Banner
    New Evolution Concepts Are Changing How We Think About Biological Aging
    By Theodore Goldsmith | September 14th 2013 10:25 AM | 20 comments | Print | E-mail | Track Comments
    About Theodore

    Theodore Goldsmith was trained in electrical engineering at M.I.T. and has an extensive background designing, analyzing, and managing digital data...

    View Theodore's Profile

    New thinking about the evolutionary nature of biological aging will profoundly affect medical research on age-related diseases – here’s why.

    Before Darwin nobody thought that the origin of lifespan was different from that of all of a species’ other traits. Whatever caused a rat to have a long tail and beady eyes also caused it to have a particular lifespan, which, like tails and eyes varied a lot between different species.  Mammal lifespans vary from less than a year for some mice to more than 200 years for some whales.

    In 1859 Darwin’s survival-of-the-fittest concept changed that idea.  Now organisms were evolving myriad traits that each caused them to live longer and/or breed more.  Because living longer and breeding more was indefinitely better, organisms were presumably evolving toward immortality.  By the present, after billions of years of evolving longer lives, why weren’t organisms immortal or at least all similarly limited by some universal and fundamental law of physics or chemistry?  Why would lifespans vary so much among even biochemically similar organisms?  Contemporaries actually wrote Darwin and asked this question!  Biotheorists have been laboring ever since to develop a theory that fits with evolution theory and simultaneously matches empirical evidence such as the lifespan observations.  

    Most gerontologists and medical researchers now believe one of two main aging theory concepts that eventually resulted:  Programmed aging theories, first proposed in 1882, say that species generally possess a lifespan regulation mechanism that purposely limits lifespan to a species-specific value in order to obtain an evolutionary benefit.  

    Non-programmed theories proposed that each species only has an evolutionary need to live to a particular lifespan and therefore only evolved the ability to overcome natural deteriorative processes to the extent necessary to live to that age.  Both concepts explain why species have such different lifespans; both require modifications to the survival-of-the-fittest idea that we all learned in high school biology class.

    Modern non-programmed theories are based on an idea by Nobel-laureate Peter Medawar who proposed in 1952 that beyond a certain species-specific age there is no further evolutionary benefit to living or reproducing longer.  In effect, survival-of-the-fittest only applies to young organisms where “young” is defined relative to the age at which the organism is first able to reproduce.  Nature doesn’t care what happens to old organisms.  Death and deterioration are not an evolutionary disadvantage unless they occur before the critical age.

    For most people who paid any attention in biology class, programmed aging, the idea that we possess a sort of suicide mechanism that purposely pro-actively limits lifespan, appears to be even more patently ridiculous and more obviously incompatible with the whole survival-of-the-fittest idea than modern non-programmed aging theory.  Indeed, as late as 2002 some prominent biologists were still writing that programmed aging in mammals was literally theoretically impossible.  Consequently, steadily increasing evidence of programmed aging such as genes that cause aging was largely ignored by medical researchers. “Impossible” trumps any amount of evidence.

    Meanwhile, beginning in the 1960’s a number of other theorists were working on trying to explain some other apparent conflicts between observations and evolution theory.  Darwin’s theory says that every individual animal is fighting for the survival of itself, its mate, and direct descendants and against competitors from its own species.  An individual surviving longer and breeding more produced more descendants having its individual design than competitors and thus better propagated its individual traits.  This is the “individual benefit clause” or the “dog eat dog” aspect of Darwinian evolution theory.  There was very wide agreement that deterioration and death caused by aging did not represent any evolutionary benefit from the point of view of an individual mammal!

    However, In addition to all of the human societal rules, laws, and commandments that limit individuals in favor of wider benefit, theorists observed animal behaviors (altruism) in which animals similarly behaved in a way that was counter to their individual best interest, apparently to obtain a wider “group” survival benefit.  A number of other apparent discrepancies with the individual benefit clause surfaced. Eventually a number of theories appeared to the effect that benefit to the survival of groups or kin, benefit to the propagation of genes (the selfish gene theory), or benefit to the evolution process itself (evolvability theory) could offset some degree of individual disadvantage and result in evolution of an individually-adverse (or neutral per Medawar) trait like programmed mammal aging.  Multiple programmed aging theories then appeared based on non-individual benefit resulting from a limited lifespan.  According to these theories, beyond a species-specific age (also associated with reproductive maturity) there is an evolutionary disadvantage from living longer.  As only one very simple example, a longer lifespan in many mammal species would lead to decreased genetic diversity.  A single long-lived male “king of the hill” might mate with many generations of his own descendants! 

    Genetics discoveries, some quite recent, exposed additional issues with traditional individual-benefit-only evolutionary mechanics theory.  At least two assumptions made by Darwin and critical to the individual/ non-individual issue are now provably false.  The emerging reality:  the evolution process, rather than being simple and elegant is actually complicated and messy.  The reader may have noticed that the two main theories are much closer to each other than to traditional evolution theory. The argument is over whether beyond the critical age aging creates zero net evolutionary disadvantage (and therefore species never evolved a longer lifespan) or whether, beyond the critical age limiting survival creates at least a small advantage (and therefore species evolved suicide mechanisms).  Arguing about the difference between zero and slightly less than zero is a lot like arguing about how many angels can fit on the head of a pin!

    It is now increasingly obvious that programmed mammal aging is the right theory.  Programmed aging theories now exist proposing that a panoply of wider evolutionary benefits would result from programmed lifespan limitations.  A number of senior advocates of non-programmed aging have even conceded the validity of the non-individual-benefit evolutionary concepts that are necessary to support programmed mammal aging. This essentially concedes the validity of programmed aging because programmed aging provides a much better fit to experimental evidence.

    Why is this development so important?  Programmed and non-programmed theories predict very different mechanisms behind the aging process and therefore behind massively age-related diseases like cancer and heart disease.  Following the wrong theory is therefore likely to substantially delay development of ways to treat or prevent the age-related diseases that in developed countries are now the main cause of death for people over 40!  For example, non-programmed theories suggest that the various manifestations of aging are functionally independent of each other and that therefore treatments and prevention techniques must be individually developed for each condition.  Programmed theories suggest that, in addition, there is substantial potentially treatable commonality between various manifestations, i.e. the program.  If aging is at least partially controlled by a program similar to the one that controls reproductive functions, we would expect the existence of a “biological clock” that could be medically altered.  We would expect the existence of signals such as hormones used to coordinate the activities of various tissues in performing the aging function that could also be altered.

    Researchers following non-programmed theories talk about preventing or contravening damage, usually associated with a particular disease.  Followers of programmed theories talk about signals, receptors, interrupting the aging program, and simulating some effect known to delay aging such as caloric restriction or exercise in order to “fool” the aging program.

    Most of us have been trained from an early age to believe that the evolution process resulted in the development of all of the “beneficial” characteristics of an organism but that all of the “adverse” aspects came from random deteriorative processes or external forces.  It is indeed a giant leap to think that aspects like muscle weakness, sensory and mental deterioration, heart disease, cancer, increased susceptibility to infectious diseases, arthritis, and other manifestations of aging are also “beneficial” as seen from the evolution process point of view and therefore ultimately result from the operation of complex evolved mechanisms similar to those that produce the traditionally “beneficial” organism features.  However unless we make this leap we will never really understand aging or age-related diseases

    References:

    Goldsmith TC.  The Evolution of Aging 3rd Ed.  Azinet Press Annapolis ISBN 0978870905 2012 also Amazon, B&N, etc.

    Goldsmith TC.  Arguments against non-programmed aging theories.  Biochemistry (Moscow)  DOI:10.1134/S0006297913090022 78:9 971 2013

    Medawar PB.  An unsolved problem of biology.  HK Lewis London 1952

    Weismann A.  Urber die dauer des lebens.  Fischer Jena 1882

    Comments

    I don't even know where to begin in considering all the things wrong with these assumptions. In the first place it presumes a directionality or purpose to evolution which doesn't exist. The second is in the way phrases like "survival of the fittest" are tossed around as if they are Darwinian dogma.

    It also seems that the concept of biological evolution is being simplistically compared to gains in efficiency, which also relates to a direction to evolution.

    The absolute first problem that must be addressed is to determine, not simply guess, as to what the selection pressure would be for aging. What is obvious is that any creature that didn't live long enough to raise its offspring, where such is necessary, or increase the probability of its offspring surviving would risk extinction. This doesn't suggest that evolution was striving for immortality. It's simply selection on the low end of aging and says nothing about the upper bound.

    Also, the crucial part to this is life expectancy which marks the probability of an organism actually surviving to any particular age. This this is generally much lower than life span, there is nothing to select for. In other words, natural selection can only increase life span if the only selection pressure present is old age. Among humans the maximum life span is 120+ years. There is absolutely nothing selectable about that value, because there is no fitness benefit to being 100 versus being 120 versus being 200. Nothing. There is nothing to select, so the entire concept is bogus.

    The moment reproduction ceases, and any applicable rearing is complete, then evolution STOPS with respect to any selection or influence the parent organism has. The only thing the parent can do is to facilitate the survival of the offspring, but there is absolutely nothing that will select for longevity.

    tgoldsmith

    The absolute first problem that must be addressed is to determine, not simply guess, as to what the selection pressure would be for aging. What is obvious is that any creature that didn't live long enough to raise its offspring, where such is necessary, or increase the probability of its offspring surviving would risk extinction. This doesn't suggest that evolution was striving for immortality. It's simply selection on the low end of aging and says nothing about the upper bound.
    I meant that Darwin said nothing about the value of survival or reproduction declining with the age of an organism. Striving for immortality is an obvious inference that would made by someone reading his book or reading modern summaries of Darwin's ideas.  Your position is more in tune with modern concepts.

    Also, the crucial part to this is life expectancy which marks the probability of an organism actually surviving to any particular age. This this is generally much lower than life span, there is nothing to select for. In other words, natural selection can only increase life span if the only selection pressure present is old age. Among humans the maximum life span is 120+ years. There is absolutely nothing selectable about that value, because there is no fitness benefit to being 100 versus being 120 versus being 200. Nothing. There is nothing to select, so the entire concept is bogus.
    Yes.  This is essentially Medawar's concept that there would be no selectable value to living longer than the age at which most wild individuals would be dead from external causes.  Again, striving for immortality applies to Darwin and not more recent thinking like Medawar or modern programmed and non-programmed theories as explained in the article.
    The moment reproduction ceases, and any applicable rearing is complete, then evolution STOPS with respect to any selection or influence the parent organism has. The only thing the parent can do is to facilitate the survival of the offspring, but there is absolutely nothing that will select for longevity.

    This true too as far as it goes.  However, the obvious question then becomes: Why didn't that species evolve the ability to keep reproducing to a later age like other similar species.  Modern programmed and non-programmed aging theories assume that cessation of reproduction is a symptom of aging as opposed to an evolutionary cause of aging. 

    There were two main points in the article: First, while everybody has heard about Darwin and "survival of the fittest." most people have never heard of Medawar or even newer ideas that there could be zero or even negative evolutionary motivation toward a longer life.  This affects popular attitudes about aging especially by suggesting that aging results from fundamental limitations and that therefore medical attempts to contravene aging or the age-caused aspects of age-related diseases are impossible.  Second was to explain the current situation regarding modern programmed vs. non-programmed theories and the rather major implications for medicine.





    Why didn't that species evolve the ability to keep reproducing to a later age like other similar species.

    That's the misconception that most people have. Species don't evolve because they can. They evolve because there is an external selection pressure that they must respond to. If there is no advantage, then there is no selection pressure. So the first problem that has to be addressed, is what would the advantage be?

    Reproduction automatically also includes liabilities. Each new animal also increases the competition for the original animal. Energy must be expended and acquired to sustain more than one individual.

    It seems that the most important point though is that evolution cannot occur without the old traits eventually being eliminated and the new ones allowed to continue. Without that aspect of it, the species would simply diverge over time.

    I'm not sure though what questions you're really asking and why it is being treated as if they exist as singular interpretations. Aging can be both, programmed and a gradual deterioration of systems and repair mechanisms. That's the most likely explanation. We already know it is programmed, because the evidence is obviously present in humans and many other long-lived species; menopause. Since there is a clear biological action and hormonal response to shut down reproduction, there can be little doubt that this is genetic and heritable.

    In that case, it becomes fairly clear that the individual has zero biological fitness, so unless their presence conveys some advantage to newer organisms, then what would the biological justification be to compete and continue to consume resources for such an individual. It makes sense that systems would eventually deteriorate and break down, since longevity would only incur a cost and provide no benefit.

    This is also evidenced by those creatures that reproduce and die almost immediately. Evolution is quite conservative about simply supporting organisms that don't support the survival of the population.

    While much of this has not been experimentally demonstrated, there are strong hints. Just as in speculating about the role of menopause, a potentially plausible explanation is that it is evolution's way of ensuring that an animal can't become pregnant or produce offspring with lower quality eggs and an increased risk of not surviving to raise the offspring to adulthood. While explanations like the "grandmother hypothesis" may play a role, issues like menopause indicate that social organization plays a significant role in such developments, over the simpler explanations of genetics alone.

    I guess another way to look at it, is that the longer traits persist in a population, the greater the likelihood that new novel traits will be lost. This is why death is such an important aspect of natural selection, otherwise one would see a trend towards homogeneity in populations. You mentioned something similar with regards to mating with genetically related offspring, but that would produce amplification which would tend to increase the detrimental traits in a population.

    tgoldsmith
    BiologyGuy:  I think we largely agree: Aging is programmed but the actual mechanism of aging involves deteriorative processes.  A program is controlling the deteriorative mechanisms and allowing them to operate on a particular species-specific schedule.  The message of the article is that traditional medical approaches are directed at slowing the deteriorative processes (e.g. anti-oxidants, anti-cholesterol medications, etc.).  The existence of a program allows for additional approaches in which efforts are made to interfere with the operation of the program (signals, blockers, mimetics, etc.)  The latter opportunities are being missed by programmed-aging-deniers.  Exploiting them could produce dramatic improvements in public health.  Because the latter approach is relatively new, we could expect to see "low fruit" and potentially dramatic improvement.  See Arguments against non-programmed aging theories for a more detailed description of the way a program can work with deteriorative processes.
    I think aging has more to do with defending against cancer. If you live long enough you will get cancer. The things your body does to control cell division to control cancer also tends to limit life span. In a sense life span is "programmed" but it is only a side effect.

    The idea of a selective pressure to a limited lifespan is total nonsense. The mortality rate from accident and disease is easily high enough to make any pressure toward reduced life span unnecessary. And even if there were some group selection mechanism for limited life span it would be blown out of the water by individual selection pressure which acts faster and stronger. And even if it didn't there are more effective ways to limit how long an individual lived like death matches between sexual rivals.

    In the natural world there is no shortage of death. No need to program for it and no advantage anyway.

    I've been waiting a while for someone to write this article.

    The greatest competition for any animal is its own species. More adapted offspring would eventually out-compete an immortal member and wipe it out.

    It is a given, then, that adaptability is designed to bring a member of a species to a specific age target that maximizes the utility of evolution: the age at which a species can bring its own offspring to reproducible independence. Any younger, and the species dwindles in numbers. Any higher, and the species dwindles in adaptability. EITHER deviation increases the likelihood of extinction.

    Tim

    Why do dogs die at 10, and people at 70. Why do mice die at 2 or 3? Why do octopuses and salmon die immediately after giving birth?

    The obvious answer is, to free up resources for the younger individuals who carry their own genes. Are we programmed to die? Of course. The amazing thing is, this isn't obvious to everyone.

    I assume that aging is an adaption that arose to prevent cancerous mutations or the tendency toward them that accumulate over time from being passed on by an aged parent. Consequently, the aged loose the ability to reproduce in order to protect subsequent generations from cancerous mutations that would otherwise cause problems in reproducing young. I can see no way for any adaptive process to automatically kill individuals immediately after the cessation of reproductive ability so consequently we have senescence. Not every cell within the aged body loses the ability to reproduce at the same time and the length of senescence might be determined by the number of critical cells and the variation in the time at which they cease producing more cells.

    tgoldsmith

    ppnl and dbohara:

    I think aging has more to do with defending against cancer. If you live long enough you will get cancer. The things your body does to control cell division to control cancer also tends to limit life span. In a sense life span is "programmed" but it is only a side effect. 

    This is one of many theories to the effect that aging is an unavoidable side-effect of some beneficial property.  There are many arguments against this.  For example, dogs have a much shorter lifespan than humans yet they still get cancer.  If cancer is a tradeoff with lifespan, why aren't dogs cancer-free?  Many other arguments against this idea are given in Arguments against non-programmed aging theories

    The idea of a selective pressure to a limited lifespan is total nonsense. The mortality rate from accident and disease is easily high enough to make any pressure toward reduced life span unnecessary. And even if there were some group selection mechanism for limited life span it would be blown out of the water by individual selection pressure which acts faster and stronger. And even if it didn't there are more effective ways to limit how long an individual lived like death matches between sexual rivals.

    In the natural world there is no shortage of death. No need to program for it and no advantage anyway.


    The idea that individual selection works much faster and stronger than group selection or evolvability was popular some time ago.  This was the basis for the idea that the non-individual theories and dependent aging theories were "theoretically impossible."  However there is now extensive theoretical basis for the idea that a non-individual benefit can trade off against an individual disadvantage and little current scientific objection.  There are also other observations that conflict with individual-benefit-only theory but have plausible non-individual-benefit explanations.  Consequently gerontologists largely concede the validity of non-individual-benefit and I have not seen recent journal articles arguing against them.  If anyone has, please advise.
    See: The Evolution of Aging 3rd Ed. for more detail.

    The idea that aging has no practical effect in the natural world has also been disproved.  If true, death rates in the wild would not vary with age after maturity.  In fact studies indicated death rates in typical wild mammals increased with age proving aging was having an evolutionary effect.

    The idea that there is no benefit to an organism surviving much beyond the age that it stops reproducing (given time for rearing, etc.) is valid. The problem is that no one has produced a plausible reason based on fundamental limitations for species to vary in the amount of reproduction they can execute.  Some negligibly senescent species can keep reproducing indefinitely. Therefore, that idea just introduces another problem: Why did species X stop reproducing at age Y when some other similar species kept reproducing to a much later age?  Why didn't X evolve the ability to reproduce longer?  In my experience the vast majority of gerontologists consider loss of reproductive ability to be a symptom of aging and not an evolutionary justification for aging.

    In my experience the vast majority of gerontologists consider loss of reproductive ability to be a symptom of aging and not an evolutionary justification for aging.

    I don't believe that perspective is a correct one. Females don't produce new eggs, so we have a relatively long period of time where eggs exist and can begin to degenerate. So, it would suggest that there is very much a "shelf-life" against which reproduction must operate.

    However, the metric of reproduction is also suspect. Superficially it seems like it has a maximizing effect, but evidence suggests otherwise. This is best observed in humans, where the birthrate correlates more readily to the death rate. In other words, the greater the likelihood of infant or youthful mortality, the higher the birthrate was. Once those numbers come down, so does the birth rate, so we don't find humans reproducing at anywhere near their biological capacity.

    This suggests that most animals are reproducing to improve the odds that some offspring will survive. I don't recall any animal that is exempt from high mortality rates among its young, whether it be through predation, starvation, or disease. If every animal born were to survive, it would decimate the local population with internal competitors, so one can draw a rough correlation of high birth numbers equating to correspondingly high death numbers.

    I also think a strong argument can be made that longevity increases the risks of injury and disease, even though there might be some offset offered by increased experience. However, one hypothesis that may be at least partially applicable is described by the "unknown futures" problem, where each organism born has to cope with a certain set of problems to which it adapts. However, the environment, situational problems, etc. change and consequently the older the animal, the more difficult it is to adapt to every changing circumstances. In the case of learned behaviors, older animals may even teach the wrong lessons, in a kind of biological generation gap.

    It's very akin to the comment attributed to Planck of saying that "science progresses one funeral at a time". Similarly one could say the same of biological populations.

    tgoldsmith
    BiologyGuy:

    Females don't produce new eggs, so we have a relatively long period of time where eggs exist and can begin to degenerate. So, it would suggest that there is very much a "shelf-life" against which reproduction must operate. 

    Again the question is: Why not?  Is this a symptom of aging? Other organisms seem able to make more eggs.  If one believes in programmed aging then programmed changes in reproductive effect are logically essentially inevitable because the evolutionary rationale is similar.  Such a reduction in reproduction could be the result of programmed termination of reproductive capability (observed), reduction in reproductive vigor (observed), or increase in puberty-age beyond what is plausibly necessary for growth of the organism (observed). 

    It's very akin to the comment attributed to Planck of saying that "science progresses one funeral at a time". Similarly one could say the same of biological populations.
    There are many arguments that uncontrolled population growth is bad for the population and that there is a group benefit to senescence or other individually-adverse trait like programmed restraints on reproduction. Here are two:

    As Darwin said the size of any population is constrained by external "checks" such as predators, etc. The life of an organism is essentially a test of its combination of traits. Therefore death rate or the rate at which lives are lived is a factor in the rate at which evolution can proceed.  If the organisms in a population lived on-average twice as long they would evolve half as fast. This a restatement of your comment above.

    Uncontrolled reproduction would tend to lead to a population in which most individuals are immature.  The evolution of adult traits is driven entirely by deaths that occurred in adults.  In other words, an organism that died prior to becoming an adult does not contribute to evolution of adult traits. Therefore a higher adult death rate increases the pace of evolution.  Traits that increase the proportion of adults in a population such as programmed restraints on reproduction and lifespan aid the evolution process.
    Females don't produce new eggs, so we have a relatively long period of time where eggs exist and can begin to degenerate. So, it would suggest that there is very much a "shelf-life" against which reproduction must operate.

    This is totally logical - this is what we are taught in school - high school,, college, even medical school - but do we know this is true? In the 1950's Lord Solly Zuckerman decided that the evidence supported that conclusion but it did not justify the conclusion that ova weren't created de novo during reproductive life and now there's considerable controversy about just this subject - and evidence which seems very reasonable that such ova are produced throughout reproductive life the 'degeneration' of the late stage ova resulting from the general decline in stem and progenitor cells with aging. [^ Johnson J, Bagley J, Skaznik-Wikiel M, et al. (July 2005). "Oocyte generation in adult mammalian ovaries by putative germ cells in bone marrow and peripheral blood". Cell 122 (2): 303–15. doi:10.1016/j.cell.2005.06.031. PMID 16051153.
    Jump up ^ Johnson J, Canning J, Kaneko T, Pru J, Tilly J (2004). "Germline stem cells and follicular renewal in the postnatal mammalian ovary". Nature 428 (6979): 145–50. doi:10.1038/nature02316. PMID 15014492.]. If you think about it - an ovum "stuck" in metaphase two for decades? How does a cell live stuck in metaphase - it's chromosomes in their most condensed form - no access to transcriptional and repair complexes - where do their enzymes come from how can they produce proteins of metabolize anything?
    I want to clarify a distinction between biology guy and Theodore Goldsmith - simply BiologyGuy agrees (and that's not so usual) with the thesis, obvious to those that have not blinded themselves, that there are programmed aspects to aging, menopause being an obvious one, but that it is a combination of programmed aging and stochastic decay that is the probably cause of aging - and Ted Goldsmith says that the deterioration due to aging is the mechanism of that deterioration. I think if you'll read my paper at you'll understand the mechanism behind that mechanism: http://www.springerlink.com/openurl.asp?genre=article&id=doi:10.1134/S00... (which also tells how aging might be cured - now), simply, the cell (stem and progenitor cells; most somatic cells are 'born to die') changes its transcription patterns; down-regulating the production of repair and maintenance proteins (at a time when repair and maintenance are seen to decline) and up-regulating the production of pro-inflammatory factors (the senescent cell is the epitome of that) and of amyloidogenic proteins (those, like presenilin that result in the formation of amyloid deposits - such as the plaque of Alzheimer's disease).
    Also, BiologyGuy also talks about finding out about selection for longevity - and this has been done in the laboratory: by only allowing the progeny of the oldest egg-laying individuals of a chohort's eggsto found the next generation and applying this selection through several generations significantly increased lifespan in flies and guppies - so there are factors which, though not obvious, can select for life span. It might simply be that such factors select for a 'slower clock speed'; we know that these speeds are set by metabolic systems, particularly those involved in insulin and insulin-like growth factor 1 (IGF-1) and that the difference between small dogs and large dogs is the the amount of IGF-1 produced and that large dogs live half as long as small ones - so I guess we've done our own breeding for longevity by breeding for size. There is considerable individual variation that can provide something select-able, say a trait like general endurance might have increased longevity as a side effect - we don't know - but we can't limit nature's ingenuity by our own. It was once argued against programmed aging that in the wild animals never reach their maximum lifespan so death of old age was not a select-able trait for evolution to work on- but this was nonsense - it's clear that old age affects an animal's ability to survive and compete for mates well before death occurs (sigh!).
    Also, Ted said something that I've not quite heard said in the way he did, that scientists have found genes that cause aging. I think at most biologists would say something like genes have been found which when incapacitated or eliminated increase lifespan - which is not necessarily the same thing - or is it?

    Okay, one more thing and I'm out of here - simply BiologyGuy said, "The moment reproduction ceases, and any applicable rearing is complete, then evolution STOPS with respect to any selection or influence the parent organism has. The only thing the parent can do is to facilitate the survival of the offspring, but there is absolutely nothing that will select for longevity." That obviously neglects the possibility that grandparents might provide groups with selective advantages - again let's not limit nature's imagination by our own. Until now the world of ageing researchers has, with notable exceptions been overlooking clear evidence that the 'wear and theories' of aging are wrong - the clear evidence that cells (tissues and organs, at least) can be rejuvenated with all of those characteristics said to cause aging (mitochondrial dysfunction, telomere shortening, reactive oxygen species production (free radicals)) being reversed by the simple addition of four transcription factors. There's more in the paper, but I'll warn you it's not easy reading.

    That obviously neglects the possibility that grandparents might provide groups with selective advantages - again let's not limit nature's imagination by our own.

    I don't think I was that restrictive in my comments. No matter what support might be conveyed to the group, there is no selection mechanism.

    To postulate a selection mechanism would require a material difference in fitness due to the survival of a parent than not. The problem, of course, is that by the time the parent can provide such assistance to their own offspring or to a group, the next generation has already been born. Therefore, the only window of opportunity would occur if a mutation would result in increased longevity and this resulted in such a dramatic difference in fitness that only those that shared comparable genes would survive.

    That argument might work if it were confined to genetic kin, but collapses when one considers the genetic diversity of groups where such mutations would tend to be diluted and such traits lost. Therefore it seems quite unlikely that there would be any direct selection pressures on longevity once the next generation's reproductive status has been secured. There's simply no means by which such a genetic influence can be made to reach across multiple generations.

    Oh - I wish that I could edit what I wrote - I'll remember next time before I hit 'submit', but I promise you the paper is better written. (It's published after all!)

    Your point that “the next generation has already been born” by the time a parent can provide assistance (not to mention a grandparent, which I did) is irrelevant if that assistance differentially helps its progeny (or it's progeny's progeny) to survive and reproduce. Perhaps you mis-stated your point (or I misunderstood it)? No one doubts that a parent must live at least long enough to ensure the survival of it's offspring – and any animal or plant that did not survive long enough to ensure the survival of its offspring would be strongly selected against right? Furthermore, if there were an incremental advantage to its progeny in having the parent live longer than merely long enough to ensure that its offspring were 'weaned' (in the case of a mammal) – if 'value' could be added to the life of the progeny, perhaps by one of the other branches of trans-generational information transfer, (say teaching what foods not to eat, or what animals to avoid) why wouldn't that result in a selective advantage? If grandparents could provide their “grand-children” with a selective advantage in terms of teaching – for example – or helping parents with 'child-rearing' (clearly I'm looking a human exemplars now, but that might apply to social animals in general – I'm not an evolutionist) – and that gave a family unit an intraspecific advantage, then there is something select-able. What I don't understand is why you say that a mutation would have to result in such a dramatic increase in fitness that only those that shared comparable genes would survive? That's never been the basis of Darwinian selection - merely providing a differential advantage would, over time result in the more fit being selected for and not an abrupt killing off of the less fit? (We could however use our imaginations here to picture a world in which modern man was fighting against the individually much stronger Neanderthals. Modern humans might, by dint of a longer life expectancy (a supposition), have grandparents that recall the weakeness of the Neanderthal's defenses such that these Neanderthals were actually exterminated due to the modern human's “grandfather advantage”.)

    The bigger point I think is the use of the antedeluvian version of Darwinian evolution to justify the proposition that programmed aging is “impossible” - or for that matter using any current variation of Darwinian evolution, to “prove” or even to deduce what the evolutionary effects on lifespan are, is not justified. Darwinian evolution is based on the proposition that evolutionary change is the result of non-directed random events that are later selected by the 'environment' (including all factors, physical and biological) and that is an unproven assumption. We now know that there are other trans-generational means of information transmission: epigenetic and behavioral, and that those two non-genetic means are directed and not random. Using computer models or simply the verbal 'model' that evolutionary selective forces are more weakly directed at post-reproductive traits might “prove” that lifespan cannot be programmed – but unlike using a 'proven' theory such as general relativity, using Darwinian evolutionary models as the basis of prediction may not lead to true conclusions if the theory itself is faulty – and there's now good reason to believe that it is, or at least is incomplete.

    I didn't say that grandparents wouldn't make a difference, I said that the difference would have to be significant to cause such a specific trait to go to fixation within a population. However, I also qualified it by saying that this would make more sense within the context of genetic kin, but would be negated if the assistance applied across the group,

    'The point is that if there is a longevity trait present in a parent, then we have to make the assumption that it is highly heritable, so that there is a virtual certainty that offspring would also carry the trait. More importantly, we also have to assume that those that lack the trait have a higher probability of experiencing reduced fitness, because without that there is no material difference in future genetic representation in the population.

    Since you had mentioned group selection, the problem becomes more pronounced, since that would presume that those possessing the longevity trait would equally assist those with it as those without it, so it becomes harder to rationalize how such a trait would proliferate through a population.

    However, in just the general sense, if we assume a population of just 10 individuals for illustration purposes. Let's assume that 5 have the longevity trait while 5 do not. However, all parents survive long enough to ensure that their offspring survive to reproduce. In this situation there would be no benefit to having the longevity gene versus not having it. Again, the point is that the grandparent must mach a substantial contribution that would affect fitness outcomes. If not, then it's purely a genetic toss up.

    In addition, if the help was spread across the group, then that would negate any specific benefit to longevity since all 10 in our example would benefit. However, if the groups were segregated, then the longevity group would actually experience the potential for more problems because their overall population would be larger [since older adults are still part of the group] which would make their subsistence requirements higher and more resource intensive.

    Again, one could think of all manner of ways in which these older adults could still provide benefit, so I'm not going to argue that they are simply a liability. However, you can see that if each generation successfully survives, regardless of the age of its oldest members, there is no selection pressure that would cause the genetic trait to ever be more than a variation. That isn't to say that it couldn't happen. That's why I qualified it by saying that the only selection pressure that could operate across generations like that would have to provide a substantial benefit to the grand-offspring to be selectable. In which case, one would expect to see a population shift occurring that is dependent on that longevity.

    So the only way I can see the argument of a longevity trait persisting and going to fixation would be because those that possessed it literally reproduced longer and produced more direct offspring. As a result, with such a trait presumably having high heritability, the trait would have gone to fixation simply because those with it out-produced those without it. There was no specific selection pressure, other than the sheer numbers that would ultimately ensure that such a gene proliferated throughout the population.

    I don't think we're disagreeing in any substantial way.

    I don't think the fact that dogs get cancer invalidates the idea that aging is largely the result of a defense against cancer. The fact that dogs have a shorter life span does not mean they have a better defense against cancer. In fact they probably have a less effective defense against cancer since their shorter life span requires less cancer protection. Life span is not a measure of how well protected from cancer you are. In fact the opposite is true. Remember the limit on life span is a side effect of cancer protection not the mechanism of that protection and certainly not a measure of that protection.

    The dogs target life span is set by the probability that they would live to a certain age without aging considerations. This is determined by food availability, predation and the probability of accidental death. Think of it as the LD50 dose of living set by environment.

    The mechanisms protecting from cancer use this target life span as a parameter. It can use any mechanism that does not reduce the life span below that target life span. Shorter target life spans mean you can use simple mechanisms that would be devastating to an animal with a longer target life span.

    If you want to live longer you need to evolve far more complex, finely tuned and effective mechanisms that do not limit life span. That is a hard problem and will only happen in species that have a chance of living long enough to take advantage of a longer life span.

    We humans seem to have recently increased our life span. Probably this happened as our rapidly increasing brain size changed our relationship with our environment. As the chances that we could live long enough to take advantage of a longer life span increased the evolutionary pressure for more finely tuned controls on cell division increased.

    Also I just don't think a very high percent of evolutionary biologists think group selection plays much of a part in evolution.

    tgoldsmith
    ppnl:

    The aging-helps-prevent-cancer theory is one of a large number of theories based on the idea that the value of survival and reproduction declines with age but not to zero, e.g. Williams 1957.  Consequently, there is a need for some compensating benefit that is somehow randomly rigidly linked to aging in such a way that the evolution process can not find a way to accomplish the beneficial function without the adverse side-effect (aging).   See extensive arguments against this idea presented in the article Arguments against non-programmed aging theories.  

    A mammal, the naked mole rat apparently does not develop cancer even though it lives to be about 30 years old, much longer than similar-size rodents.
    Also I just don't think a very high percent of evolutionary biologists think group selection plays much of a part in evolution.
    First, there IS wide agreement that the evolution process is much more complicated than it was thought to be in, say, 1950.  Claims by someone to the effect that they understand the evolution process so perfectly that they can confidently state that something is "impossible" because of THEIR evolutionary mechanics concept are now seen as overreaching and naïve.  The group, kin, gene-oriented, and evolvability theories were developed because of a perceived need to explain a number of observations that were incompatible with traditional theory (in addition to aging).

    Second, modern non-programmed aging theories depend on the idea that at some age the net (counting all tradeoffs) individual benefit of living longer and reproducing more declines to zero.  This is said to be why that species did not develop a longer lifespan.  Therefore the non-individual benefit of limiting life could be very small and still outweigh the zero individual disadvantage of limiting life. To show that programmed aging theories are invalid therefore requires showing that group selection and the other non-individual theories play ZERO part in evolution.  "Much of a part" does not get it!  I have not seen any recent article that actually attempts to show why the non-individual theories are invalid.  Incidentally, evolvability theory is not really a "group" theory because the evolutionary mechanics of evolvability are very different.  That is why I use the term "non-individual."  The Guru of non-programmed aging, Tom Kirkwood, has conceded that non-individual benefit is at least somewhat valid. 

    Third, there is very extensive and growing direct evidence of programmed aging.  Back in the day, when programmed mammal aging was thought to be "impossible" and there was no theoretical support for it, such evidence was widely summarily dismissed (E.g. evidence in non-mammals was declared "irrelevant"). The rationale for such exclusion would not withstand scientific review today.