Mitochondria and male lifespan: Women outlive men. An evolutionary curiosity may explain this

Mitochondria and male lifespan: Women outlive men. An evolutionary curiosity may explain this

May 31st 2014 | From the print edition

WHY past generations regarded women as the weaker sex is a mystery to anyone who has examined the question objectively, for they are far stronger than men—outliving them in pretty well every society in the world. Partly that is because men are more violent, and their violence is largely directed at other men. But partly it is physiological. Men seem to wear out faster than women do. Yet no one knows why.

Madeleine Beekman of the University of Sydney, Australia, and her colleagues, however, have a hypothesis. As they outline in a paper in the Philosophical Transactions of the Royal Society, they think at least some of the blame lies with subcellular structures called mitochondria (pictured), which provide the body with its power by burning glucose and using the energy thus released to make ATP, a molecule that is biology’s universal fuel.

Mitochondria are intriguing. They are descendants of bacteria that teamed up with the ancestors of animal and plant cells about a billion years ago. As such, they retain their own genes. And this is where the problems start. To avoid fights between genetically different mitochondria in the same cell, most species have arranged for their mitochondria to come from only one parent—usually the mother. This means, as Dr Beekman notes, that a male’s mitochondria are stuck in an evolutionary dead end. They cannot evolve in male-specific ways, because no matter how much good they do a male body they inhabit, they will not be passed on to the next generation.

Male and female physiologies are sufficiently similar for this not to be a central problem, but Dr Beekman thinks it may matter at the margins. She observes that one disease, called Leber’s hereditary optic neuropathy, which is caused by a faulty mitochondrial gene, occurs in only 10% of women whose cellular power-packs include the damaged gene, but in 50% of men whose mitochondria are so encumbered. The gene in question, in other words, is less likely to harm a woman than a man. She then lists a lot of other diseases, including ones far commoner than Leber’s hereditary optic neuropathy (such as cardiomyopathy, diabetes and several forms of deafness) that sometimes or always have a mitochondrial component, and speculates that some of these, too, may prove to be either more common or more serious in men than in women. As far as her searches of the literature can show, this is not something that has yet been looked into.

Part of the reason for this absence of information may be that few doctors think like evolutionary biologists, so they fail to ask the appropriate questions. Dr Beekman’s hypothesis may turn out to be wrong. But it sounds eminently plausible, and certainly worth investigating.