Menopause wars: can male preferences for young women explain ‘the change’?

Why would an otherwise healthy animal stop reproducing? Natural selection usually favours genes that elevate reproductive success because the very act of reproduction is how genes proliferate. So adaptations that involve self-limited reproduction call for unusual evolutionary explanations.

Sterile worker ants and honey bees present one such unusual adaptation. These females forego any chance to reproduce so that they can help their sisters become queens. Insect sociobiologists have shown just how special the evolution of sterile workers is. The massive genetic lottery win that comes when a sister ascends to head a hive of her own more than compensates the worker for her life of sterile devotion.

But human women also stop reproducing around their late 40s. Menopause remains among the most hotly debated products of human evolution. I have written here before about the competing theories. And earlier this month Dyani Lewis wrote a very clear overview of the ideas surrounding the evolution of menopause.

But today I’d like to consider a computer simulation model published last Friday in PLOS Computational Biology. In the breathless style so beloved of journal publicity departments, the press release quotes author Rama Singh as saying:

Menopause is believed to be unique to humans, but no one had yet been able to offer a satisfactory explanation for why it occurs.

Singh, together with McMaster University colleagues Richard A. Morton and Jonathan R. Stone argue that the reason menopause evolved was that older men preferred young women as mates. Their logic resembles that behind successful theories for the evolution of ageing: natural selection grows weaker on older cohorts, allowing late-acting mutations to accumulate. Likewise, when older women get left on the shelf, late-acting mutations that rob them of their fertility are allowed to accumulate.

The paper builds on an intriguing earlier model in which men’s ability to sire offspring late in life, and the fact that many wealthy and powerful men have done just that for millenia, can have the incidental consequence of prolonging female lifespan as well, by weeding out some of the late-acting mutations that would otherwise act after women have ceased reproducing. That idea has some merit for explaining why women live a long time after menopause, but it says nothing about why they stop reproducing in the first place.

The new model shows that genes that lower the fertility of older women (but not men) can accumulate. But they do so in a rather artificial situation: the genes that alter age-dependent survival affect both males and females the same. I will wage that if the researchers had allowed mutations to affect male and female survival independently, female survival would have waned at least as much as female reproduction did. I think the assumptions of this model were artificially disposed to getting the observed outcome.

That’s not to say the idea lacks merit. I’m just not convinced that the study lives up to the press-release hype. Hype, I might add, that has seen more cut-and-paste action in the print and electronic media than a Year Three school project. Complete with stock images of ageing male celebrities stepping out with twenty-something “latest” girlfriends. Check out the Sunlight Foundation’s Churnalism, analysis of the Guardian’s version of the story.

In fact, my go-to source for garbled science news, The Daily Mail did a slightly better job than the Guardian and several other sites. They quote Oxford post-doc, Dr Maxwell Burton-Chellew, who didn’t mince his words, calling the study just ‘plain wrong’.

It seems to me infinitely more plausible and more consistent with decades of evidence that men’s preference for younger women evolved as a response to the declining fertility of older women, and not the other way around. That said, however, science doesn’t work by rejecting ideas on plausibility grounds alone. This new idea should be developed and considered more thoroughly, including the possibility of feedback loops between reproductive ageing and preferences for younger mates.

Rob Brooks does not work for, consult to, own shares in or receive funding from any company or organisation that would benefit from this article, and has no relevant affiliations.

The Conversation

This article was originally published at The Conversation.
Read the original article.

Is human longevity due to grandmothers or older fathers?

Why do humans tend to live such a long time? Our closest relatives, the chimpanzees, can last into their mid forties in the wild. Yet somewhere in the last six million years, human lifespans have lengthened dramatically, so that living into our seventies is no big surprise.

The last few weeks have seen some exciting new developments in this area. First, a recent paper featured in The Conversation showed that at all ages, humans are less likely to die than chimps.

Excitingly, however, modern health care, diets and the steady decline in violent deaths have slashed mortality rates of young adults. People in societies like Japan are now almost 200 times less likely to die in at a given age than people of the same age in hunter-gatherer societies.

The dramatic declines in modern mortality rates are almost entirely due to technological developments, but the lengthening of the maximum potential human lifespan since we diverged from the other great apes poses an intriguing evolutionary problem.

Our bodies only function as well as they do because we have a quiver-full of cellular repair and maintenance mechanisms. For example, we have systems that correct mistakes in DNA replication, and others that detect and kill off pre-cancerous clusters of cells.

But natural selection optimises those mechanisms to operate during our expected lifespan. Modern people who live beyond seventy are much more likely to suffer from cancers, dementia and other diseases of old age. Few of our ancestors – even the most recent ones – lived that long, and these late-onset diseases didn’t interfere with their successful reproduction. By the time they got the diseases, our ancestors had already passed their genes on – and that’s why we carry those same genes.

Six million years ago, the diseases of old age probably kicked in before our great-ape ancestors hit forty. The evolution of a longer lifespan involved a steady postponement of ageing. But only if older individuals contribute to the success of their own genes can this actually happen. Continue reading Is human longevity due to grandmothers or older fathers?