TEXAS TOWNSHIP, Mich. (WOOD) — A 4-month-old from the Kalamazoo area is one of only a few in the world with a rare condition similar to the one that recently took the life of British baby Charlie Gard. 
 
 Russell Cruzan III’s parents are fighting to find him treatment that could save his life. Even though doctors say Russell’s chances of survival are slim, his parents are hoping he’ll defy the odds. 
 
 Held by his mother in his Texas Township home Monday, Russell’s breathing was labored. 
 
 “It’s really hard to be told that your child’s chances of even making it to 2 are like 50 percent,” his mother, Michelle Budnick-Nap, said tearfully. 
 
 She and Russell’s father noticed something was wrong in early June. 
 
 “(We) kept asking the nurses why. Why is he not eating? Why isn’t he thriving?” Budnik-Nap recalled. 
 
 There were no answers. And Russell kept getting worse. Dehydrated and lethargic with a low body temperature, he was admitted to Bronson Children’s Hospital for a week. 
 
 Doctors treated the symptoms, but Russell’s parents say they weren’t ever given a reason why their child was sick. 
 
 Two days after Russell was released, his parents rushed him back to the hospital when he started having severe respiratory problems and then developed pneumonia. Russell was in the hospital for a month. 
 
 Still, no answers. 
 
 Until a test on his kidneys came back. 
 
 “When those labs came back the doctor called and she was like, ‘You need to bring him into the hospital right now. His labs are looking kind of crazy. We need to find out what’s going on,'” Budnik-Nap said. 
 
 The diagnosis was mitochondrial DNA depletion syndrome 13, which can cause a loss of muscle mobility and strength, decreased kidney function and an inability to swallow. 
 
 Charlie Gard also had mitochondrial depletion syndrome. 
 
 The baby in the United Kingdom was at the center of a legal battle over whether his parents should be allowed to bring him to the United States for experimental treatment. Doctors objected, saying it wouldn’t help and could in fact hurt Charlie. Eventually, his parents ended their fight when it became clear that the treatment could no longer save their son. 
 
 Charlie died last week. He would have turned 1 this week. 
 
 After Russell’s diagnosis, doctors told his parents the the odds were against him. 
 
 “‘We know the seriousness of this diagnosis. We know what the prognosis is. Do you want to keep fighting or do you want to give up and let nature take its course?'” Burdik-Nap said she was told. “Which is a really, really hard thing to hear. But I always tell them, ‘Bo, we want to do everything we can. We want to fight.'” 
 
 That’s why she and Russell’s father are working to get to Boston. 
 
 “If anything if they can’t save him or whatever — maybe he can be used to save kids in the future,” Russell Cruzan II said. 
 
 They say a doctor at Boston Children’s Hospital, who is one of the top mitochondrial physicians in the country, has agreed to treat Russell if a doctor at Bronson can get the insurance company will authorize it. If Russell goes to Boston, he would get a treatment aimed at helping his healthy mitochondria replicate. 
 
 “I don’t want to say that we’ve come to terms with it. We love him more than anything in the world,” Budnik-Nap said. 
 
 They may be able to get treatment for their son, but insurance isn’t covering the costs. A YouCaring page has been set up to help cover medical costs. 
 
 Share this: Email 
 
 Print 
 
 Facebook 
 
 Twitter 
 
 Google 
 
 Pinterest 
 
 More 
 
 LinkedIn 
 
 Tumblr 
 
 
 
 Reddit ||||| A 5-month-old local boy is fighting the same, rare life-threatening disease that took the life of baby Charlie Gard in London, despite a court fight over acquiring experimental treatment. 
 
 Local doctors say baby Russel Cruzan III might not live to see his second birthday. But his parents aren't giving up the fight. 
 
 
 
 Baby Russell has mitochondrial DNA depletion syndrome. But his parents told Newschannel 3 that they're hopeful experimental treatments could save their baby. 
 
 Baby Russell is a happy little boy who likes to coo and grunt to his parents. A sweet boy with a lot of strength-it says so on his onesie. 
 
 “As many times as he's been poked as many times as he's been messed with, he just smiles and carries on like nothing ever happened," said his father, Russell Cruzan II. 
 
 His mother, Michelle Budnik-Nap, said, “He does, he'll cry for a couple minutes, then he's back to his little happy self." 
 
 Mitochondrial DNA Depletion Syndrome affects energy in his cells. 
 
 
 
 “Ultimately, it affects the major organs because the major organs require the most energy," Budnik-Nap said. "So right now he's dealing with some kidney problems, some liver problems, heart problems, definitely some muscle weakness, although we're definitely working on getting that fixed." 
 
 His parents say 50 percent of children with the rare disease don't make it to age 2. 
 
 “When we came in to get the diagnosis they just said there's no treatment, there's no cure. We would encourage you to take Russell home and enjoy the time that you have with him,” Budnik-Nab, said. 
 
 They plan on doing that, but his parents also say they're working to get him experimental treatment from a doctor in Boston willing to help. 
 
 “It's time to fight we're not taking no for an answer,” Budnik-Nab, said. 
 
 And in their fight, it's Russell’s strength they say will help them live his life to the fullest. 
 
 “Happy and healthy as possible for as long as possible. And when that's not possible any longer we hope that we have done something to help other children with his condition,” Michelle said. 
 
 Next week, the family will see a neurologist to check how Russell's brain is doing. 
 
 They're planning a golf outing and spaghetti dinner to help fund treatments, travels, and lodging as they work to save their child. They've also started a crowdfunding page to help with some of the expenses. ||||| Blackout Concepts/Alamy 
 
 It’s a boy! A five-month-old boy is the first baby to be born using a new technique that incorporates DNA from three people, New Scientist can reveal. “This is great news and a huge deal,” says Dusko Ilic at King’s College London, who wasn’t involved in the work. “It’s revolutionary.” 
 
 The controversial technique, which allows parents with rare genetic mutations to have healthy babies, has only been legally approved in the UK. But the birth of the child, whose Jordanian parents were treated by a US-based team in Mexico, should fast-forward progress around the world, say embryologists. 
 
 The boy’s mother carries genes for Leigh syndrome, a fatal disorder that affects the developing nervous system. Genes for the disease reside in DNA in the mitochondria, which provide energy for our cells and carry just 37 genes that are passed down to us from our mothers. This is separate from the majority of our DNA, which is housed in each cell’s nucleus. 
 
 Advertisement 
 
 Around a quarter of her mitochondria have the disease-causing mutation. While she is healthy, Leigh syndrome was responsible for the deaths of her first two children. The couple sought out the help of John Zhang and his team at the New Hope Fertility Center in New York City. 
 
 Zhang has been working on a way to avoid mitochondrial disease using a so-called “three-parent” technique. In theory, there are a few ways of doing this. The method approved in the UK is called pronuclear transfer and involves fertilising both the mother’s egg and a donor egg with the father’s sperm. Before the fertilised eggs start dividing into early-stage embryos, each nucleus is removed. The nucleus from the donor’s fertilised egg is discarded and replaced by that from the mother’s fertilised egg. 
 
 Meet your mitochondria: The powerful aliens that lurk within you 
 
 
 
 But this technique wasn’t appropriate for the couple – as Muslims, they were opposed to the destruction of two embryos. So Zhang took a different approach, called spindle nuclear transfer. He removed the nucleus from one of the mother’s eggs and inserted it into a donor egg that had had its own nucleus removed. The resulting egg – with nuclear DNA from the mother and mitochondrial DNA from a donor – was then fertilised with the father’s sperm. 
 
 Gene editing: A guide to the genetic revolution on our doorstep 
 
 
 
 Zhang’s team used this approach to create five embryos, only one of which developed normally. This embryo was implanted in the mother and the child was born nine months later. “It’s exciting news,” says Bert Smeets at Maastricht University in the Netherlands. The team will describe the findings at the American Society for Reproductive Medicine’s Scientific Congress in Salt Lake City in October. 
 
 Neither method has been approved in the US, so Zhang went to Mexico instead, where he says “there are no rules”. He is adamant that he made the right choice. “To save lives is the ethical thing to do,” he says. 
 
 The team seems to have taken an ethical approach with their technique, says Sian Harding, who reviewed the ethics of the UK procedure. The team avoided destroying embryos, and used a male embryo, so that the resulting child wouldn’t pass on any inherited mitochondrial DNA. “It’s as good as or better than what we’ll do in the UK,” says Harding. 
 
 A remaining concern is safety. Last time embryologists tried to create a baby using DNA from three people was in the 1990s, when they injected mitochondrial DNA from a donor into another woman’s egg, along with sperm from her partner. Two of the fetuses developed genetic disorders, and the technique was halted by the US Food and Drug Administration. The problem may have arisen from the fetuses having mitochondria from two sources. 
 
 When Zhang and his colleagues tested the boy’s mitochondria, they found that less than 1 per cent carry the mutation. Hopefully, this is too low to cause any problems; generally it is thought to take around 18 per cent of mitochondria to be affected before problems start. “It’s very good,” says Ilic. 
 
 Smeets agrees, but cautions that the team should monitor the child to make sure the levels stay low. There’s a chance that faulty mitochondria could be better at replicating, and gradually increase in number, he says. “We need to wait for more births, and to carefully judge them,” says Smeets. 
 
 Two women, one man and a baby A Jordanian couple has been trying to start a family for almost 20 years. Ten years after they married, she became pregnant, but it ended in the first of four miscarriages. In 2005, the couple gave birth to a baby girl. It was then that they discovered the probable cause of their fertility problems: a genetic mutation in the mother’s mitochondria. Their daughter was born with Leigh syndrome, which affects the brain, muscles and nerves of developing infants. Sadly, she died aged six. The couple’s second child had the same disorder, and lived for 8 months. Using a controversial “three-parent baby” technique (see main story), the boy was born on 6 April 2016. He is showing no signs of disease. 
 
 At the clinic’s request we have removed the names of the family The story has been updated to clarify that it was fetuses that developed genetic disorders in the 1990s ||||| A promising technique to prevent mothers from passing on devastating mitochondrial diseases was thrown a biological curve ball this week: A paper published Wednesday in Nature shows that such diseases can come back to sicken a child, even when 99 percent of the mother’s own mitochondria are eliminated. 
 
 Mitochondria are the tiny power plants that provide the energy every cell needs to function. When a large percentage of these organelles malfunction, cells cannot do their jobs—and everything from weakness to death can result. Mothers with certain conditions may have such low levels of faulty mitochondria that they have no symptoms, but their kids can inherit a higher burden of these defective mitochondria, leading to devastating illness. 
 
 In attempt to combat this problem, researchers have essentially been—as one doctor described it—taking the “yellow part” of a mother’s egg and inserting it into the “white” of a donor’s egg. Because the child ends up with DNA from its mother, father and a donor, this mitochondrial replacement therapy has been nicknamed the “three-parent baby” technique. An apparently healthy boy was born using the approach in April in Mexico. He carries about 1 percent of his mother’s mitochondria, which if allowed to pass to him in full might have caused Leigh syndrome, a severe neurological disorder that is generally fatal in early childhood. His parents had two previous children who died of the disease, one at age 6 and one at 8 months, New Scientist reported. 
 
 But the new laboratory study shows that the mother’s mitochondria can sometimes replicate faster than the donor’s and come to dominate again, potentially bringing disease with it. Still, that effect is likely to be rare, says Shoukhrat Mitalipov, the developmental biologist who led the research and has used the technique on mice and monkeys, reportedly without seeing any health problems. Mitalipov and Paula Amato, a reproductive endocrinologist also at Oregon Health & Science University in Portland, said at a news conference that they think mitochondrial replacement therapy should be tested in a clinical trial—despite concerns about the mother’s defective mitochondrial DNA making a comeback. “Because these diseases are so debilitating and often fatal and there are no cures, we think it’s still worth trying to move this research forward to prevent those diseases if we can,” Amato says. Congress currently bans such three-parent procedures for clinical use in the United States, but the United Kingdom has approved a similar technique that would allow even more of the mother’s mitochondria to be passed on to the child and a trial could likely be conducted there, Mitalipov says. 
 
 Although mitochondrial diseases are fairly rare, affecting about one in 5,000 children, Mitalipov and Amato say the three-parent technique could theoretically also be used to treat infertility and help with some stem cell treatments. Mitochondria (which have their own DNA, separate from the DNA in a cell’s nucleus) are inherited solely from the mother. Some consider the three-parent procedure controversial because of this mix of DNA, and because scientists worldwide have agreed to avoid making changes to human genetic inheritance. 
 
 A number of experts have also argued that mitochondrial replacement therapy is too little understood to try in people. Klaus Reinhardt, an evolutionary biologist and zoologist at Germany’s Technische Universität Dresden, thinks the mismatch between the donor’s mitochondrial DNA and mother’s nuclear DNA could cause mitochondrial problems in about one in 50 children born using the three-parent process. Inherited together, the nuclear and mitochondrial DNA can resolve each other’s defects. But when they come from different people, this mismatch can create problems for the child, says Reinhardt, who was not involved in the new research. The human genome, he explains, has 6 billion pairs of DNA and mitochondria have about 16,000, making it very challenging to predict their interactions. “We have no idea who ‘talks’ with whom,” he says. 
 
 Dan Mishmar, a mitochondrial evolutionist and geneticist atBen-Gurion University in Israel, who was not involved in the new study, says his own research shows large differences between the mitochondrial genomes of Africans and Caucasians. When the parents’ DNA match their mitochondrial DNA, these gaps don’t matter, he says. But he worries about taking the mitochondrial DNA “out of context” when the donor and the mother have very different ethnic and racial backgrounds. Like Reinhardt, he worries that the DNA mixture itself could cause illness. “If you reduce the compatibility, you increase the susceptibility to complex disabilities, such as diabetes, Parkinson’s and … Alzheimer’s. That’s the thing we are afraid of.” But Mitalipov believes such problems can largely be avoided by matching the mitochondrial DNA of the mother with that of the donor, in much the same way that organ donors are matched to recipients by immune type. 
 
 Juan Carlos Izpisua Belmonte, a stem cell scientist at the Salk Institute in California who worked on the paper with Mitalipov, suggests an additional way to reduce the risks. He says his lab has developed a technique to cull mutant mitochondria from a mother’s egg before its nucleus is transferred to the donor’s. Reducing levels of the dangerous mitochondria should limit the number that reach the child, he adds. 
 
 For the new study, four women whose children had mitochondrial diseases underwent hormone therapy typically used for in vitro fertilization and provided eggs. Researchers took the DNA from the nucleus of these egg cells and transferred it into donor egg cells whose nuclei had been removed, a process called spindle transfer. The eggs with the mother’s nuclear DNA and the donor’s mitochondrial DNA were fertilized and allowed to divide and grow for five days. Then the embryos were turned into embryonic stem cells, ending their potential for development. These stem cells were transformed into brain, heart and other types of cells to see how their mitochondria would behave. In cells from one mother, the mitochondria reverted to the mutant type that she carried before the spindle transfer. 
 
 Although the new study raises questions about the safety of mitochondrial replacement therapy, Belmonte says it should also quell any fears that the research is moving too quickly. “We have to be convinced in the laboratory that we have done every possible experiment to make sure this is safe—as safe as we can [make it],” he says. “This is a wonderful way to avoid diseases, but we found a problem and we need to make sure we have ways to minimize or solve that problem before we go into the clinic.” ||||| Alana Saarinen loves playing golf and the piano, listening to music and hanging out with friends. In those respects, she's like many teenagers around the world. Except she's not, because every cell in Alana's body isn't like mine and yours - Alana is one of a few people in the world who have DNA from three people. 
 
 "A lot of people say I have facial features from my mum, my eyes look like my dad… I have some traits from them and my personality is the same too," says Alana. 
 
 "I also have DNA from a third lady. But I wouldn't consider her a third parent, I just have some of her mitochondria." 
 
 Mitochondria are often called the cell's factories. They are the bits that create the energy all of our cells need to work, and keep the body functioning. But they also contain a little bit of DNA. 
 
 Alana Saarinen is one of only 30 to 50 people in the world who have some mitochondria, and therefore a bit of DNA, from a third person. She was conceived through a pioneering infertility treatment in the USA which was later banned. 
 
 But soon there could be more people like Alana, with three genetic parents, because the UK is looking to legalise a new, similar technique which would use a donor's mitochondria to try to eliminate debilitating genetic diseases. It is called mitochondrial replacement and if Parliament votes to let this happen, the UK would become the only country in the world to allow children with three people's DNA to be born. 
 
 The structure of a cell 
 
 Nucleus: Where the majority of our DNA is held - this determines how we look and our personality 
 
 Mitochondria: Often described as the cell's factories, these create the energy to make the cell function 
 
 Cytoplasm: The jelly like substance that contains the nucleus and mitochondria 
 
 Alana was born through an infertility treatment called cytoplasmic transfer. 
 
 Her mum, Sharon Saarinen, had been trying to have a baby for 10 years through numerous IVF procedures. 
 
 "I felt worthless. I felt guilty that I couldn't give my husband a child. When you want a biological child but you can't have one, you're distraught. You can't sleep, it's 24-7, constantly on your mind," she says. 
 
 Cytoplasmic transfer was pioneered in the late 1990s by a clinical embryologist Dr Jacques Cohen and his team at the St Barnabus Institute in New Jersey, US. 
 
 "We felt that there was a chance that there was some element, some structure in the cytoplasm that didn't function optimally. One of the major candidates that could have been involved here are structures called mitochondria," he says. 
 
 Cohen transferred a bit of a donor woman's cytoplasm, containing mitochondria, to Sharon Saarinen's egg. It was then fertilised with her husband's sperm. As a little bit of mitochondria was transferred, some DNA from the donor was in the embryo. 
 
 Image copyright Science Photo Library 
 
 Seventeen babies were born at Cohen's clinic, as a result of cytoplasmic transfer, who could have had DNA from three people. 
 
 But there was concern about some of the babies. 
 
 "There was one early miscarriage, considering there were twelve pregnancies that is an expected number," says Cohen. 
 
 He and his team believed that miscarriage occurred because the foetus was missing an X chromosome. 
 
 "Then there was another twin pregnancy, where one [of the twins] was considered entirely normal and the other had a missing X chromosome. 
 
 Find out more Listen to Mum and Dad... and Mum? on BBC Radio 4 at 21:00 BST or on the World Service at 18:30 on Monday 1 September, or watch the film on BBC Newsnight at 22:30 on the same date Or catch up on iPlayer 
 
 "So that's two out of the small group of foetuses that was obtained from this procedure. This did worry us and we reported that in the literature and in our ethical and review board that oversees these procedures," he says. 
 
 At the time of birth, the other babies were all fine. A year or two later, another of the children was found to have "early signs of pervasive early developmental disorder which is a range of cognitive diseases which also includes autism." Cohen told me. 
 
 He says it's difficult to know if the abnormalities happened by chance or because of the procedure. 
 
 Other clinics copied the technique and Cohen estimates that around 30 to 50 children worldwide were born who could have DNA from three people as a result. 
 
 But in 2002 the American regulator, the FDA (Food and Drug Administration) asked clinics to stop doing cytoplasmic transfer due to safety and ethical concerns. All of them did. 
 
 "There was a reaction from scientists, ethicists, the public at large, I think most of it was supportive, some of it was critical - I think this is normal, every time an experiment is done in medicine there is a reaction - what are the risks here?" says Cohen. 
 
 At the time, some were concerned because they felt this was germ line genetic modification. What "germ line" means is that a child like Alana would pass her unusual genetic code down to her children. And their children, would pass it to their children and so on. 
 
 Because we inherit our mitochondria only from our mothers, only female children would pass their unusual genetic code on. Crossing the germ line as it is known has never been done before so very little is known about what the outcome could be. 
 
 Due to a lack of funding, Cohen says, it hasn't been possible to find out about how any of the children like Alana who were born from cytoplasmic transfer are doing. But the St Barnabus Institute is now starting a follow up study to check their progress. 
 
 Sharon Saarinen says her daughter Alana is a healthy, typical teenager 
 
 "I couldn't ask for a better child. She is an intelligent, beautiful girl inside and out, she loves math and science … she does really well in school. She helps me around the house… when she's not texting!" 
 
 "She has always been healthy. Never anything more than a basic cold, or a flu every now and then. No health problems at all." 
 
 The health of the children, like Alana, born from cytoplasmic transfer is under scrutiny now because of the UK's decision to consider legalising mitochondrial replacement, where the mitochondria of a donor woman will be used to create a child. 
 
 It would not be available for people with fertility problems but for those who carry diseases of the mitochondria and would otherwise pass down these genetic abnormalities to their children. 
 
 Exactly how it is done still needs to be determined as there are two ways of doing the procedure, depending on when the eggs are fertilised. 
 
 Eggs from a mother with unhealthy mitochondria and a donor with healthy mitochondria are collected 
 
 The nucleus, containing the majority of the genetic material, is removed from both eggs. The donor nucleus is destroyed 
 
 The mother's nucleus is inserted into the donor egg - it now has healthy mitochondria. The egg is then fertilised by the father's sperm 
 
 Both the mother's and donor's eggs are fertilised with the father's sperm to create two embryos 
 
 The pronuclei, the nuclei during the process of fertilisation, contain the majority of the genetic material. They are removed from both embryos. The donor's is destroyed 
 
 A healthy embryo is created by putting the parents' pronuclei into the donor embryo 
 
 "Mitochondrial diseases tend to involve tissues or organs which are heavily dependent on energy," says Prof Doug Turnbull from The University of Newcastle. He has treated people with mitochondrial disease for decades and is one of those who has developed these new techniques to try to cure these debilitating diseases. 
 
 "The conditions can therefore involve the heart, the brain or sometimes the skeletal muscle," he says. 
 
 "People can have very bad heart problems which can cause the heart to fail eventually, they can be very weak and require respirators or be in a wheelchair. With the brain, they can get epilepsy, strokes and eventually severe dementia." 
 
 Turnbull estimates that around 1 in 3000-5000 people in the UK have a mitochondrial disease. "We can treat the symptoms. We can improve the quality and length of peoples' lives but we can't cure them." 
 
 The mitochondria carry some DNA, around 13 "important genes" says Turnbull. 
 
 That compares to the "23,000 important genes" in the nucleus where most of our DNA is held. This is the DNA that determines our traits and personality. 
 
 "We're not trying to create some characteristic that makes this person a stronger person or [someone who] will have blonde hair. We're trying to prevent disease and I think that is the only justification for doing this," he says. 
 
 Sharon Bernardi, from Sunderland in the North of England, is someone who mitochondrial replacement could have helped. 
 
 Image copyright other 
 
 Bernardi has lost seven children to mitochondrial disease. 
 
 "I have babies in three different cemeteries," she told us in her sitting room, surrounded by photographs of all her children. 
 
 "That is not the way you plan your life when you're trying to have a family. I have lovely photos and lovely memories but obviously that's all I have got now." 
 
 I have to slip back into reality and think don't be silly, Edward's not there. He's not in his room Sharon Bernardi 
 
 The doctors didn't know why Bernardi's babies kept passing away only hours after they were born. So that's why she kept trying, hoping she would have a healthy child. 
 
 With her fourth child, Edward, at first everything seemed different. He was healthy until he was about four and a half. But it was then that he was diagnosed with Leigh's disease, a type of mitochondrial disease, and his health deteriorated throughout the years. 
 
 "From the age of 20 Edward [found] getting around more difficult. He started to get new symptoms - spasms. He'd start screaming... four, five, six hours at a time. His muscles used to tense up, his hands, his face. It was like dystonic spasms - a really bad spasm. [For] eight hours he'd be in pain, screaming. His face would twist up and his hands would get really stiff. It was hard to see." 
 
 Edward Bernardi passed away three years ago, when he was 21. 
 
 "My life was totally for Edward. Even now sometimes if I have gone to sleep, I still wake up, and think, 'It's very quiet.' I have to slip back into reality and think, 'Don't be silly, Edward's not there. He's not in his room'." 
 
 "Without a heartbeat I would have gone for this [mitochondrial replacement]. I hope this is a new option. I hope people take it seriously and it's approved. 
 
 "I don't want my son to have just died for nothing. I want him to have made a difference." 
 
 "His life was robbed at 21. We're trying to stop this. People have to understand this is a life disease. We're trying not to pass it on to children and make it better for future families." 
 
 Image copyright other 
 
 But some people believe this technique could set us on a slippery slope towards genetically modified humans. 
 
 "These regulations would authorise the crossing of a rubicon for the first time. It would authorise germ line therapy... to alter the genes of an individual. This is something defined by the EU Charter of Fundamental Rights as effectively constituting eugenics," says British MP Fiona Bruce who chairs the All Party Parliamentary Pro-Life Group. 
 
 "We will have approved a technique and what that technique could be used for in the future who knows. We're opening a Pandora's box." 
 
 The regulator in the UK, the HFEA or Human Fertilisation and Embryology Authority, has held three independent reviews to scrutinise the safety of this technique. The conclusions were that mitochondrial replacement is "not unsafe". 
 
 There have been few episodes I'm aware of in the history of assisted reproduction that have had to be stopped because of hazard Professor Braude, Kings College London 
 
 That means "it would be reasonable, with some additional experiments, to take it into clinical practice if all circumstances are fulfilled" says Peter Braude, emeritus professor of obstetrics and gynaecology at Kings College London. He sat on all three HFEA scientific reviews. 
 
 "In any move from science to clinical practice there is a leap of faith - it has to be done," he says. 
 
 He adds that many of the concerns being raised now about this are the same as the ones cited in the early days of IVF. The UK has for decades been a leader in assisted reproduction science and is where the world's first test tube baby, Louise Brown, was born in 1978. 
 
 "The headlines then were 'playing God' and 'genetically modified humans'," says Braude. 
 
 "There have been few episodes I'm aware of in the history of assisted reproduction that have had to be stopped because of hazard. It's all gone pretty swimmingly as far as I'm aware." 
 
 Braude says that mitochondrial replacement has gone through much more scrutiny than previous, now well established, assisted reproduction techniques did, such as IVF. 
 
 "Whereas the original techniques were used with only [experiments from] mice, rabbits, lab animals... the big difference here is we also have issue of human embryos and this work has been tested in macaque monkeys in primates. All those were very useful, reassuring… hence why we came to the conclusion that this is not unsafe." 
 
 The experiments done on macaque monkeys were done in Oregon, US and the monkeys are now five years old and seem to be healthy. 
 
 Braude also points out that having a third person's DNA in your system is "nothing particularly new". 
 
 "Think about bone marrow transplants, let's say unfortunately you have leukaemia and you have to have your bone marrow radiated for the cancer to be killed and then it is replaced by bone marrow from someone else - say me. Effectively from that time onwards, you will have circulating in your body DNA from me. You won't be related to me, you may be grateful to me, but you will have DNA from a third person circulating in your body." 
 
 What is different, say critics, about mitochondrial replacement, is that DNA from the donor will be passed down future generations. 
 
 Image copyright Science Photo Library 
 
 Dr Ted Morrow, an evolutionary biologist from the University of Sussex, and colleagues have carried out mitochondrial replacement experiments on other animals. He raised safety concerns about mitochondrial replacement to the scientific reviews. 
 
 "For mice, there were changes in cognitive ability... to learn and do things using their brain. In fruit flies and seed beetles there were changes in male fertility, changes in ageing, a range of different traits were effected in various experiments," he says. 
 
 The HFEA's scientific reviews dismissed Morrow's findings as not relevant to humans because they were done on inbred animals. 
 
 Morrow stands by his research and says the scientific panels should not have dismissed his findings so quickly. 
 
 I'm a scientist but I'm not a pro-lifer. I think this is a genuine safety concern - that's it Ted Morrow, University of Sussex 
 
 It is Morrow's evidence that critics such as Fiona Bruce cite when saying this technique is not safe enough. 
 
 She has called a debate in the House of Commons today to discuss mitochondrial replacement. She does not believe there has been enough debate about what the UK is proposing to do. "The technique itself could allow the child to inherit untried untested medical complications," she says. 
 
 Morrow says that all the coverage of his research has been "a rather odd experience". 
 
 "In the press it's sometimes portrayed that the scientists think this, and the pro-life group this. I'm a scientist but I'm not a pro-lifer. I think this is a genuine safety concern - that's it." 
 
 Alana and Sharon Saarinen have been watching the debate in the UK with interest. 
 
 Media playback is unsupported on your device Media caption Watch the Newsnight film in full 
 
 "I wish I could meet her, the donor, to tell her I am so grateful for what she did for us. How can you thank someone for giving you a life? That's impossible," says Sharon. 
 
 Alana agrees with her mum. "I think it would be nice to thank her. But I wouldn't want to have a relationship or connection with her. The DNA I have of her is just so small." 
 
 "I know she might have another person's mitochondria, [but] look what a great person she turned out to be, and healthy. Just because she'll pass it on to her children it won't bother me in the least. I know it was the right thing to do. I have the living proof every day to see how great it turned out." 
 
 Subscribe to the BBC News Magazine's email newsletter to get articles sent to your inbox.
– Mitochondrial diseases afflict an estimated one in 4,000 people, most notably in the recent high-profile case of Charlie Gard in the UK, whose parents unsuccessfully sought to transport him to the US for experimental treatment. The fault lies in mitochondrial DNA, which is inherited from mothers and is responsible for powering every cell in the body, per Quartz. Now a 5-month-old baby in Michigan has been diagnosed with mitochondrial DNA depletion syndrome 13, which claimed the life of Gard last week. His parents will attempt experimental treatment in Boston, they tell NewsChannel3. With only a 50% chance of reaching his second birthday, they say at least their baby might "help other children with this condition." Russell Cruzan III, or "Bubs," first worried his parents in early June, when they wondered why he wasn't eating or thriving and was lethargic. After several hospital visits, respiratory problems, and eventually pneumonia, they got the grim diagnosis: His body lacked the energy to power his major organs. The couple doesn't have help from their insurance provider, per WOOD TV, so they've set up a YouCaring page to help with the initial test. This is the type of disease that geneticists hope to be able to stop in its tracks using so-called three-parent IVF, where a donor egg supplies a healthy set of mitochondrial DNA (37 genes) and the biological mother supplies her egg's nucleus (thousands of genes) without passing on mitochondrial diseases. (A baby was born in Mexico using this technique.)