As we grow older, we experience declines in our health, fertility and survival. Explaining why this is once posed an enormous challenge to evolutionary biology. Although we now broadly understand why we age, many outstanding questions about the evolution of aging remain. Our paper considers one of these – as we grow older, why do men die but women suffer?
Men are more likely to die than women at most ages but spend a greater proportion of their lives in good health. This is the male-female, health-survival paradox. We first heard about this paradox from human demographers using powerful data-sets to tease apart how lifestyle, biology and survey methods might contribute to it. When we delved into proposed biological mechanisms underpinning the paradox, we realized that most focus on why men die earlier – explanations that include the unguarded Y chromosome and the deleterious effects of testosterone. As evolutionary biologists working on sexual selection, when we see one sex doing something well (being healthy late-in-life) and the other sex doing it poorly (being unhealthy late-in-life), we immediately think of sexual conflict. As far as we could tell, sexual conflict did not feature in the literature on this paradox even though we believed it could be central to it.
Intralocus sexual conflict occurs because males and females express many shared traits, but often have different optimal values for these traits. Weapons are a good example – in many species males use weapons to fight off competitors but in females weapons represent wasted resource that could otherwise be spent on egg production. When this occurs, there is selection for weaponry in males, but against it in females. The genes underpinning non-sex-limited weapons would therefore be subject to an evolutionary tug-of-war, being pulled towards different trait values when expressed in either sex. This conflict can mean that genes that make a good male do not necessarily make a good female and vice versa. We know that alleles with sexually antagonistic effects exist in humans, for example there are alleles that are associated with high male attractiveness, but reduced female health.
Our paper expands on this to make a simple point: a sexually antagonistic allele that increases male fitness but reduces female health will increase in frequency if its affect are felt after the age of menopause. That is, if males keep reproducing past this point. Selection against such alleles in females will be weak because women have stopped reproducing. This may allow the accumulation of male-benefit sexually antagonistic alleles, which could drive sex-differences in health late-in-life – having masculinised gene profiles might not be good for females and menopause must relax the conditions under which male-benefit female-detriment alleles can accumulate (because selection is weak in females).
What next? While we present basic data from flies generally supporting our ideas, the theory needs testing in people. If our theory is supported more generally, we can ask what (if anything) can we do about it to improve human healthy aging? More generally, the work highlights the importance of communication between biomedical sciences and evolutionary biologists – while human health is shaped by society and lifestyle, novel insights can emerge by applying evolutionary theory to biomedical problems.
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