For the past four years I have been a member of the panel that has provided independent advice to the government on this topic. It is our considered view that the techniques are not unsafe and are likely to be effective. As long as these views are not contradicted by further research currently under way, they should be made available.

However, a recent article in 91av on some of the properties of mitochondria, together with an accompanying leader, claimed that “we may have seriously underestimated the influence that mitochondria have” and that “recent research suggests that they play a key role in some of the most important features of human life”, and are not just simply the cell’s power plants.

The leader concludes by saying that the “emerging science and the issues it raises have not had a proper airing” and “need to be brought to parliament’s attention, debated and settled before a decision is made”.

I was rather taken aback by this, given our almost four years of work exploring all the issues relating to the science, safety, efficacy and ethics, and to conduct an informed public debate in the UK.

Amazing biology

“We” are fully aware of the amazing biology in which mitochondria are involved in addition to their main function of generating energy, including their roles in steroid synthesis and cell death, and their complex behaviour when they replicate, fuse or change shape and position within cells. People with mitochondrial diseases can experience a myriad of symptoms related to these functions. None, however, is relevant to mitochondrial replacement.

of an unfertilised or fertilised egg (zygote) from the woman at risk of having affected children to a donor egg or zygote with its nuclear DNA removed; the donor has normal mtDNA. The resulting child will have nuclear DNA from the patient and her partner, and mtDNA from the donor.

The scientific review considered many issues in depth. But, with respect to the issues raised in the article, the following questions are the only ones that are relevant:

Is a trait attributed to mitochondria one that is encoded by nuclear or mitochondrial DNA? If nuclear, then it is not relevant to MR because all these traits – and we know there are at least 1000 nuclear genes encoding products required for mitochondrial functions – will be inherited by the child in exactly the same way as if MR had not been used.

Effect on the child

If a trait is encoded by mtDNA, will mitochondrial replacement have any consequences for the child’s future that are different from those of natural reproduction? If so, are the consequences worth worrying about, especially given that without replacement the child would suffer from a debilitating disease and die young?

We know that variation in mtDNA can alter mitochondrial function. Notably, variations in the 37 well-studied genes in the mitochondrial genome have been associated with subtle differences in energy metabolism, such as the ability to cope at high altitudes.

Is this relevant? Any effect of mtDNA variation has to be considered in the light of the extensive variation in the nuclear genes that impact on mitochondrial function. Will variation in mtDNA make itself heard above the noise of this variation in nuclear DNA? The answer is probably not.

But let us assume that a child born after MR has slightly different energy metabolism compared to his or her parents. Will this matter? Assuming the child is healthy, I very much doubt it will concern anyone.

Humanin

What about other possible mtDNA-encoded traits? The 91av article discusses the role of “humanin” and of non-coding RNAs encoded in mtDNA. Are either of these likely to be relevant?

Humanin is a peptide (a short chain of amino acids) that was discovered in a screen for biomolecules that might protect against the neurodegeneration seen in Alzheimer’s disease. It was given its emotive name in the hope that it would restore humanity to Alzheimer’s patients.

As to its function, we don’t really know. Research papers report it acting both inside and outside of cells and having protective effects against several types of neurodegeneration, stroke, heart and cardiovascular disease, cancer, and death of cells in the testis. It has also been reported to be involved in the action of insulin, and declining humanin levels in blood plasma are claimed to be associated with ageing.

I am a little suspicious when something is said to be so powerful. Nevertheless, even if humanin is able to carry out a fraction of all these functions, then it would be important.

But is it relevant to MR? To be so, humanin would have to be a product of mtDNA and to vary in a meaningful way between individuals. But the evidence for both is weak at best. A genetic sequence potentially encoding humanin is present within a much longer stretch of mtDNA that encodes an essential component of the protein synthesis machinery within mitochondria. But despite many years of work, no one has yet described how humanin could be made from this.

Like for like

Moreover, no variants in the putative sequence for the peptide have been associated with any trait, such as increased susceptibility to Alzheimer’s. If these don’t exist, then MR will simply involve a like-for-like exchange: it will have no consequences.

In addition, the mitochondrial “humanin” coding sequence is so poorly conserved in evolution that some mammals, including Rhesus monkeys, would be unable to make it.

Even if some humanin is made within mitochondria, we know of no mechanism by which it could be transported out. On the other hand, there are at least 13 nuclear DNA sequences that could encode humanin-like peptides. These seem much better candidates to produce the peptide.

Far less has been published on the small non-coding RNAs. However, there is no evidence that they have any role outside the mitochondria. Nor is any mechanism known by which they could get out.

Once again, the critical question is: is there any variation in the sequence that might be relevant to MR? The simple answer is no. Although there must be some variants, no consequences have been reported to date.

In summary, the significance of humanin and non-coding RNAs is, to say the least, unsubstantiated and controversial. The reported data do not warrant a wholesale rethink of MR techniques.

Matching DNA

Moreover, if haplotype matching – that is, finding a donor with mtDNA similar to the mother’s, as suggested by the HFEA’s scientific panel – is practical, then even hypothetical problems due to variation in mtDNA sequence will disappear.

All told, my view is that neither humanin nor small RNAs are relevant.

Women at risk of passing on mitochondrial disease currently have a range of options that many find unpalatable. They can avoid having children, or any further children if the first was affected. They can hope that their child will be OK, which is very risky. They can adopt or use egg donation, in which case the child will not be genetically related to them. Or they can use pre-implantation genetic diagnosis to look for embryos with a sufficiently low proportion of mutant mtDNA. This, however, is not possible where there is a high proportion of abnormal mtDNA or where it is all abnormal, which is common.

Mitochondrial replacement could provide an additional choice that is suitable for all these patients and, based on all the data we have seen so far, it should mean children free of mitochondrial disease.

The only known traits that could come from the donor mtDNA concern energy production, and these are likely to be extremely minor or unnoticeable. It will ultimately be up to the parents to decide if this is a “risk” worth taking in order to avoid mitochondrial disease in their children.

There is a consensus among scientists that certain types of research require the use of animals. The UK government has repeatedly said .

However, a small but vocal minority has been eroding British research by targeting an unexpected group – the transport sector – with the effect that the movement of lab animals into, out of and within the UK is now threatened.

Activists accuse airlines and ferry companies involved in this of acting immorally. While it is clear that carrying animals used in life-saving research is legitimate, these activists have created the illusion that these companies are going against their human passengers’ wishes by doing so, and many firms are refusing to continue the practice.

Ironically, research animals may suffer as a result. When a direct route is shut off, they have to be taken on increasingly circuitous journeys. One breeder flying animals from London to Edinburgh has said they now go via Frankfurt, because no airline with direct flights will carry research animals.

No other option

It is right that companies listen to their customers, but in this case, those protesting are a minority. A 2010 showed that 87 per cent of the public support well-regulated animal research for medical benefits, if there is no other option. UK science is meeting these conditions.

We constantly see medical benefits from such work. Either by uncovering basic physiology using animal systems or testing a new treatment before human trials, every medical advance will have involved animals at some point. We also have extremely high standards of animal care of which we should be proud.

Many are asking why this is an issue at all. Surely research facilities can breed their own animals? On the whole, they do, but in a small number of cases this is not an option and so animals must be imported or sent from the UK to scientists elsewhere.

Science is an international endeavour. In my own research, with genetically altered mice, we collaborate with teams on the other side of the world whose expertise complements our own, and must use animals with the same genetic make-up. Usually a few mice of a specific strain are shipped, in carefully controlled environments, and bred to establish a breeding colony at the receiving institute.

Making things worse

If we cannot transport animals, experiments will be repeated unnecessarily, and it will be difficult to compare results. This goes against the principles of reducing and refining the use of animals, which are important to reduce suffering. Activists are therefore making things worse, not better. They are also putting research into certain medical conditions at risk. If they succeed, some new treatments will not be developed. People will suffer needlessly.

Fortunately, action is being taken to stop this happening.

This week the UK’s science minister, David Willetts, said that his department has been working to get a deal with the whole transport industry so that the movement of research animals can continue. Government, the bioscience sector and transport companies must work together to achieve this.

As scientists, we also have a role to play. A question that has come up again and again in interviews on this is: “What exactly do you do to these animals?” This is what the public want to know. Scientists should not be afraid to speak out in support of their research and to explain why it is necessary. Perhaps if they do, they will be able to drown out the voices of the tiny minority who are now endangering us all.

is a stem cell biologist and geneticist at the Medical Research Council’s National Institute for Medical Research in London, a member of the Council of Understanding Animal Research and president of the Institute of Animal Technology