GENETICALLY speaking, everyone has two parents. But that could soon change. Several countries, led by Britain—whose legislators approved the idea last year—are working on a procedure called mitochondrial donation, which would result in a child with DNA from three people: its mother, its father and a female donor sometimes dubbed a mitomum.

The mitomum supplies the child’s mitochondria. These are tiny structures (one is pictured below), present in most cells, that liberate usable energy from food and oxygen. People with defective mitochondria suffer debilitating illness and often die young because the tissues of their bodies are starved of the energy they need to work. Mitochondrial diseases are hereditary, and at the moment incurable. Mitochondrial donation is designed to prevent them by replacing faulty mitochondria with healthy ones.

But mitochondria are, or used to be, creatures in their own right. They are the descendants of ancient bacteria that once lived free, but then entered into a symbiotic union with other cells. As such they have their own tiny genomes, separate from the main genome in the host cell’s nucleus. A baby born through mitochondrial donation would thus inherit maternal nuclear DNA, paternal nuclear DNA and a helping of mitochondrial DNA from the mitomum.

The effects of such mixing seem benign—and certainly better than inheriting misfiring mitochondria. But, to the surprise of almost everybody, a paper in Nature by José Antonio Enríquez of the Carlos III Centre for Cardiovascular Research, in Madrid, suggests they may be more than merely benign. The very act of transplanting mitochondria, regardless of any pre-existing disease, might bring benefits.

Dr Enríquez and his colleagues worked on that scientific stalwart, the mouse. Many genetic strains of lab mice are available, and the team started with two whose mitochondria had been shown by DNA analysis to have small but significant differences—about the same, Dr Enríquez reckons, as the ones between the mitochondria of modern Africans and those of Asians and Europeans, people whose ancestors left Africa about 60,000 years ago. They then copied the procedure for human mitochondrial transplants by removing fertilised nuclei from eggs of one strain, leaving behind that strain’s mitochondria, and transplanting them into enucleated eggs of the second strain, whose mitochondria remained in situ. A group of the first strain, left unmodified, was employed as a control. The researchers raised the mice and kept an eye on how they developed.

While the animals were young, few differences were apparent between modified and unmodified individuals. But as murine middle age approached, at around the animals’ first birthdays, differences began to manifest themselves. Modified mice gained less weight than controls, despite having the same diet. Their blood-insulin levels fluctuated less after fasting, suggesting they were more resistant to diabetes. Their muscles deteriorated less rapidly with age. And their telomeres—protective caps on the ends of their chromosomes whose shortening is implicated in ageing—stayed lengthier for longer.

Not all of the changes were beneficial. Young, unmodified mice had lower levels of free radicals—highly reactive (and therefore damaging) chemicals produced by mitochondria—than did their modified brethren, though even that difference reversed itself after the animals were 30 weeks old. But the combined result of the various changes was that the modified mice lived longer. Their median age at death was about a fifth higher than that of their unmodified cousins.

Given the fundamental metabolic role played by mitochondria, it makes sense that replacing one set with another, more distantly related set causes profound changes. The surprise is that those changes seem largely positive. Most biologists would have predicted the opposite, assuming that nuclear and mitochondrial DNA would co-evolve to interact optimally, so that mixing versions which have not co-evolved would be harmful.

Though unsure what to make of his discovery, Dr Enríquez suggests that a concept called hormesis might offer an explanation. This is the observation that a small amount of adversity can sometimes do an animal good, by activating cellular repair mechanisms that go on to clear up other damage which would otherwise have gone untreated. The biochemical cost of coping with mismatched mitochondria might, therefore, be tempering the animals’ metabolisms in ways that improve their overall health.

It is an intriguing idea. And regulators, in Britain and elsewhere, will examine Dr Enríquez’s results with interest. But it would be foolish to assume that something similar would happen in people. After all, human beings live much longer than mice do. And Doug Turnbull of the University of Newcastle, who is one of the pioneers of mitochondrial donation in Britain, points out that both strains of mice used in the study are highly inbred—much more so than humans. A better lesson to draw, until many more experiments have been done, is that a mismatch between parents and mitomum can indeed have profound physiological consequences. For the time being, Dr Turnbull thus argues, the safest approach to human mitochondrial donation is to make sure that the mitomum is as closely related to the biological parents as possible.