On July 26, Shoukhrat Mitalipov woke up to headlines about his research: “First human embryos edited in US,” said one; “Genome of viable human embryos edited in controversial study,” said another. Normally, this would be a cause for celebration for the Oregon Health & Science University (OHSU) professor. But in this case, all the media coverage did was stress him out—his study wasn’t supposed to be published until Aug. 2. 
 
 “I don’t know how it got leaked,” Mitalipov said on July 28. “It’s likely because of a combination of hot words: Crispr, gene-editing, and designer babies.” 
 
 He sounded annoyed, and justifiably so. The articles had rung alarm bells about “designer babies” engineered to have advantageous genetic traits, but his research was far from proving that a possibility. Although it did involve the use of human embryos—which is a union of egg and sperm—it also wasn’t particularly controversial. In 2015, after a long debate, experts at the US National Academies of Science, Engineering, and Medicine concluded that this sort of research on human embryos should be encouraged. And in fact, one prominent news story that called Mitalipov’s study “controversial” actually contained testimonies from two bioethicists who supported the study (the headline has since been changed). 
 
 Today (Aug. 2), Mitalipov’s study was published in the journal Nature. It shows the first highly successful use of the gene-editing technique called Crispr to improve human health: his team was able correct a genetic mutation that causes a life-threatening cardiac disease. None of the embryos were allowed to come to term. But if Mitalipov has his way, future projects could eradicate a disease that affects millions—one in 500 people carry the mutation—and even kills unsuspecting, seemingly fit adults. 
 
 Picking the target 
 
 On Mar. 4, 1990, Loyola Marymount University basketball player Hank Gathers dunked the ball to put the Loyola Lions well ahead of the University of Portland Pilots. Immediately afterwards he collapsed and stopped breathing. There were 13 minutes left in the basketball game; he’d given everything to the sport. The cause of death was later determined to be hypertrophic cardiomyopathy (HCM), the most common inherited cardiac disease and the most common cause of death in young athletes. 
 
 Mitalipov began working on the project three years ago. He knew he wanted to try to use Crispr to cure a genetic disease, but first he needed to pick which mutation in the human genome to target. He could have chosen from thousands, but Sanjeev Kaul, a cardiovascular specialist at OHSU, convinced Mitalipov to go after the HCM gene mutation. 
 
 “It’s such a terrible disease to deal with it, and it’s present in a large population,” Mitalipov says. “In India, for instance, nearly one in ten people carry it.” 
 
 The most common cause of HCM is a genetic mutation in one of nine genes. Mitalipov’s research shows that you can take a human embryo with one such mutation, where the human genome is missing four base pairs (or letters of DNA) and simply correct it. In theory, if you let that embryo grow, it would develop into a human without HCM. 
 
 Substitutes won’t do 
 
 Next Mitalipov had to convince the OHSU review board to approve the use of human embryos. That part took about two years. 
 
 Most research to understand what happens at the embryonic stage of human development is done on embryo-like cells, created by exposing adult stem cells to a special handful of chemicals. But though embryo-like cells have been a boon for research, they are not a perfect replacement for embryonic cells. Certain things, like DNA repair systems, can be quite different in embryos than they are in embryo-like cells. 
 
 And DNA repair was key to Mitalipov’s research. Crispr is the most precise gene-editing technique we have, but it doesn’t actually “edit” genes. Instead, it seeks out the gene it has been programmed to target and then makes a snip. The next step almost always involves relying on the cell’s own DNA repair system, which finds the cut and does its best to fix it. 
 
 In most cells in the body, there are two repair systems. The system most often used by the body requires less effort, but it also does a sloppy job: sometimes inserting a letter of DNA where it doesn’t belong and other times deleting a letter of DNA that should be there. The other repair system produces more accurate results, but the cells need to put in more effort to make it happen, so it’s rarely used. However, past research hinted that human egg cells tend to use the second system. Mitalipov needed this especially strong DNA repair system to accomplish his Crispr-HCM edit. 
 
 With the case made and approval secured, Mitalipov’s team went into full gear. A group of collaborators recruited a man with the HCM mutation who would donate sperm, and a dozen healthy women who would donate eggs for the research. 
 
 Beating China 
 
 Three previous studies that used Crispr in human embryos—all conducted in China—produced poor results. The first, published in 2015, injected Crispr in 86 non-viable embryos (all discards from in-vitro fertilization treatment), in an effort to cure the inherited blood disorder β-thalassemia. It only worked in about 33% of the samples, and even then in those cases it was far from perfect: each had undesirable cuts in other locations on the genome (called “off-target effects”). 
 
 Another attempt published in 2016 tried a different tack. Instead of removing a mutation, it sought to induce one that would provide resistance to HIV. Gene insertion was only successful in 25% of the 26 non-viable embryos, and many of those “successes” ended up with the wrong mutation. 
 
 Earlier this year, the researchers made the case that the reason their 2016 study failed wasn’t because Crispr wasn’t doing its job. Instead, they suspected that the embryos used, because they were non-viable, were too abnormal to effectively test Crispr’s precision. But in a new study using six viable human embryos, they were still able to fully correct the mutation in only one. In another two, they fixed the mutation but in only some of the cells of the embryo—leading to a condition known as “mosaicism.” In these cases, if the embryo were to come to term, it would create a human whose body has some cells with the mutation and others without. The upshot would be that there’s no guarantee the adult would be free of the disease. 
 
 Mitalipov had a plan to avoid both off-target effects and mosaicism. Instead of injecting Crispr after the embryo had formed, he decided to make the snip during the process of fertilization. So while injecting sperm, he also injected Crispr. 
 
 OHSU The first sign of successful in vitro fertilization, after co-injection of a gene-correcting enzyme and sperm from a donor with a genetic mutation known to cause hypertrophic cardiomyopathy. 
 
 The programmed Crispr system located the position in the sperm DNA where the man’s genome was missing the four key base pairs and it made a simple cut there. The fertilization process began with the cut in place. However, at some point during the early stages of the development of the embryo—and Mitalipov doesn’t know exactly when—the egg’s DNA repair system kicked in. The new embryo contained one strand of DNA from the mother, which the team knew to be healthy and without the HCM mutation, and another strand from the father that included a snip at the location of the HCM mutation. 
 
 When the egg’s more accurate DNA repair system detects the cut in the paternal strand, it started fixing it, using the maternal strand as a model. And because the maternal strand was healthy, the repair system added the four missing base pairs to the paternal strand, and the HCM mutation in the embryo was corrected. (This method is only applicable to situations where one parent has the mutation; if both parents have the same mutation, this type of DNA repair system has no functional model to copy.) 
 
 Mitalipov’s team tested their technique on a total of 163 viable embryos, and the mutation was corrected successfully in nearly 50% of them. Better still, only one of those embryos showed mosaicism and none showed any off-target effects. 
 
 Two independent experts Quartz contacted—Dieter Egli of Columbia University and Maria Jasin of the Memorial Sloan Kettering Cancer Center—weren’t sure Mitalipov’s claims were water tight. Based on the information provided in the study, Egli couldn’t confidently say for sure that the tests used to detect mosaicism caught all mosaics. In other words, it’s possible that results appear to be more positive than they actually are. Jasin pointed out that more evidence was needed to back up the claim that it was the more accurate method of DNA repair that the embryo used. She acknowledged that working with human embryos has extra constraints because researchers need to justify the use of every extra embryo, but still felt there were some gaps in the study. 
 
 The father of human genetic engineering 
 
 If the results do stand up, they are orders of magnitude better than the three previous Chinese attempts—both because of the rate of success and the number of viable embryos tested. But Mitalipov acknowledges that it’s still not good enough. “A 50% success rate is too low,” he says. 
 
 Reuters/Richard Clement Shoukhrat Mitalipov of Oregon Health & Science University. 
 
 His exacting standards have paid off in the past. Mitalipov’s groundbreaking work in the late 2000s paved the way for “three-parent babies;” last year, a technique he developed contributed to the birth of the first genetically engineered baby born with DNA from two females and one male. 
 
 The technique cures mitochondrial disease, which is caused because of faulty mitochondria, the power packs in each human cell that converts sugar into a usable form of energy. Children born with mitochondrial disease either die young or live disabled lives. 
 
 Most human genes are jammed into the cell’s nucleus, but there’s a tiny fraction (37 out of 20,000) present in mitochondria. These genes are only passed down from mother to child. Mitalipov developed the technique to replace a mother’s faulty mitochondria with healthy ones from a female donor. Though the baby will mostly still be the genetic child of one man and one woman, he or she will have a small number of genes from another woman, technically a third “parent.” 
 
 “In 2009, when I published my research on mitochondrial replacement, people laughed at me,” he says. “They said ‘You will never bring it to clinic.’ Look where we are today.” 
 
 He first developed the technique in monkeys, and then progressed to human embryos—reaching success rates of 99%. He has the same ambition for Crispr-edited human embryos. 
 
 “I have a very strong opinion on clinical applications. I didn’t do this research to satisfy my curiosity,” Mitalipov says. “This was done to develop the technology and bring it to clinics. It may take a decade, but we will be there.” 
 
 Slippery slope? 
 
 Crispr-editing of human embryos is a much more complex endeavor than the three-parent baby technique. There is no guarantee, for instance, that the steps used by Mitalipov to fix the HCM mutation would work on other similar mutations or on more complex ones. However, if the technique is perfected, it will have a much greater impact on human health than anything the three-parent technique could ever offer. 
 
 The complexity is also a safeguard against the use of the technique to, say, create babies with traits such as higher intelligence or greater strength. We don’t yet understand the sheer number of genes involved in the creation of those traits, let alone what it would take to make such detailed edits to the human genome. In other words, even if you think it’s an ethical hazard to the Crispr to provide advantageous mutations, there’s no reason to worry right now; those “designer babies” are decades away. 
 
 A more immediate threat is unregulated use. Genetic engineering of humans has already begun, and there is real danger in people with inadequate understanding of the risks starting to use Crispr to edit out inherited illnesses and bring the embryos to term. The baby is likely to suffer mosaicism, off-target effects, or other as-yet-undetected consequences, and we don’t know what that could do to the person born with them. 
 
 The first three-parent baby was born in Mexico, because at the time the country had no regulations on the use of the technique. Though the baby was reported to be healthy few months after birth, the risks of things going awry are much higher without the rigorous checks provided by clinical trials in a country with strong regulations. (The second three-parent birth was reported to have occurred in Ukraine.) 
 
 OHSU Embryos after co-injection developing into blastocysts, which could someday be used in fertility clinics to help people trying to have children free of genetic disease. 
 
 “Unfortunately, that’s a risk,” admits Paula Amato, a gynecologist who collaborates with Mitalipov at the OHSU. “Obviously, we would prefer clinical applications occur in a regulated environment. But it’s not something we can control.” In the US, the Food and Drug Administration (FDA) forbids the use of human embryos in clinical trials. “So it’s not surprising to me that people would attempt to circumvent such restrictions,” Amato says. 
 
 In the US, only pre-clinical research involving human embryos is allowed and even for that government funds aren’t available. Mitalipov’s work was supported mostly by OHSU’s institutional funds and the rest through charitable foundations. His collaborators in South Korea, where human embryo research is strictly forbidden, had to get lawyers and were only able to handle DNA extracts from the test embryos, and not the embryos themselves. 
 
 There are some places that offer regulated environments without stifling experimentation and clinical use. Amato points to the UK, the first country to offer licenses to create three-parent babies, if those applying could make the case for it. The country spent years debating the topic among experts and holding public consultations before it reached that stage. 
 
 Ultimately, if society would like to see the use of Crispr or other techniques to rid humanity of devastating diseases, countries will need to undertake a process similar to what the UK went through. Without hearing the voice of the public and putting the right regulations in place, the fear of “designer babies” could not only lead to dangerous experimentation in unregulated environments, but also quash the true potential of this powerful tool. ||||| 
 
 
 
 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. 
 
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 ||||| Please report potential fraud and Terms of Service violations only. Personal disputes will not be reviewed. 
 
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 Subject * Choose One Suspicious activity This fundraiser is offensive, vulgar, or divisive Money not being used as the fundraiser states This is a duplicate fundraiser This fundraiser contains copyright information Violates Terms of Service Other ||||| Mitochondrial disease is an inherited chronic illness that can be present at birth or develop later in life. It causes debilitating physical, developmental, and cognitive disabilities with symptoms including poor growth; loss of muscle coordination; muscle weakness and pain; seizures; vision and/or hearing loss; gastrointestinal issues; learning disabilities; and organ failure. It is estimated that 1 in 4,000 people has Mito. It’s progressive and there is no cure. 
 
 What are Mitochondria? 
 
 Mitochondria are tiny organelles found in almost every cell in the body. 
 
 They are known as the "powerhouse of the cell." 
 
 They are responsible for creating more than 90 percent of cellular energy. 
 
 They are necessary in the body to sustain life and support growth. 
 
 They are composed of tiny packages of enzymes that turn nutrients into cellular energy. 
 
 Mitochondrial failure causes cell injury that leads to cell death. When multiple organ cells die there is organ failure. 
 
 Watch the 5-minute video, "How energy is made" 
 
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 What is Mitochondrial Disease? 
 
 Mitochondrial disease is a chronic, genetic disorder that occurs when the mitochondria of the cell fail to produce enough energy for cell or organ function. 
 
 The incidence is about 1:4000 individuals in the US. This is similar to the incidence of cystic fibrosis of caucasian births in the U.S. 
 
 There are many forms of mitochondrial disease. 
 
 Mitochondrial disease is inherited in a number of ways. 
 
 Mitochondrial disease presents vary differently from individual to individual. 
 
 There may be one individual in a family or many individuals affected over a number of generations. 
 
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 What are the Symptoms of Mitochondrial Disease? 
 
 The severity of mitochondrial disease symptoms is different from person to person. The most common symptoms are: 
 
 Poor growth 
 
 Loss of muscle coordination, muscle weakness 
 
 Neurological problems, seizures 
 
 Autism, autistic spectrum, autistic-like features 
 
 Visual and/or hearing problems 
 
 Developmental delays, learning disabilities 
 
 Heart, liver or kidney disease 
 
 Gastrointestinal disorders, severe constipation 
 
 Diabetes 
 
 Increased risk of infection 
 
 Thyroid and/or adrenal dysfunction 
 
 Autonomic dysfunction 
 
 Neuropsychological changes characterized by confusion, disorientation, and memory loss. 
 
 Detailed information about symptoms can be found in the Clinician's Guide to Mitochondrial Disease 
 
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 How common are mitochondrial diseases? 
 
 Infants, children, and adults may develop mitochondrial disorders. Experts in mitochondrial medicine agree there is a spectrum of the disease, ranging from mild to severe. 
 
 In adults, many diseases of aging have been found to have defects of mitochondrial function; these include, but are not limited to, Type 2 diabetes, Parkinson's disease, atherosclerotic heart disease, stroke, Alzheimer's disease, and cancer. In addition, many medicines can injure the mitochondria. 
 
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 What causes mitochondrial disease? 
 
 For many patients, mitochondrial disease is an inherited genetic condition. An uncertain percentage of patients acquire symptoms due to other factors, including mitochondrial toxins. 
 
 It is important to determine which type of mitochondrial disease inheritance is present in order to predict the risk of recurrence for future children. The types of mitochondrial disease inheritance include: 
 
 DNA (DNA contained in the nucleus of the cell) inheritance. Also called autosomal inheritance. If this gene trait is recessive (one gene from each parent), often no other family members appear to be affected. There is a 25 percent chance of the trait occurring in other siblings. If this gene trait is dominant (a gene from either parent), the disease often occurs in other family members. There is a 50 percent chance of the trait occurring in other siblings. 
 
 
 
 MtDNA (DNA contained in the mitochondria) inheritance. 
 
 There is a 100 percent chance of the trait occurring in other siblings, since all mitochondria are inherited from the mother, although symptoms might be either more or less severe. 
 
 Combination of mtDNA and nDNA defects: 
 
 Relationship between nDNA and mtDNA and their correlation in mitochondrial formation is unknown. 
 
 Read more about genetics and the inheritance of mitochondrial disease. 
 
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 Random occurrences 
 
 Diseases specifically from deletions of large parts of the mitochondrial DNA molecule are usually sporadic without affecting other family member. 
 
 Medicines or other toxic substances can trigger mitochondrial disease. 
 
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 How is Mitochondrial Disease Diagnosed? 
 
 There is no reliable and consistent means of diagnosis. 
 
 Diagnosis can be made by one of the few physicians who specialize in mitochondrial disease. 
 
 Diagnosis can be made by blood DNA testing and/or muscle biopsy but neither of these tests is completely reliable. 
 
 Read about the vitamins and supplements used to treat Mito 
 
 How is Mitochondrial Disease Treated? 
 
 The goal is to improve symptoms and slow progression of the disease. 
 
 Use vitamin therapy 
 
 Conserve energy 
 
 Pace activities 
 
 Maintain an ambient environmental temperature 
 
 Avoid exposure to illness 
 
 Ensure adequate nutrition and hydration 
 
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 Misdiagnosis 
 
 Lack of understanding of the disease and misinterpretation of symptoms can lead to misdiagnosis. 
 
 Further progression of symptoms can occur if the symptoms are missed and opportunities for treatment and support are not recognized. 
 
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 What are the Challenges of Living with Mitochondrial Disease? 
 
 Affects multiple organs, affects multiple family members, affects multiple generations. 
 
 Lack of awareness and understanding of the disease. 
 
 Families are continuously forced to expend their very limited energy to explain their disease, advocate for themselves and fight for services. 
 
 Mitochondrial disease is often an "invisible disease." Good day - Patients look fine and healthy. They have more energy and appear rested. Bad day - - Patients appear tired to significantly ill. They are obviously fatigued and/or have significant illness. Repeated "bad days"often lead to decompensation and patients have difficulty returning to baseline. 
 
 Mitochondrial disease is unpredictable. Day to day, hour to hour patients can develop symptoms and their stability can be threatened. 
 
 Difficulties establishing a diagnosis interfere with a patient's ability to obtain adequate recognition, medical care, insurance coverage, healthcare supports, and disability services. 
 
 Lack of understanding of the disease and misinterpretation of symptoms can lead to misdiagnosis. Further progression of symptoms can occur if the symptoms are missed and opportunities for treatment and support are not recognized. 
 
 An individual can become symptomatic at any time in life despite the fact that it is inherited. 
 
 It is difficult to diagnose. 
 
 Meet other parents and patients in our closed Facebook group. 
 
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 What is the Prognosis for Someone? 
 
 The prognosis is variable. Some people live a normal life and are minimally affected; others can be severely compromised with the disease. 
 
 It is completely individualized. 
 
 The prognosis is unpredictable. 
 
 Browse medical & support topics in our Medical Blog 
 
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 MitoAction's Goals 
 
 To improve quality of life for adults and children affected by mitochondrial disease. 
 
 To internationally raise awareness about mitochondrial disorders, and their relationship to other diseases. 
 
 To provide specifc and practical materials that help patients to manage their symptoms. 
 
 To aggregate and connect the international mitochondrial disease community. 
 
 To create tools that empower patients and caregivers to be advocates for themselves or their children. 
 
 Other Mito organizations 
 
 Read more about the mission of MitoAction 
 
 back to top ||||| 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.
– 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.)