A recent post on the Gene Expression blog (here) alerts me to an article on selection for human longevity in PLoS One (here).
Explaining ageing is actually harder than it might seem and there is no particular reason to suppose that ageing should occur at all. One explanation, described by Peter Medawar, is that genes with deleterious effects later in life are relatively less effectively selected against because of a general increase in mortality with age (the longer you live the higher the chance of accidental death) and can persist in a mutation-selection balance. Decreases in the intensity of selection with age can also favour genes with beneficial effects earlier in the lifespan and deleterious effects later. This scenario, first described by George Williams, is called antagonistic pleiotropy and can take a number of forms depending on the sorts of trade-offs lying behind these gene effects.
But there is a problem which is unique to humans (ed. it turns out I am wrong that this is unique see here!) and that is the female menopause. As Hamilton pointed out there should be a sudden increase in mortality after the age of menopause in both sexes because an expected fertility of zero effectively negates selection against deleterious genes acting at this time. Arguments aimed to try to fell this “wall of death” are generally focussed on intergenerational transfers and the best known of these is the “grandmother” hypothesis which suggests that the continued presence of post-reproductive females can enhance survivorship of grandchildren and other relatives through the provision of resources and time. In this way longevity is kin selected.
But the PLoS One article by Tuljapurkar et al. offers a new explanation, which is that male reproduction past the age of female menopause can strengthen selection for longevity and assuage the rise to infinite mortality predicted by Hamilton. Collating data from several cultures they show that males continue to show non-zero fertility rates after the age of female menopause (which is not surprising given that males tend to mate with younger females across the board), but also they show that the shape of the fertility function is different in males compared with females. It is not simply an echo of female fertility rates at younger ages, but instead shows an extended tail of male fertility with increasing age. This effect is likely a result of several factors including serial monogamy (wherein males are more likely to re-marry than females), polygyny (in which males have multiple partners) and the existence of high status males (who show persistent sex appeal into old age). It is important to remember that genes for longevity can be shared between the sexes so that theories of ageing should take account of fertility in both sexes. Tuljapurkar et al. explicity modelled the dynamics of fertility in both sexes to produce a model supporting their conclusion that male age-specific fertility rates can explain the persistence of human longevity past the menopause and the absence of a “wall of death”.
Evolving Ideas 
Personally I don’t see the differences in fertility between men and women all that surprising. It all comes down to the “implementation”:
Sperm is the smallest of cells, generated “on demand” … eggs are the largest of cells, stored over a lifetime. It is obviously more difficult to get a good quality fresh egg than fresh sperm, so there better be a point at which the system shuts down.
Of course there is the question of just why exactly did things end up the way they are … but that is requires a different approach, in which say the menopause is a unavoidable consequence of the way human reproduction evolved rather than being the mechanism that explains other effects.
Your alternative non-adaptive explanation for menopause is difficult to falsify because it could take make many forms, but there are two problems I perceive with it: 1. females do not literally run out of eggs and 2. even if they do decline in quality surely it is still worth attempting reproduction in hopes? But I was not addressing the existence of menopause per se, instead I was taking it as a given and asking why survival after this time is possible in the absence of selection for viability. One non-adaptive possibility is simply that it is unlikely that mutations could arise with lethal effects reliably timed to occur after menopause. In this case the cost of dying before menopause is sufficiently high that mutations with any level of uncertainty in their timing of action would be selected against. However it occurs to me that antagonistically pleiotropic alleles with beneficial effects early and deleterious effects triggered by post-menopausal hormonal changes could perfectly well arise and contribute to a wall of death. I therefore believe an adaptive explanation is required.
Ben said: “why survival after this time is possible in the absence of selection for viability.”
there is not “absence of selection”, you forget that one has to raise the child that was born right before the menopause. That’s adds a good 15 years of very strong selection.
Also “2. even if they do decline in quality surely it is still worth attempting reproduction”
No, again you only look one step ahead. I won’t get into details here because I’m afraid that I formulate in a way that may be insensitive to other people but here again you forget that having a special needs child puts can put tremendous strain on all members of a family and thus acts as a strong counterselection.
Your first point about raising children born before the menopause: fair enough – this is, after all, a form of intergenerational transfer although admittedly not of the sort I originally described (where the transfers were to grandchildren). The only problem with this is that it could only delay the wall of death by 15 years right? An abrupt menopause gives an abrupt end to child-rearing even if this is delayed to rear the last. Perhaps not though – because the strength of the selection you describe will depend on the level of care provided by siblings and others in a group – something that might be heterogeneous enough to break down the rapid decline in selection for viability.
Your second point about the costs of reproduction at later ages depends on the relative likelihood of birthing children with disabilities (the cost you highlighted) versus spontaneous abortion and also on the likelihood of infanticide (which is another, albeit disturbing, way to mitigate the cost). One would need to posit a threshold effect to explain how this might lead to an abrupt decline in fertility at menopause.
You are, of course, right to say that I have only looked one step ahead in my previous reply. But it may take several more steps in thinking to explain the existence of menopause and the non-existence of the wall of death. Certainly absent from my discussion, for the purposes of assessing non-adaptive explanations, is a description of menopause itself which is something I do not well understand.