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Human Fertilisation and Embryology Bill [HL]

As it appears that we are now discussing this whole group of amendments, it is appropriate that I should comment on my Amendment No. 4, which was referred to in detail by my noble friend Lord Alton. The purpose of the amendment is quite simple: to remove the need for research on the prevention of mitochondrial disease to be subject to regulations made by both Houses of Parliament, simply leaving the responsibility for licensing such research with the Human Fertilisation and Embryology Authority. I shall come to that in just a moment. I remind your Lordships that mitochondrial disorders are a cruel class of inherited disease— life-threatening conditions coupled with great unpredictability about how future children will be affected. They can include fatal liver failure, stroke-like episodes, mental retardation with intractable epilepsy, muscle weakness, diabetes and deafness. All cells in the body contain between 1,000 and 10,000 mitochondria in the cytoplasm that surrounds the nucleus. They are tiny energy-producing structures, or organelles, vital to cell function. If they malfunction, organs will eventually fail. Because there are no mitochondria in sperm but only in the ovum cytoplasm, when mutations occur in the mitochondrial genes, causing these devastating diseases, those mutations are transmitted by the female who has those genes to all her children of either sex. They are therefore inherited only from the mother. Mitochondria carry only a very small number of human genes—just over 0.1 per cent. It is in those genes that the mutations may occur. The Human Fertilisation and Embryology Act 1990 permits laboratory research into human cytoplasmic transplantation. Such a research licence was granted by the Human Fertilisation and Embryology Authority to a team at Newcastle University in 2005, and the laboratory studies are ongoing. The team is working on animal studies in which it is carrying out the procedure, to which I referred in detail at Second Reading, of taking an ovum, removing the nucleus from it and transplanting the nucleus from another ovum into it so that that nucleus will contain 99.5 per cent of the DNA of the donor nucleus but will also contain the normal cytoplasm. The proposal that we are discussing now is the next step—when safety has been assured and when all the evidence, scientific and otherwise, has accumulated to make it clear to the Human Fertilisation and Embryology Authority that this is a practical possibility—which is to be able to take an ovum from a women carrying these devastating mitochondrial abnormalities in her cytoplasm, take the nucleus containing 99.5 per cent of her DNA and transplant it into a donor ovum from which the nucleus has been removed but which has normal cytoplasm. The decision to allow that to happen is hinted at in the Bill, which allows regulations to be introduced in the future in respect of the clinical application of the current animal research to prevent the transmission of mitochondrial disease. This amber signal is welcome, but is it not just introducing yet another stage of bureaucracy in allowing the research to proceed? The decision to introduce this technique as a clinical treatment must be based on whether researchers can produce convincing evidence of safety and efficacy. The decision to grant a licence for such new clinical treatment involving embryos and gametes ordinarily rests with the HFEA. Similarly, there is a strong case for the HFEA to be allowed to determine whether to license cytoplasmic transplantation in human subjects. It will be ideally placed to assess the safety and efficacy of each case and to incorporate detailed scrutiny by members of the scientific community with appropriate expertise. There is a need for such research to progress to therapeutic application for the prevention of such serious, life-threatening diseases. The idea that the resulting child has three parents is nonsense. The DNA in mitochondria carries no information that defines any human attributes whatever, so it cannot be parental in any way either. On this reasoning, one might well claim that people with a kidney transplant have four parents; indeed, that is a stronger claim, as the kidney carries nuclear DNA from the donor and not just cytoplasmic DNA. This treatment is not the same as reproductive cloning, which describes the situation where any baby created would be genetically identical to a donor through the transferring of a nucleus from that donor into an egg from which its own nuclear DNA had been removed. Reproductive cloning is, and must remain, illegal in the UK. However, in mitochondrial disease treatment, there is in effect the exact opposite: a transfer of a cytoplasm and, with it, normal mitochondria from the donor. People have asked whether this is the same as germ-line gene therapy, a term used for modifying a gene in the nuclear genome at the beginning of development. It is not germ-line therapy, because mitochondrial genomes are not being modified; they are simply being replaced. It is true that, once normal mitochondria are in place, subsequent generations will have normal mitochondria, too, which is hardly a bad thing. This is a crucial piece of evidence, which is of inestimable value to many women and many families where this group of mitochondrial diseases has been present—I have seen many such in my professional life. We cannot miss this opportunity.