It is well known that females of many species live longer than males. Some fundamental aspects of gender roles in mating and reproduction tend to lead to this outcome. It isn't peculiar to our species, so it can't have anything to do with technology or the sociology that comes with intelligence. Thus the dominant arguments really have to be evolutionary in nature. It is less well known that, in our species at least, women have worse health than men in later life, despite a greater life expectancy. This also probably arises at root from fundamental aspects of gender roles, but there is a great deal of room to argue for any specific position on how exactly it is that evolutionary processes lead to the observed result.
In the paper noted here, researchers take a swing at explaining how we could arrive at the position of worse female health, invoking the selection of gene variants that benefit males in late life but harm females in late life. This is a sort of cross-gender antagonistic pleiotropy to complement the usual understanding of how genetic variants that harm individuals in later life might arise. The size of the effect may depend upon the existence of menopause, which is only observed in a few species, however, which makes it harder to support any theoretic position with solid data. The paper makes for interesting reading, as is the case for most such research.
That said, I disagree with the authors' assertion that we need to understand this and other similarly subtle evolutionary mechanisms in order to produce greater human longevity. Understanding is not a bad thing, mind, and science is a worthy goal, but here understanding is near completely orthogonal to progress in the treatment of aging as a medical condition. Both men and women age for same underlying reasons, the accumulation of molecular damage is the same in both genders. After the research and medical communities have built therapies that can repair that damage, then it won't matter in the slightest how evolution has handled or mishandled late life resilience to high levels of damage. No-one will have high levels of cell and tissue damage any more.
Scientists have long wondered why older women are less healthy than older men, given that men at any given age are more likely to die than women (a puzzle known as the "male-female, health-survival paradox"). The answer, according to recent research, is "intralocus sexual conflict" - genes that benefit one sex but harm the other. The researchers used mathematical models and experimental data on flies to show that such genes can easily spread if they take effect after female reproduction stops.
"Shared genes tether the sexes together in an evolutionary tug of war. Selection is trying to push females and males in different directions, but the shared genome means each sex stops the other from reaching its optima. Basically, certain genes will make a good male but a bad female, and vice versa. However, after females reaches menopause, they no longer reproduce to pass on their genes which means selection (which is reproduction) on females is greatly weakened. So after that point, any genes that improve late-life male fitness will accumulate, even if they harm female fitness."
While we broadly understand why mortality risk rises as fertility and general performance decline with age, it is less clear why the tempo and severity of these changes often differ between the sexes. In humans, survival, fertility, and performance show sex-specific patterns of decline with age. Strikingly, women stop reproducing decades before dying, while men can reproduce throughout their adult lives. Additionally, men are more likely to die than women in most age-classes, but are healthier than women late-in-life. To be clear, this is not just due to the selective loss of low quality males, as female mortality rates are lower than male rates at nearly all ages despite poorer female health. This sex difference has been termed the "male-female, health-survival paradox", and while its causes are not well understood, some resolution of it is needed if we are to ensure healthy aging as human lifespan increases.
Here we focus on the health aspect of the paradox and suggest that intralocus sexual conflict might explain why women are less healthy than men late-in-life. Intralocus sexual conflict occurs when the sexes have different optimal values for a shared trait with a common genetic basis. For example, male broad-horned flour beetles develop enlarged mandibles and males with larger mandibles have higher fitness. However, daughters of males with large mandibles have lower fitness because of the masculinisation of the body that occurs with these genotypes. This means that alleles associated with mandibles are subjected to an intersexual tug-of-war over optimal values, with high fitness male genotypes making low fitness females. This type of conflict means that the alleles encoding a high-quality male often produce low quality females and vice versa.
For intralocus sexual conflict to explain the health-survival paradox, male-benefit sexually antagonistic alleles with late-acting effects must accumulate. This is entirely feasible because women experience the menopause. This means that selection against any alleles with costly effects when expressed in females will weaken dramatically once women undergo the menopause and stop reproducing, because these alleles can only have indirect effects on female fitness. However, in men there will be selection for male-benefit alleles over the entire lifespan because men can keep reproducing until advanced ages. This would allow late-acting, male-benefit sexually antagonistic alleles to spread and accumulate in the human genome and reduce female health late-in-life, as females carrying late-acting male-benefit alleles express trait values closer to male than female optima.
To formally test this hypothesis, we assessed whether a male-benefit, sexually antagonistic allele could spread through a diploid population using an evolutionary modelling framework. We show theoretically that under biologically realistic assumptions of costs and benefits, such antagonistic alleles can accumulate. Using Drosophila model systems, we then assessed whether sexual conflict solutions are feasible by testing whether populations evolving with selection for late-life male reproduction, but with no direct selection on females (as is the case for post-menopausal women), developed late-life costs to females. Our data broadly support the predictions and suggest that intralocus sexual conflict could help explain the male-female, health-survival paradox.