 胚胎干細胞研究還未能在治療疾病上取得突破 |
bbc新聞兩則
設計嬰兒
《泰晤士報》報道，一對英國夫婦獲准對胎兒進行基因檢測，以診治能導致高膽固醇和心臟病風險的基因。
文章說，這一決定將引發新的倫理爭議。儘管這一技術是被用來診斷罕見的重症，但也可以用來判斷一些可以藥物治療的疾病，這樣可能會導致一些夫婦將那些具有一般病症基因的嬰兒墮胎。
批評者說，檢測會帶來史無前例的道德困境，因為很難產生毫無疾病基因的胚胎。
From The Times
December 15, 2007
Designer baby fear over heart gene test
Mark Henderson, Science Editor A British couple have won the right to test embryos for a gene that leads to high cholesterol levels and an increased risk of heart attacks, The Times has learnt.
The decision by the fertility watchdog will reopen controversy over the ethics of designer babies, as it allows doctors to screen embryos for a condition that is treatable with drugs and can be influenced by lifestyle as well as genes.
While the procedure is designed to detect a rare version of a disease called familial hypercholesterolaemia (FH), which often kills children before puberty, it will also identify a milder form that can be controlled by drugs and diet.
Critics argue that the test will allow couples to destroy embryos that would have had a good chance of becoming children with fulfilling and reasonably healthy lives.
The test will also create an unprecedented moral dilemma for some couples, as it could show that they have produced no embryos completely unaffected by the disease. This would force them to decide whether to implant embryos that they know have a genetic risk of premature heart disease and death, or to throw them away and deny them a chance of life.
Britain’s first licence to test embryos for FH will be awarded next week to Paul Serhal, of University College Hospital in London, by the Human Fertilisation and Embryology Authority (HFEA).
Its decision breaks new ground because it permits Mr Serhal to screen out not only the severe form of the condition but also the milder type, which is usually treatable.
Embryo screening has previously been approved only for disorders in which a gene invariably causes a serious disease, or for conditions such as breast cancer in which mutations carry an 80 per cent lifetime risk.
FH occurs in two forms. The more common version, heterozygous FH, affects 1 in 500 people. It is caused by a single mutated gene, which raises cholesterol and thus the risk of hardened arteries, heart disease and stroke. It can usually be managed with statin drugs and diet.
One in 250,000 people inherits two defective copies of the gene and develops homozygous FH, which is much more serious. Sufferers show severely elevated cholesterol from the age of 5, and can suffer angina by 6 or 7. Many die in childhood, and most have suffered at least one heart attack by the end of their twenties.
Mr Serhal’s patients, who are in their thirties, both have the milder heterozygous FH. They discovered their status only when they had a daughter, now 5, with the homozygous form, and they also have an unaffected son.
They said yesterday that they were delighted. “We had no idea that we both carried a gene for high cholesterol until the double gene was expressed in our first child. We are very lucky that our child has responded so well to the very high-dose drug regime. We have been led to understand that other children with the same double gene may not be so lucky.”
The couple, who approached Mr Serhal after learning that he was offering the pre-implantation genetic diagnosis test for a breast cancer gene, will have IVF next month, even though they are naturally fertile.
A single cell will be removed from each embryo at the eight-cell stage, and be tested for defective FH genes. Any that have homozygous FH will be discarded. The test will also determine whether the remaining embryos are completely clear of FH, or whether they have the heterozygous form. There may be none that are unaffected, leaving the couple with a difficult ethical decision.
Mr Serhal said: “This obnoxious disease can cause cardiovascular accidents at a very young age. Ideally, we will find embryos with no FH genes, but it is possible we will not and it will be up to the patients to choose. Some people would think twice about using embryos that they know have a risky gene, and others would say you shouldn’t screen out a condition that can be managed so people can live with it. It will be an awkward choice.”
Mr Serhal said that the HFEA had also indicated that it would be prepared to sanction screening for the milder form of FH alone for couples in which one partner was a carrier and the other was not, though he was not yet proposing to do such screening.
From The Times
December 15, 2007
Testing Issue
Genetic screening is permissible but only under strict regulation
Inevitably, whenever the words “lifestyle” and “designer babies” are used in a report on genetic screening or embryo testing, free rein is given to speculation on the more repulsive fantasies of Aldous Huxley's hatcheries and Nazi eugenics. The ethics of human reproduction and scientific intervention in this delicate area are a moral minefield, provoking strong emotions and a cacophony of opinions. It is not surprising, therefore, that the decision by the Government's fertility watchdog to allow a couple to test their embryos for a gene that causes high cholesterol levels is as controversial as it is misunderstood. It appears, at first glance, to open the way to designing children who will never grow fat or to speeding the acceptance of bioengineering to produce superbabies. It is no such thing.
The procedure that has been allowed by the Human Fertilisation and Embryology Authority is designed to detect a rare version of a disease called familial hypercholesterolaemia (FH), which often kills children before puberty. The condition occurs in two forms — a relatively mild one, caused by a single mutated copy of a gene, that nevertheless raises cholesterol levels to dangerous levels, causing heart disease, hardened arteries and strokes; and a far more deadly version, when the sufferer inherits two defective copies that cause high levels of cholesterol from the age of 5, angina and likely early death.
The principle of screening embryos to avoid such suffering has already been accepted for such conditions as Huntington's disease and cystic fibrosis. Other diseases, caused by genetic defects, have recently been added to the list. This pre-implantation genetic diagnosis, using embryos obtained by IVF, screened and then re-introduced to the womb, is costly, invasive and must be regulated by clear guidelines. But there is no reason why FH should be excluded. It does, however, raise a moral dilemma: while embryos with double mutations should not be implanted, what should be done with those affected by only the milder condition? Should parents — and the State — be obliged to support the birth of a child who will, inevitably, face a life of some suffering and much expense? Or should even partially affected embryos be discarded and the mother obliged to undergo again the full IVF procedure?
Several clear principles must be paramount when framing a moral and legal response. The first is that the parents should decide. The circumstances of each case may differ. Only parents can judge what they and their offspring are prepared to undergo. Secondly, medical regulation remains essential. Sanction for pre-implantation diagnosis does not apply to other situations: abortion of a foetus in the womb is a very different issue that raises other ethical questions. Thirdly, the scientific possibilities of screening must not be abused. Parents who choose this rigorous and sometimes distressing procedure over natural conception do so out of determination not to pass on genetic defects. They are not trying to manipulate their genes to raise IQ, breed a top athlete or “design” a baby — nor could they, when limited by their own gene pool. But a technique to prevent suffering must never be used for eugenics, with a promiscuous shopping list of genes to be screened out. That way not only moral madness lies, but present fears of Frankenstein science could prove all too true.
英國寬帶
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