating senescent phenotype to a continuously growing negligibly senescent phenotype, the species must pass through the transitional trait pair phenotype.   On a population basis negative selection of the transitional phenotype constitutes a "Transition Barrier" stabilizing the non-transitory phenotypes as depicted in Figure D below.  The magnitude of this transition barrier accounts for phenotypic persistence in similar species  across the spectrum of phenotypes from negligibly senescent, to senescent, to semelparous.  

The other possible transitional trait pair, growth-terminating and negligibly senescent,  does not mitigate future risk as well as the continuous growth phenotype and it does not maximize Trans-Generational Fitness as effectively as the growth-terminating senescent phenotype.  

In Figure D. below, the transitional trait pair are negatively selected-for relative to the other trait pairs as shown in the boxes labeled A and B.   In the non-transitional trait pair each trait drives natural selection to favor their partner trait in the pair.  The curved arrows in the green shaded boxes below depict the reinforcing aspect of the phenotypic trait pairs.   The figure also depicts the role DES plays in determining which phenotype is utilized by a given species.  

Figure D.         DES Actuated Self-Stabilizing Phenotypes


Figure D, illustrates how changes in the magnitude of the DES's (bottom arrow) imposed on the organism by modification of their niches represents the specific type of selective pressure that can drive the evolution of the species enabling it to transition across the phenotypic barrier to the alternate self-stabilizing state. Morphological change also can cause increases or decreases in the DES's acting on the organism.   The  MSSA proposes that morphogenic change can also cause organisms to repetitively transition between the two stable states over evolutionary time.   These transitions can be driven by morphological change just as it can be driven by environmental change.   Multiple transitions between these two stable phenotypes will have the effect of cleansing the genome of "disposable soma" and antagonistic pleiotrophic type mutations.  

The Semelparity Hole

Another example of self-stabilizing phenotypes is semelparity which is a more extreme example of a growth-terminating senescent phenotype.   This trait confines reproductive opportunity to a single event and as a result drives natural selection to minimize cellular repair to the point that large reductions in predation and large reductions in DES cannot tip the balance toward another phenotype.  Such a phenotype is essentially a self-reinforcing lock-step, since once established, the organism essentially incorporates into its genome a very high mortality rate in young adults.  This will permit the inclusion of many disposable soma and antagonistic pleiotrophy type deleterious changes to the genome that further precludes improved fitness via increasing cellular repair.   Any improvements in cellular repair will detract from the resources that can be dedicated to the only reproductive event that can occur and so will be strongly selected-against.   Semelparity represents a very strong bias towards Trans-Generational Fitness at the cost of individual fitness.

Figure E.         Metabolic Characteristics of Semelparity

Figure E, provides an example of the semelparous animal such as the pacific salmon.  At sexual maturation the metabolic parameters change migrating along the trajectory of the arrow which depicts the animal strongly conserving both the anabolic and catabolic activity of cellular repair.  It should be noted that the organism maintains some overall bias to growth which accounts for the continued morphological changes such as the hooked jaw and humped back etc.   The pacific salmon drives its metabolism deep into the zone of senescence conserving large energy resources to power the migration to up stream spawning grounds but eliminates the option of iteroparity due to programmed death.    

Filial Cannibalism

MSSA proposes that filial cannibalism is an attribute of the negligibly senescent non-terminating-growth phenotype.  By consuming its offspring this phenotype continues to favor its own growth and future reproductive capability.  Of course, the fact that any given cannibalized offspring will carry only half of the parents genes contributes greatly to the logic of this mechanism.   In this model, offspring represents competition for available food supplies that could be used by the parent to increase their own future fitness.   Additionally, offspring produced early in the reproductive life of the parent will compete with the parent in the future.

CR and Senescence

As described earlier, Calorie Restriction (CR) results in life extension in vertibrates  by preventing the suppression of autophagy via the insulin-IGF-1 axis.    CR up-regulates autophagy above the basal level that has been down-regulated by the effects of the IDM.  Modulators of anabolic biosynthesis other than the insulin-IGF-1 axis that do not suppress the up-regulation of autophagy, sustain cellular repair at levels that prevent the accumulation of senescent cellular constituents in CR.  However under CR the TDM is still active and is not strongly suppressed by these mechanisms and as a result, vital parenchymal cells will still be lost and not replaced due to intrinsically driven apoptosis.  Fibrosis and decrepitude will continue to occur though at a some what slower rate.   This, I propose, is the reason that CR does not produce negligible senescence only species specific increases in lifespan.

Senescence and the Colonization of Land


As fish colonized the land they gave up the bouncy of water and subjected themselves to a very large and abrupt increase in the DES effects that are the by-product of gravity.   If the fish progenitor of land vertebrates was a species that executed a continuous-growth phenotype it is probable that growth-terminating regulatory genes were again released from constraints of inhibition concurrent  with other major changes in form and function that were needed to survive on land.   

Water was a very competitive place containing many large and evolved predators, as a result, natural selection strongly favored the adaptions to a land existence.  However, leaving the water subjected these species to large amounts of DES resulting in the adoption of a growth-terminating, senescent, phenotype.   Because this adaptation  afforded great protection from predation, it dramatically and immediately lowering the mortality rate of young adults.   Until large differentiated populations of animals emerged on the land and predation resumed, natural selection strongly favored the rapid increases in  life-span in such growth-terminated species.    

Cleansing the Genome

The Disposable Soma and Antagonistic Pleiotrophy theories illuminate the experimentally demonstrable reason why deleterious mutations will accumulate in the genome of post reproductive individuals.  However, growth-terminating species do not commonly possess a multitude of  genetic diseases similar to Huntington's Disease, which  expresses a deleterious phenotype some period of time after sexual maturity.  

The rarity of genetic diseases that display antagonistic pleiotroyph effects  supports the idea that a growth-non-terminating, negligibly senescent species recently existed in the ancestry of mammals.  The existence of such an ancestor species would have had the effect of cleansing the genome of these type mutations as they would negatively effect fecundity in animals that exhibit iteroparity, continuous growth and and a low mortality rate in young adults.  The existence of a recent ancestor that was growth-non-terminating again supports the idea that the controlling mechanism of growth-termination is fundamental and highly conserved in trans-species evolution.

Basal Metabolic Rate and Autophagic Down-Regulation

Speculating, it seems plausible that the basal metabolic rate that is regulated by the "Hypothalamus > Pituitary > Thyroid > T3,T4"  mechanism, could be involved in regulating the basal rate of autophagy and through it, the rate of intracellular repair.  

Slow Growth VS Terminated Growth

The question arises as to whether turtles and tortoises are growth-terminating negligibly senescent species, the evidence may show that these animals like snakes and other reptiles implement slow, perhaps in-perceptively slow growth throughout life.    However many of these animals experience a low mortality rate in young adults which could also provide some selective pressure toward delayed senescence.   Growth-termination cycling is another option that could exist somewhere between growth-terminating phenotypes and continuous growth phenotypes.  In this scenario, turtles would have growth-terminating regulatory genes that cycle within the course of a year between varying degrees of activity and inactivity.  This cycling could account for the annualized markers of age that are present in species that exhibit what appears to be continuous growth.  

Growth-Termination Without Attenuated Stem Cell Differentiation

Blanding's Turtles appear to stop growing at some point in life while seemingly remaining negligibly senescent.  This species may maintain negligible senescence by establishing a permanent  equilibrium between cell replacement and apoptotic processes.  This, like the hydra, would constitute growth-termination with negligible senescence. If the Blanding's turtle does effectively terminate-growth in this manor,  then this species could stand as an excellent example in nature for our scrutiny of the capability of achieving negligible senescence under terminated-growth.  However, its applicability to the human condition may be limited as it may be a very recent split from a growth-non-terminating ancestor.  If this is the case, then evolution may simply have not optimized the resource conservation mechanism to drive the species into a slightly senescing state.  This speculation seems reasonable since the Blanding's turtles mortality rate and reproductive capability may drive selective forces to only weekly discount the fitness of adults.  

It has been reported that older females are better at locating and securing superior nesting places, their brains in effect may be providing these turtles with a way to continue to increase fitness over time without maintaining growth.  


From the perspective of evolutionary theory, menopause has been seen as perplexing.  For this reason much has been written speculating on the evolutionary sensibility for the persistence of menopause across mammalian species.   I would like to propose another alternative, within the context of this theory.   Menopause can simply represent a cessation of reproductive capability that has been overtly shutdown to prevent risky pregnancy because the body has determined the degree of senescence has compromised the health state to the point that there is a low probability that pregnancy will result in offspring that live long enough to reproduce.  If this is the case, then in theory, fertility could be reinstated if the senescent condition could be reversed to some degree.  

This idea unifies the menopause that results from aging with the temporary menopause that results in elite athletes and anorexics which is triggered by insufficient fat stores and is reversible.   In this case menopause is just a senescence induced example of the same mechanism.

Two Types of Senescence Mechanisms

It is a proposition of this paper that Trans-Generational Fitness is implemented primarily through the operation of two fundamental types of mechanisms that conserve resources by withholding them from use by body repair processes in the adult.   Both of these types of mechanisms reinforce each other but senesce the organism in distinct ways.  I have labeled these mechanisms types as the "Intracellular Depreciation Mechanism" (IDM) and the "Tissue Depreciation Mechanism" (TDM).


The Intracellular Depreciation Mechanism

Entropy And The IDM  

The IDM represents a specific down-regulating extension of  control on the components of  cellular metabolism that are responsible for the effectiveness of entropy mitigation within the cell.  The IDM under-mitigates entropy by over conserving resources via the body-wide under-recycling of intracellular components.  This attribute establishes the IDM as one of the primary mechanisms by which evolution implements and optimizes species specific rates of senescence.  (See Appendix A. in the Supplementary Materials at the end of the paper for a discussion of this topic).

 Intracellular Repair And Senescence

Autophagy The Intracellular Recycling Mechanism  

Autophagy comprises much of the catabolic half of the intracellular recycling and repair process.  Autophagy is a critically important complementary mechanism to growth, antioxidants, and DNA repair enzymes in the regulation of the rate of senescence, and in the realization of negligible senescence.  In support of the primacy of autophagy, it has been proposed, by ETTORE BERGAMINI et al. that autophagy is the primary mechanism by which calorie restriction increases lifespan. 

The Utilization Of Conserved Resources

I propose that the IDM does not determine how or when conserved resources are exploited, the unique reproductive strategy of each species determines how the conserved resources are utilized to improve Trans-Generational Fitness.   It may seem that the generality of this resource conservation mechanism does not provide enough benefit to the organism to drive its persistence across species and niches.  However, this paper proposes that this objection is answered by the fact that the individual bares little cost from implementing the processes of selecting a mate on the basis of criteria that include altruistic traits.  See the Supplementary Materials sections titled: "The Sensibility Of The IDM And the TDM As The Cause of Senescence", and the section that follows it titled,  "Persistence of Senescent & Negligibly Senescent Phenotypes", for an explanation. 

Optimal Resource Conservation And Optimal Senescence

The IDM is the regulatory mechanisms that implements intra-cellular resource conservation by down-regulating the intracellular repair mechanisms.  The IDM down-regulates intracellular repair until the resultant level of activity produces a species specific rate of accumulation of senescent  constituents that is optimal relative to the species specific level of extrinsic risks to the fitness of adults.  This "optimal senescence" proposal is supported by the observation that rates of aging is highly species specific and by the long history of failures of antioxidants such as lipoic acid, vitamin E, vitamin C, Acetyl-L-Carnitine, to slow senescence in vivo.  

The concept that senescence results from non-incidental, optimized, mechanisms, is also supported by the large body of experimental evidence observed across species that have demonstrated that rates of senescence can be up or down regulated by changes in predation rates and through delayed breeding.   This malleability in the rates of senescence points to the existence of these mechanisms of autophagy regulation.

The Dynamics of Autophagy Regulation

Though the IDM is a powerful control mechanism that down-regulates the basal rate of autophagy,  some degree of intracellular repair as initiated by autophagy is normally maintained.   Cells are  not under exclusive regulation by the IDM,  other mechanisms such as ones that respond to a shortage of specific amino acids that cannot be synthesized by the organism can cause the up-regulation of autophagy and biosynthesis to levels above the basal rate established by the IDM.

Programmed Cell Death And Senescence

The autophagic component of intracellular repair is not capable of preventing the accumulation of damage to DNA, and so, is not sufficient to prevent deleterious effects over the long term.  However Daf -16 type transcription factors are up-regulated along with autophagy driving DNA repair.  Unfortunately, DNA repair is not completely effective leaving some types of DNA damage unrepaired.  For this reason Programmed Cell Death (PCD) is required to destroy cells that may harbor defective DNA.  Though this process is essential to the health of the individual, it is also involved in the production of senescence.

Over time PCD will deplete tissue reserves of parenchymal cells when these cells are no longer being replaced at a sufficient rate to maintain functional tissue mass 20.   The depletion of the tissue reserves in one or more essential tissues results in the decline and death of the individual.   For example, if pace maker cells in the heart undergo PCD heart failure results.   PCD is instrumental to the functioning of both senescent and negligibly senescent phenotypes and constitutes a fundamental element in the second major type of resource conservation mechanism in the organism, this mechanism is called the Tissue Depreciation Mechanism of senescence.  

The Tissue Depreciation Mechanism (TDM)

Importance Of The TDM

The TDM could be responsible for the majority of the seemingly intractable aspects of senescence.  The TDM represents a down-regulating extension on the body's primary Growth-Termination Mechanisms (GTM).   I propose that the TDM constitutes the foundational mechanism that controls age related fibrosis and is one of the primary cause of the progressive degradation of tissue function we observe in aging .  The TDM  drives processes that define the lifespan of a species independently of the action of the IDM.   Note: See, "Growth Termination and Scale" for a detailed description of the evolution of growth deceleration and growth termination.  

Second Order Senescence Effects Of The TDM


Though the action of the GTM produces the terminated-growth phenotype, like all other mechanism in the body, it is not exempt from the selection pressures exerted on it by the phenotype it produces.  As a result, the second order effects of terminated-growth on the function of the GTM are significant and are factored into the evolution of the total mechanism, this constitutes the second order effect that drives what I call the TDM    

Conditions that favor Trans-Generational Fitness, discount the fitness of the individual by driving selection forces to favor the action of the IDM, these same forces also drive optimization of the GTM's rate of tissue growth/repair, the mechanism of this optimization constitutes the TDM.  The TDM achieves optimization of resource conservation by down-regulating  the production of tissue-specific replacement cells until the quantities produced are insufficient to fully maintain the functional capacity of tissues.   

It is proposed that the TDM qualifies as a mechanism of resource conservation because it drives the replacement of tissue specific cells with fibroblasts and extra-cellular matrix (ECM).  Because scar tissue or ECM consists of dispersed cells in an extra-cellular protein matrix fewer metabolic resources  are required to sustain this tissue than are needed by the equivalent volume of non-fibrotic tissue.

Mechanistically, once deceleration of the cell replacement rate has reached an equilibrium with the rate of tissue cell death, growth-termination occurs.   The resulting terminated-growth phenotype produces the second order effects that then drives the further down-regulation of the differentiation of stem and progenitor cells yielding numbers of parenchymal cells that are insufficient to replace dying cells in the target tissue.   Over time this process results in the incremental fibrosis of body tissues as fibroblasts and ECM are substituted to replace many of the parenchymal cells that have died due to, injury, the accumulation of senescent cellular components, or due to intrinsically or spontaneously driven apoptosis.  

Stem cell differentiation pathways that lead to the production of fibroblasts are not equivalently down-regulated and continues to operate within the phenotypic environment of terminated-growth, sustaining the supply of fibroblast cells and ECM required to maintain the volume and basic structural integrity but not the optimal functionality  of the tissues.  


Parenchymal Cell Attrition and Senescence

Jeffrey Baron et al, have also proposed a model of the relationship between parenchymal cell attrition, growth termination and senescence in several papers such as "An Extensive Genetic Program Occurring during Postnatal Growth in Multiple Tissues".

Incomplete Tissue Repair Theory of Senescence

Others have recognized the relationship between the processes of fibrosis associated with tissue-damage, repair, and aging, expressing the view that, tissue-damage repair mechanisms contribute to senescence (see "Aging AS A CONSEQUENCE OF MISREPAIR" (2009) ).  However the authors conclude that "Misrepair" is ultimately a manifestation of entropy, not the result of a genetically determined mechanism of overt tissue degradation as proposed here.

Senescence And The Regulation of Stem Cell Differentiation

Support for this and other theories of senescence propose that systemic factors control the production rate of many types of parenchymal cells by down-regulating the differentiation pathways of stem and progenitor cells in favor of pathways that increase production of fibroblasts and ECM.   See the article in Science titled:  Rejuvenation of aged progenitor cells by exposure to a young systemic environment.   In this and other similar research, heterochronic parabiotic pairings have been used to demonstrate that it is soluble systemic factors and are regulatorily "upstream" of the cell to cells contact, that are responsible for modulating the stem or progenitor cell differentiation pathways.   This research also supports the conclusion that these growth factors are anti-senescent in there action on a variety of stem cell types.

Modification Of The GTM For Senescence Accumulation

The TDM - A Non-Incidental Source of Senescence 

The argument has been made in this paper, that the IDM is a non-incidental mechanism of senescence that results as a direct consequence of the favoring of Trans-Generational Fitness which, to a large extent, is driven by terminated-growth.  This same logic applies to the TDM,  once established in the genome, the terminated-growth phenotype drives second order effects that favor the evolution of a metabolically efficient mechanism of growth-termination, one that conserves resources.

Cell Turnover And The GTM

Other growth-termination mechanisms that are not under the control of the TDM exist and are utilized by specific tissues.  For example, the mechanism implemented by the intestinal mucosa achieves terminated-growth via continuous proliferation and differentiation of progenitor cells to produce the cells that compose the lining of the intestinal mucosa.  In this mechanism, a high rate of cell proliferation is balanced by an equally high rate of apoptotic activity maintaining static tissue size.   Growth-termination mechanisms such as this, with a very high metabolic cost, are appropriate for tissues such as the intestinal mucosa, which has exposure to high levels of carcinogens, viruses, and very high glucose concentrations.   It should be noted that this type of growth-termination mechanism is not optimal for other tissues within the context of a growth-terminated phenotype where natural selection is favoring resource conservation and Trans-Generational Fitness.

The IDM Drives the TDM

As it was described, the IDM will senesce cells over time producing incremental disfunction of proteins and organelles such as mitochondria.  As mitochondria become senescent they leak more free radicals which can further damage their host cells.   As a result, over time, cells will either become senescent or self destruct via apoptosis.   The cells eliminated via apoptosis places increasing demands on stem cell differentiation for the production of more replacement cells, just at the time when the TDM is exerting its influence to decelerate the production of tissue specific cells.   For these reasons the IDM amplifies the senescence mechanisms of the TDM.  

The TDM Drives Senescence Independently of the IDM

Even if an animal is calorie restricted and up-regulated autophagy is preventing the IDM from senescing cells, apoptosis will continue to occur at some rate due to a large number of other drivers.  For this reason calorie restriction and other IDM modulating approaches to mitigating senescence are insufficient,  intervention at the level of the TDM is required to achieve negligible senescence.

Dwarfism and Senescence

Dwarfism can be viewed as the phenotype that results from mechanisms that knockout the IDM mechanism by driving  the continual down-regulation of the anabolic half of metabolism via the insulin-IGF axis and as a result chronically  up-regulates the autophagic, catabolic side of metabolism.  However I know of no example where dwarfism has resulted in negligible senescence in a species.  Instead dwarfisms ability to increase maximal life span by some limited fraction of normal life span is strong evidence for the existence of another senescence mechanism, namely the TDM which is not effectively attenuated by the various causes of dwarfism.  

In the context of the above logic, the question still remains, why doesn't dwarfism protect the organism from the effects of the TDM?  Dwarfism does prevent the individual from reaching the size threshold at which the GTM / TDM down-regulates the differentiation of stem cells into parenchymal cells, so why are dwarfs not negligibly senescent?   One possible answer to this question is embodied in research demonstrating that the proliferation of stem cells which is an anabolic, growth process, is driven by the insulin-IGF-1 axis.   Without the initial proliferation step the differentiation step in stem cell morphogenesis does not produce sufficient numbers of parenchymal cells to meet the demands resulting from continuing apoptosis in the tissues.  

Proposed experiment to test hypothesis that Mate-Selection drives the persistence of the aging phenotype in Drosophila melanogaster.

Significant experimental evidence exists that supports that both male and female Drosophila melanogaster (DM) engage in sexual selection of mates, for this and other practical reasons this species could be an ideal experimental animal to investigate the proposal that  the rate of senescence is a sexually selected trait.   M Rose and others have bread files for many years that senesce at varying rates, it seems reasonable to employ these lines to see if flies preferentially select mates on the basis of rate of aging and not not absolute age of its potential mates age for example.


If flies have a mate-selection preference for young or older flies the following experiment might address this question.  However this will not shed light on the question of how senescence comes to presist in the population.  

The first step in this process is to demonstrate the hypothesis that a population of young adults will preferentially mate with older flies.  


A preference for Senescing mates may be restricted to females, males may have a preference for virgin females as a way to maximize reproduction, however if female selection is stronger senescence will still remain a sexually selected trait in this species.

By using larger population of sterile older flies mixed in with a newly mature population of fertile flies it should  be possible to demonstrate by the number of hatching eggs if a preference for older mates exist in the younger and older flies.  The logic here is, if a preference exists for selecting mates that show signs of  senescence there should be fewer viable offspring produced than would be expected based on the simple numeric ratio of young to old, that is if young flies are preferentially mating with older flies and the older flies are preferentially mating with older flies we should see fewer offspring than the simple ratio of old steriles to young fertile would predict.    

Step 1.

Introduce a small mixed sex population of newly mature virgin Drosophila melanogaster to  a X times larger population of old (in the last quarter of reproductive life ) males and females that are tetracycline dependent sterile.

Compare the reproductive yield to the theoretically expected yield when no mate-selection bias against senescence has been established in the species via selection caused by the experiment itself.  This will be used as a base line for the study.

Step 2.

Repeat step 1 utilizing successive generations of offspring, until the reproductive yield per generation significantly exceeds the offspring yield derived from step 1.

Note:  If the hypothesis is correct this process should eliminate the preference for senescence and install a mate-selection preference for non-senescence , in the population.

Step 3.

Introduce a population of newly mature virgin female flies, that are progeny of step 2, to a small population of young tetracycline sterile males and a large population of old senescing males ( in their last quarter of reproductive life ) and compare the progeny yield to the expected yield to test for a bias for youth in mate-selection and to account for the possibility that the females can detect tetracycline dependence.  

Note:   This step should test for the complement to the selective pressure of step 1.

Step 4.

Introduce successive virgin female populations constituting progeny of step 2 to successive populations of tetracycline sterile old males and fertile males of the same age that constituting progeny for step 2. 

Note:  This experimental design may not differentiate young flies interest in senescing mates from the preference of senescing individuals for non-senescing individuals.  This could be tested by utilizing flightless senescent sterile populations in such a way as to require the non-senescent fertile males and females to actively do the selecting by flying to achieve mating contacts with the sterile senescent flies. This result can then be compared with the matings where both populations are flightless and where both populations can fly and where the non-senescent population is paired with a flighted sterile senescent population.

Note:  If we have successfully removed the female preference for senescence in step 1 the populations should evolve longer life spans over time.   Repeat steps 1, 2 and 4 to fix and enhance the phenotypes.  

End of Supplementary Material




If, as I have proposed, the process of sexual maturation is linked by the same mechanism with the process of growth termination then sexual maturation can be used as a “tell” to the individual that its prospective mate has terminated growth.  Such a linked mechanism could have a great economy, in that sexual maturation can simply be executed as a reallocation of resources from growth to the growth and differentiation of tissues constituting the primary and secondary sexual tissues and organs.


Complete sexual maturation can be viewed as a "tell" that a potential mate has or is in the process of becoming  growth terminated though this is not absolute.  Therefore it seems likely that animals can detect whether an animal has actually terminated growth or not is some more direct or absolute fashion.  This is not to say that an animal can detect directly that a prospective mate has capped it growth surfaces on its bones or not.  Perhaps it is expressed through pheromones that indicate that growth is still occurring.    

Also maintaining a juvenile, infertile state, allow animals to dedicate resources to growth in order to reach  optimal size quicker and not to dedicate resources to changes required for secondary sexual characteristics and competition for mates or actual reproduction.

Even trees and other plants have juvenile periods, presumably to  provide time for the plant to reach the height necessary to access sufficient quantities of sunlight and as a result produce sufficient sufficient food stores to produce seed.  

Mammals can also use juveniles as a way to prevent incestuous matings.  This could be the case since human adult males do not develop aversion to mating with females that they have come to know as adults regardless of how closely they are genetically related.  The juvenile state reduces likelihood of such matings and eliminates the chance of offspring being produced when it does occur.  

In many mammal  species and other higher animal forms the length of larval or fetal form plus juvenile life span correlates positively with overall life span.  Why, if species attempt to maximize reproduction, does long juvenile periods exist in species when the juveniles are already very large?

Additionally this theory explains why a juvenile period exists in species.  Put another way why do species with large offspring fail to be capable of reproduction within days after being born?  

Why do large animals that have long gestation periods like humans and elephants have long gestation periods and juvenile periods where the young are not fertile for over a decade after birth, when at birth they are larger than related species ever attain in their life


Another related question is why are larval forms of insects infertile, for example some insect larvae like 17 year cicadas are not reproductive, why not, they are as large or larger than the reproductive adult since the reproductive adults do not feed?

Why are the rivers of the world not full of single celled human ameba that are reproductive?  Why have not some of the trillions of living ameboid cells found in human feces not colonized the river beds after 100,000 years of human habitation near rivers?  Why have mutations not enabled some of these cells to become capable of executing asexual and sexual reproduction when they possess all of the required foundational genetic equipment necessary to do so?  

The following is my theory of why this is true.  

The answers to these questions are found in developmental biology.

 It is an advantage for individuals to produce large offspring.  However large offspring require the parent to be even larger.  In terrestrial animals large size requires complex organs and body structures to mitigate growing diseconomies of scale that grow ever larger as bodies get bigger.  In both cases for the individual to be large requires a complex body plan due to increasing diseconomies of scale with increased size.  

Since both large and small animals start out as a single cell that then multiply and metamorphose through a variety of body plans as it grows, a large species need a way to sequester resources for their offspring so that it can traverse these stages quickly and in safety, this is done via the development of large eggs.  

Eggs allowed for a variety of body plans to be passed through in an express fashion because a large food source is sequestered to support it.  

In evolutionary time variations on these developmental body plans represent a body plan that was once a mature body plan that was reproductive.  As one body plan evolved from the other an additional layer of developmental morphogenesis was invented to get to this new form and the old form was pushed down into a gestational body plan and shortened in its duration.  This process of driving old body plan into the gestational realm required considerable evolutionary time.  One important element of this process is that the individual not be reproductive when not possessing the final body plan.  

Another option here is that the change always occurs in the metamorphic process not in the final mature form.  


Aging likely represent both the oldest and simplest mechanisms capable of terminating growth in that it does not require the evolution of any additional mechanisms but can simply be accomplished by deterioration, or dysregulation or “defunding” of existing mechanisms of body development.  Aging at its essence simply constitutes a  deceleration of developmental growth processes to a level beyond the point at which no further body growth occurs.   Aging, as growth termination mechanism, does not requiring a mechanism to measure the moment at which growth has terminated and it does not need regulatory elements necessary to constantly balance the body's metabolism on the growth or no-growth knife edge.