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    New Study Lends Additional Support To Grandmother Hypothesis
    By Eve Hardy | October 24th 2012 09:06 AM | 8 comments | Print | E-mail | Track Comments
    About Eve

    I graduated from Rutgers University with a B.A. in Molecular Biology & Biochemistry, and currently work in a molecular biology lab using Drosophila...

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    Kids driving you crazy? Most parents don’t hesitate to pick up the phone and call grandma when they need a hand in caring for their children. Grandparents are often an invaluable resource when it comes to childrearing, and can be a lifesaver for frazzled parents everywhere. 

    A study led by Kristen Hawkes with mathematical biologist Peter Kim found that in a computer simulation of a population of chimpanzees the contribution of grandmothers in caring for infants and children increased the average lifespan by almost 25 years. Their findings ultimately support the ‘grandmother hypothesis’, which attempts to explain why humans survive long after their childbearing years have passed, a quality which is somewhat unique to humans. 

    The postmenopausal survival of humans is anomalous because at first glance it appears to be at odds with the dogma of evolution. Ultimately our evolutionary prerogative is to pass on our genes, and so more children means a greater contribution to the gene pool. Once an organism is past its reproductive years, the reasoning goes, they become an evolutionary dead end. Sustaining older organisms without the ability to reproduce is also an added draw on the resources available to the rest of the community. Humans, therefore, are unusual in that they survive for decades post-menopause, long after they have lost the ability to reproduce. 

    One explanation for this phenomenon is the grandmother hypothesis, which posits that post-menopausal grandmothers help care for their grandchildren, thereby conferring an evolutionary advantage. In doing so they are simultaneously increasing their grandchildren’s probability of survival and allowing their daughters to bear more children, as they are partially relieving them of their parental responsibility of childrearing. In this way they are ensuring that their genes will be passed on through their offspring and subsequently on to their grandchildren. 

    The grandmother hypothesis was first proposed by evolutionary biologist William Hamilton in 1966, but only gained popularity after a field study of Tanzanian hunter-gatherers by anthropologist Kristen Hawkes. Hawkes found that when grandmothers helped with foraging, their grandchildren were often heavier and healthier and weaned at a younger age. Earlier weaning also decreased the interval between births, as once children were fully weaned their mothers were free to give birth again at little cost to their other children. 

    In the years following researchers began to put the grandmother hypothesis to the test. A 2010 mathematical simulation began with a population of 1,000 people and tracked changes in lifespan in populations with the aid of grandmothers and without. The researchers who conducted the study found that the average lifespan was not affected in either population, casting doubt on the validity of the grandmother hypothesis. Hawkes countered by pointing out several flaws in the simulation, and the authors ultimately conceded that their simulation did need several adjustments. 

    A new study led by Kristen Hawkes which was published today in the Proceedings of the Royal Society employed a new simulation that began with animals with chimpanzee lifespans. Female chimpanzees do not live long past their childbearing years, whereas humans survive for decades even after they have lost the ability to reproduce. When the simulation began each individual only lived an average of 25 years after reaching adulthood, making their lifespan closer to that of a chimpanzee. After 24,000 to 26,000 years of evolution, however, the length of time that the individuals survived as adults doubled. Researchers found that the simulated creatures survived an average of 49 years after reaching adulthood, a lifespan which is more similar to humans. 


    Living Longer? Thank Grandma. Credit: Shutterstock

    The simulation began with only 1% of females reaching grandmother age, and a 5% possibility of newborns acquiring a gene mutation which would decrease or lengthen their lifespan. By the end of the simulation the number of females which reached grandmother age climbed to 43%. To avoid artificially inflating the grandmother’s contribution the researchers included several parameters which limited the contribution of grandmothers: women were only considered grandmothers between 45 and 75 years of age, and they could only care for one child after the age of 2 at any given time. Even with these constraints, and only a minimal amount of 'grandmothering', the contribution of grandmothers still had a significant effect on the lifespan of the simulated creatures. 

    These findings come on the heels of a study published in Science in September in which the authors reported that ‘grandmother’ killer whales increase the survival of offspring. Their contributions were most pronounced in aiding the survival of grown male killer whales, but less so among their daughters. These results were widely touted as additional support for the grandmother hypothesis, and suggest it may also be relevant for the few other animals with a similar lifespan. 

    Another explanation for the increased longevity of humans contends that it is just an artifact of decreased predation. Before modern humans mastered the art of hunting they were more susceptible to attack by other animals, but as of now humans have virtually no natural predators. Over the past few years, however, the grandmother hypothesis has been gaining support as it has been accruing evidence in its favor. The grandmother hypothesis, however, is not an explanation for the steadily rising lifespan of humans, especially in developed countries: it is only supposedly working in conjunction with other variables such as increased hygiene, medical intervention, etc. So the next time Grandma complains about looking after the kids, remind her that it is her evolutionary duty to do so. Or maybe not- chances are that won't go over well, and you're probably better off staying on Grandma's good side.

    Comments

    Bonny Bonobo alias Brat
    Another explanation for the increased longevity of humans contends that it is just an artifact of decreased predation. Before modern humans mastered the art of hunting they were more susceptible to attack by other animals, but as of now humans have virtually no natural predators. Over the past few years, however, the grandmother hypothesis has been gaining support as it has been accruing evidence in its favor. The grandmother hypothesis, however, is not an explanation for the steadily rising lifespan of humans, especially in developed countries: it is only supposedly working in conjunction with other variables such as increased hygiene, medical intervention, etc. So the next time Grandma complains about looking after the kids, remind her that it is her evolutionary duty to do so. Or maybe not- chances are that won't go over well, and you're probably better off staying on Grandma's good side.
    It is probably best to stay on Grandma's good side as the Monty Python's team showed another possibly evolutionary significant grandmother behaviour that may be relevant to the Grandmother hypothesis, where Grandmothers were turning into predators and attacking and terrorising young men, as shown in this video :)
    My article about researchers identifying a potential blue green algae cause & L-Serine treatment for Lou Gehrig's ALS, MND, Parkinsons & Alzheimers is at http://www.science20.com/forums/medicine
    Bonny Bonobo alias Brat
    Sorry if I seemed a bit flippant putting in that Monty Python Hell's Grannies video link, but I do think it was relevant here. You said that :-
    Just because one hypothesis doesn’t adequately explain everything in its entirety doesn’t mean its not valid if the evidence supports it- there is never a smoking gun, things are always messy, complicated, and there is always an ‘x factor’ to be reckoned with. But you can’t reject everything all the time just because you want a catch-all answer, otherwise science would never move forward.
    But I'm afraid I have to agree with Gerhard that there are way too many factors and variables here for anyone to make any very credible deductions about whether a possible grandmother longevity gene has been or can be positively selected for by evolution. Some other genes are obviously much more straightforward, for example, I suffer from a genetic disorder called hemochromatosis otherwise known as the Scottish warrior or iron overload disease, this was a gene that evolution did appear to have positively selected for in Celtic societies, because it allowed women to produce a baby each year, often shedding large amounts of blood but still surviving to breastfeed and produce another baby the following year when females without this gene may well have died or become very anaemic and much less fertile. 

    Hemochromatosis also enabled the men, women and children carrying the gene to extract more iron from an often meagre, mineral deficient diet and gave the fighting men an advantage when they fought and occasionally lost copious amounts of blood that would have killed other men without the gene. 

    Nowadays the same gene is a positive disadvantage for these women who have a few if any children and for these men who rarely fight and shed blood, it is also very detrimental to people eating mineral rich diets especially with iron supplementation because undiagnosed and untreated iron overload can cause people to suddenly drop dead of heart attacks, making them much more prone to develop cancers than the average person that doesn't carry the gene as well as arthritis and many other health problems. If diagnosed in time it can be easily treated by the genetic disease sufferers giving regular blood donations and/or phlebotomies, it is thought that well over a million people in the US are currently suffering from this undiagnosed disease and its symptoms which has to be diagnosed with a specific genetic test.

    Unlike this quite easily comprehensible hypothesis of how evolution has positively selected for the hemochromatosis gene the grandmother longevity gene hypothesis is a lot less comprehensible and obvious. As Gerhard pointed out there is no evidence that the genetically programmed human lifespan has changed for thousands of years, even though it may vary slightly between individuals. The human life expectancy does however vary enormously because of so many factors, too many to list really and whether a woman lives to be a grandmother will always have been affected by many of these variables. 

    It is also easy to see how the survival of a woman to grandmotherhood could have both positive and negative effects upon the survival chances of her offspring. She may be a competitor for food and resources so that could be a negative effect but she may also have knowledge about child rearing and childbirth which could be a positive effect. Her continued existence might simply reflect the tolerance or aggression levels of the dominant males or females in that society and the liklihood of their offspring surviving or it might simply reflect increased male demise from other causes, fighting other tribes for example or diseases affecting more males than women. Maybe she survived to grandmotherhood because she was less fertile than other females and therefore had lower risk of dying in childbirth than her counterparts but that doesn't imply that she would be genetically fitteror more fertile as she would have had less offspring, so that would have been a negative and so on....... 

    I think that the possibilities of so many positive and negative factors and variables affecting whether a woman becomes a more or less fertile grandmother or not are endless, so I can't see how the implications for this study giving support for the grandmother hypothesis' or the evidence from the simulation can really be used to deduce anything much more than mere speculation to support the grandmother hypothesis. It reminds me of the promiscuous female guppies Science20 blog that also had many unknown but potentially significant factors and variables that were not included in the experiment and which made that study and its deductions also rather dubious. The promiscuous female guppies in that study produced more grandchildren than the singly mated female guppies regardless of whether they lived to see or even eat their grandguppy offspring or whether they lived fast and died young :)
    My article about researchers identifying a potential blue green algae cause & L-Serine treatment for Lou Gehrig's ALS, MND, Parkinsons & Alzheimers is at http://www.science20.com/forums/medicine
    Gerhard Adam
    The grandmother hypothesis, however, is not an explanation for the steadily rising lifespan of humans, especially in developed countries:
    Sorry, but there's no evidence for this.  It seems like you're conflating life expectancy with life span. 
    Humans, therefore, are unusual in that they survive for decades post-menopause, long after they have lost the ability to reproduce.
    Actually this is specifically females, but even so, given the normal issues of disease, predation, etc. on what basis would one conclude that there is any genetic component that would have increased longevity?  There is no doubt that more people [related or not, male or female] would improve the likelihood of a child surviving to adulthood, although this also has nothing to do with life span, rather it is life expectancy.

    However, unless humans were routinely living into their 70's and 80's, there's no basis for assuming that genetics would have favored a longer lifespan for either sex, if their life expectancy was considerably lower.  There couldn't be a fitness advantage, since few ever lived that long.
    Earlier weaning also decreased the interval between births, as once children were fully weaned their mothers were free to give birth again at little cost to their other children.
    The missing element here is indicating how many children actually survived to adulthood. 

    As an example we can see that approximately 1/3 to almost 1/2 don't live to 15, after which another 1/3 don't live through adulthood [although they may live long enough to reproduce]:
    ...we see that on average 57 percent, 64 percent, and 67 percent of children born survive to age 15 years among hunter-gatherers, foragerhorticulturalists, and acculturated hunter-gatherers. Of those who reach age 15, 64 percent of traditional hunter-gatherers and 61 percent of forager horticulturalists reach age 45. The acculturated hunter-gatherers show lower young adult mortality rates, with 79 percent surviving to age 45, conditional on reaching age 15.
    http://www.anth.ucsb.edu/faculty/gurven/papers/GurvenKaplan2007pdr.pdf
    Mundus vult decipi
    ehardy52

    Your expectancy vs. lifespan point isn’t really relevant here, as it doesn’t affect any of the conclusions, but regardless of shades of meaning, I still don’t know how you could take issue with the first sentence you quoted. It is only taking into account the “normal issues of disease and predation” which you refer to later. In your article you attempt to minimize (a tad overly so, in my opinion) the effect of medicine, technology, and other ‘modern’ variables on prolonging lifespan, but you do concede that “it becomes reasonable to argue that advances in technology have probably contributed little to human longevity while it may have contributed (along with numerous other social and lifestyle changes) to improving the probabilities of surviving the earlier years”. That sentence was only to point out that there are other important variables in determining life expectancy AND lifespan.

    To an extent, however, longevity preceded many modern interventions and there is very likely a genetic/evolutionary component. So why are you excluding genetics entirely as being one possible contributor? You say that “there's no basis for assuming that genetics would have favored a longer lifespan for either sex, if their life expectancy was considerably lower. There couldn't be a fitness advantage, since few ever lived that long.”

    It has been well documented that lifespan does in fact have a genetic component. At the very least one could conclude that it is one possible factor on the basis that there is a proven correlation between longevity and heredity. One that is not completely dependent on environmental factors, but of course eating well, exercising often, quitting smoking, and having a pill for everything sure helps.

    You also assume that genes that favor a longer lifespan would come at cost, and therefore there would not be a fitness advantage, but there is no support for that assumption. A Nature study from several years ago also says otherwise, and supports many aspects of the hypothesis- including that women who live longer tend to have not only more grandchildren, but more healthy grandchildren who reach adulthood. This has been shown time and time again. (This also addresses the ‘missing element’ you refer to- a greater percentage [not number] of ‘grandmothered’ children make it to adulthood and tend to be healthier overall)

    Sear, R., Mace, R., McGregor, I. A. 2000 Maternalgrandmothers improve nutritional status and survival of children in ruralGambia. Proc. R. Soc. Lond. B 267, 1641–1647. doi:10.1098/rspb.2000.1190

    Lahdenpera et. Al. 2004 Fitness benefits of prolongedpost-reproductive lifespan in women. Nature 428, 178–181

    Ragsdale, G. 2004Grandmothering in Cambridgeshire, 1770–1861. Hum. Nat. 15, 301–317. doi:10.1007/s12110-004-1011-y)

    The fitness benefits only wane after their offspring are no longer able to reproduce. And in the instances where life expectancy is exceeded- ie, early humans avoid getting eaten by a tiger or whatever it is they were threatened by- the benefit of being able to live past their reproductive years and ensuring that their genes (which would include the tendency towards longevity) are passed on would be a considerable fitness benefit.

    Say that we started out with a fairly set lifespan: regardless of all the things that could kill them, early humans could only live 30 years (this is purely hypothetical), at which point they die of old age. But most die by age 20 anyway. Now say that a mutation which allows the carrier to live longer starts getting passed around. Even if only 1 out of 100 enjoyed the benefit of that mutation- only 1 in 100 lived to 40, had offspring which then went on to bear many healthy, long-lived grandchildren, they would still have an advantage. They would have had a more sizable contribution to the gene pool, and there would be a better chance that one of their many grandchildren would pass on the same genes. Factor in tens of thousands of years and this effect would eventually be amplified- which is exactly what happened in this study. In their simulation “the population [was] subject to an extrinsic, population-dependent deathrate that affects everyone equally. Calculation of the population-dependentdeath rate is explained in the Agent-based model algorithm describedin the electronic supplementary material”, and so there was a sort of ‘built-in life expectancy’ in their simulation.

    Analyzing the issue from an evolutionary perspective is just one way of looking at it. It is also particularly tricky because so much of it is speculation and hypothesizing and then putting it to the test with statistics and measurements,as there is no way to examine, manipulate, or directly observe these things. No self-respecting scientist would confuse this as a sole explanation for a perceived trait, so I think you aren’t putting this in context. Just because one hypothesis doesn’t adequately explain everything in its entirety doesn’t mean its not valid if the evidence supports it- there is never a smoking gun, things are always messy, complicated, and there is always an ‘x factor’ to bereckoned with. But you can’t reject everything all the time just because you want a catch-all answer, otherwise science would never move forward.

    “There is no doubt that more people [related or not,male or female] would improve the likelihood of a child surviving to adulthood,although this also has nothing to do with life span, rather it is life expectancy.”

    If that were the case, then that would actually detract from the fitness benefits of grandmothering. In the article the authors actually used this principle to weaken the grandmother effect, but still got the same results. They say that:

    "Rather than grandmothers helping only their own daughters, our model distributes grandmothering to any eligible dependents in the population. It may seem that this would not only weaken selection for grandmothering, but undercut it altogether. Those with shorter life spans spend little or no time grandmothering and have higher rates of offspring production.If females with lower L free-ride on grandmothering supplied by others, this should halt the spread of grandmothering and the evolution of increasing life spans."

     In this instance, ‘females with lower L’ should have an equal contribution to the gene pool, and so there wouldn’t be a bias towards ‘females with higher L’ passing on their genes (and thus the average lifespan increasing over time).And yet we still see this increase, so it must be conferring some benefit, which does seem to be the case based on other research and what was observed inthe study. They explain this by saying “Increasing L raises the number of grandmothering years and grandmothering gives greater benefits to females with higher L because their offspring probably have higher L as well. The latter point matters because offspring with higher L have higher survival and are dependent longer, making themmore likely to be adopted. In addition, grandmothers take oldest dependents first, disproportionately accepting those with higher L. Although adoption does not benefit the dependents themselves, it does benefit their mothers. This differential benefit that mothers with higher L gain from grandmothering drives the evolution of increased longevity”.

    In addition to this, there is also no reason to assume that more people would automatically improve the likelihood of a child surviving to adulthood, because that also means less resources per child, especially if they didn’t have adequate help obtaining those resources (mom, grandma), and more work for everyone else withall of those extra mouths to feed. According to the most basic evolutionary biology/psychology, we are on a very primal level far less invested in other people’s children when we have our own genetic contribution to worry about (and yes, this is a somewhat broad/superficial statement, because once you start talking communities and civilized society many of ourevolutionary impulses are repressed and things get complicated).

    You also say that this is specific to females, but the authors of the study did account for the fact that for males, living longer would come ‘at cost’- and they found that the outcome was always the same, the only difference being the length of time it took to reach the doubling took more or less time. They also ignored the importance of pair bonds in their study. In some primates, females who have a disproportionate amountof caretaking duties tend to live longer, while in populations where childrearing duties are shared equally between the sexes their lifespans are approximately the same.

    Gerhard Adam
    In your article you attempt to minimize (a tad overly so, in my opinion) the effect of medicine, technology, and other ‘modern’ variables on prolonging lifespan...
    That's just it though, there is no technological change that has contributed to lifespan.  The changes are for life expectancy.   The human lifespan is fundamentally what it has always been, which life expectancy has changed dramatically depending on the environment and lifestyle.
    It has been well documented that lifespan does in fact have a genetic component. At the very least one could conclude that it is one possible factor on the basis that there is a proven correlation between longevity and heredity. One that is not completely dependent on environmental factors, but of course eating well, exercising often, quitting smoking, and having a pill for everything sure helps.
    I don't dispute that lifespan has a genetic component, but you then turn around and invoke longevity, which is life expectancy.  Eating well, exercise, etc. etc. have nothing to do with lifespan.
    You also assume that genes that favor a longer lifespan would come at cost, and therefore there would not be a fitness advantage, but there is no support for that assumption. A Nature study from several years ago also says otherwise, and supports many aspects of the hypothesis- including that women who live longer tend to have not only more grandchildren, but more healthy grandchildren who reach adulthood.
    Of course there's a cost, because there are more individuals that have to consume resources belonging to the group at large.   However, you then talk about healthy grandchildren, which again, has nothing to do with life span.  That is a life expectancy issue.  This isn't merely parsing terms, they are two separate and distinct things.  A normal human lives for about 7-8 decades.  That is the typical lifespan.  No matter what else an individual does, that is what the biology says [with obvious variations].  However, an individual that smokes, engages in risky behaviors, etc. may have a shorter life expectancy, despite their biological lifespan.
    You also say that this is specific to females ...
    Yes, because your reproductive argument doesn't apply in the same way to males.  Older males will be constrained by their ability to provide resources for their offspring, but the ability to reproduce doesn't wane in the same way, so it is entirely possible for a 70 year old male to still be reproductively viable.

    The entire argument about the "grandmother hypothesis" only addresses children having a better chance to reach adulthood.  It says nothing about human lifespan; it is only improving life expectancy for children. 

    Women appear to live about 5.2 years longer than men with respect to life expectancy, not lifespan. 

    So, in a nutshell, what it comes down to is that life expectancy is the time you expect to live within the biological constraints of your lifespan.  Therefore to argue that there is a genetic contribution is meaningless if people do not actually achieve their lifespan potential.  To argue that people improved their life expectancy by these behaviors indicates absolutely nothing about the genetic basis for one's lifespan.
    Say that we started out with a fairly set lifespan: regardless of all the things that could kill them, early humans could only live 30 years (this is purely hypothetical), at which point they die of old age. But most die by age 20 anyway. Now say that a mutation which allows the carrier to live longer starts getting passed around.
    Yes, if we make that assumption that humans only lived such a short span, then your conclusion would be based on the knowledge of how long humans live today.  Yet, there is no reason to believe that lifespans were ever that short for humans, so if the lifespan is not appreciably different today than it was then, the argument denies any genetic contribution.

    This link indicates that human lifespans have been fundamentally constant for the past 2000 years.  If we consider the oldest human mummy [Otzi] we find a relatively active adult from about 5300 years ago, presumed to be 45 years old that was killed by an arrow, so again, this argues against any notion that somehow humans were living in "old age" at the time.

    So, the problem isn't whether genes can contribute to an increased lifespan.  Certainly they can.  What has to be demonstrated is that human lifespan has changed significantly enough to warrant such an assertion.  In the absence of such evidence, then one must conclude that the notion of the "grandmother hypothesis" in contributing to the human lifespan by genetics is simply speculation.
    Analyzing the issue from an evolutionary perspective is just one way of looking at it.
    I fully agree, which is precisely why I've raised the issue.  Evolution is rife with all manner of "just so" stories, because it becomes a convenient way to presume that we know how things came to be the way they are.  There might even be a reasonable point here if one could demonstrate increased fitness due to cooperative groups, amplified by familial support, etc. 

    Again, at best, the "grandmother hypothesis" can demonstrate that this may have contributed to increasing life expectancy for children. 
    Mundus vult decipi
    ehardy52
    Longevity, by definition, means "long life". You define life expectancy as "a statement about probabilities and has little to do with life span(1). In other words, expectancy is determined by taking all the things that can kill you and averaging them out to determine what your "expectation" of survival is", yet you say longevity and life expectancy are the same thing. You are thoroughly confusing your argument by harping on trivialities (especially when they are inconsistent), so lets move away from which-word-is-used-where. 

      You acknowledge the genetic aspect, yet you are ignoring it. You say that "at best the grandmother hypothesis can demonstrate that this may have contributed to increasing life expectancy for children". That is true, but if we weren't biologically capable of living past a certain age- if we reached senescence immediately our reproductive years were over- then most people wouldn't live long enough to meet their grandchildren. 

     In the paper they refer to it as "L". Lets say L is a gene. People with "L", which confers the biological capability of longevity relative to their peers, end up with more grandchildren. Additionally, an increased percentage of their already increased number of grandchildren make it to adulthood and reproductive age. All (or most) of their grandchildren now carry "L", and over time "L" is overly represented in the gene pool because there has been a much higher contribution by individuals with "L". 

    But "L" wouldn't have been selected for in the first place if it didn't make a difference one way or another whether or not they lived longer. If there were no advantage to living longer, when it doesn't actually affect the length of time one is capable of reproducing, then individuals that could live well past their reproductive years would be outliers.

     Unless, of course, this quality is somehow selected for, if it increases fitness and has some benefit that outweighs the costs. If this were the case, you would see more people able to live past their reproductive years, with more/healthier grandchildren, and in this way the hereditary aspect of longevity is passed on. Eventually such a desirable trait would be selected for, and as of now women live on average just long enough to see their children reach menopause. 

    The point is that there must be a reason that "L", as a trait, has been so strongly selected for over time, and this is one possible explanation (or at the very least, a contributing factor). And we are not talking about life expectancies here, we are talking about the average human lifespan, and possible reasons why it would be so drastically different from the rest of the animal world above and beyond life expectancy and any associated variability therein.
    Gerhard Adam
    In the paper they refer to it as "L". Lets say L is a gene. People with "L", which confers the biological capability of longevity relative to their peers, end up with more grandchildren.
    Yes, I get that's what they say in the paper, and that's where the nonsense begins.

    (1)  First one has to demonstrate that human lifespan has changed over the reported time interval.  If humans 50,000 years ago had the same lifespan as those today, then this study is irrelevant and false.

    (2)  One has to demonstrate that there is a gene that is both selectable and can be demonstrated to be heritable within a population.  This is flatly wrong.
    The genes isolated so far are only a few of what scientists think may be dozens, perhaps hundreds, of longevity- and aging-related genes.
    http://www.antiagingresearch.com/secrets_of_aging.shtml

    In reality there are many genes and pathways that govern the aging process of the body, as well as environmental factors that can have an affect.
    http://www.bio.davidson.edu/courses/genomics/2004/mcdonald/longevity_gene.htm

    A newly discovered suite of 150 "long life" variants in about 70 genes allows scientists to guess, with 77 percent accuracy, whether a person can live into their late 90s or longer, a new study says.
    http://news.nationalgeographic.com/news/2010/07/100701-boston-university-health-genes-live-100-longevity-genetic-science/
    The point being that if lifespan is determined by a complex interaction of genes, then that argues against there being any particular gene that can be singularly selected for.  In short, the more complex the interactions, the lower the heritability, indicating that such a genetic mix has already gone to fixation within the population.

    Even in those cases, where select populations demonstrate fundamental differences that could infer an increased lifespan, this isn't by any means clear [i.e. Ashkenazi Jews]

    So, not only does this study make the serious mistake of inventing a scenario that may never have existed [i.e. humans living less than their current lifespan], it then creates a model based on a single genetic trait [which has no scientific support] and presumes that it is directly capable of being selected for to produce the desired result.

    There is no evidence to suggest that this is even remotely correct.

    Current human lifespan is defined as being about 120 years [based on the oldest recorded age of a human - 122], despite few ever getting close to this number. 
    However, it's more problematic than that.  Consider Besse Cooper who lived to be 116 years:
    Besse Cooper did not come from an especially long-lived family. Her seven siblings died in their 60s and 70s. “Her mother died in her 60s; her father lived to be 72,’’ Sidney Cooper says.
    http://www.georgiahealthnews.com/2012/08/healthy-life-georgia-besse-coopers-world-beating-longevity/
    While this is only one instance, it creates a problem because it suggests that there is no direct genetic correlation between long-life [at least not in the "single-gene"] sense.  After all, if it were a single allele, this would suggest that it was recessive and not particularly prone to being passed on.  Of course, this would depend on someone further in her ancestry actually demonstrating that they lived as long.  If not, then we're right back to where we started. 
    Her secret to longevity: "I mind my own business," Cooper said. "And I don't eat junk food."
    http://www.huffingtonpost.com/2012/08/27/besse-cooper-worlds-oldest-living-woman_n_1833864.html
    I can make up any argument about a make-believe trait and how it could be selected for.  However, unless the change being proposed can actually be demonstrated as having occurred, then such speculation is meaningless.  Suppose I wanted to argue that a select group of people have a selectable gene that allows them to grow to be 10 feet tall "giants".  Now there are no 10 foot tall individuals, but that doesn't matter, because we can argue that this is due to environmental factors that prevent us from being able to maximize the gene's potential.  We can also define the range of "giant" as anyone between 6-10 ft tall.  We can then argue about how such a height advantage could be selected for, despite no one actually achieving 10 feet, and I will guarantee that if I ran their simulation with the same criteria, it would also demonstrate how this was possible.

    So, other than this being a complete fantasy, the model would "prove" my assertion. 

    Mundus vult decipi
    randallmayes
    Eve- in the intro you discuss how females are programmed to be disposable, in theory anyway. This implies a controlling mechanism. Assuming it is true, the mechanism could be reversed. From synthetic biology I have learned these types of mechanisms are governed by natural laws towards equilibrium. In bacteria the mechanism is quorum sensing and in insects epigenetics. Insect castes have different life spans. In humans we have similar forces that regulate gender births. Do you think that these forces are involved?
    Randall Mayes