Nature, Published online: 04 June 2025; doi:10.1038/d41586-025-01456-7In mice, a lack of maternal iron impairs an iron-dependent enzyme that activates the male sex-determining gene, causing some XY embryos to develop ovaries.

The anti-aging supplement industry is valued at many billions of dollars, with North America offering the largest market worldwide. Through clever marketing, many such supplements have promised consumers everything from halting to reversing the aging process — often without clear scientific evidence to back it up.However, recent findings from a long-term randomized controlled study have put a widely used and potent supplement into the anti-aging spotlight: Vitamin D.A sub-study from the Vitamin D and Omega-3 Trial (or VITAL Trial), published in The American Journal of Clinical Nutrition and led by researchers at Mass General Brigham and the Medical College of Georgia, has revealed that long-term Vitamin D supplementation may actually slow aging on a cellular level. This adds even more promise to Vitamin D’s already impressive list of health benefits.There's More to Vitamin D Roughly a quarter of Americans take Vitamin D supplements daily — and for good reason. While this fat-soluble vitamin is best known for maintaining bone health by helping regulate calcium and phosphorus, its role in the body extends far beyond that. Vitamin D also supports immune function, regulates inflammation, and influences cell growth to name a few.That said, getting enough Vitamin D naturally can be challenging. It’s found mainly in fatty animal products like fish, red meat, and eggs. Our skin can also synthesize it through sun exposure — which isn’t always a reliable source due to lifestyle, geography, or sunscreen use. This is why many people end up deficient.With the latest findings from the VITAL Trial, the benefits of adequate Vitamin D supplementation may now include not just stronger bones and better immunity but also support for healthy aging.Read More: What's the Difference Between Vitamin D2 and D3?Vitamin D Prevented Aging on Cellular Level“VITAL is the first large-scale and long-term randomized trial to show that vitamin D supplements protect telomeres and preserve telomere length,” said JoAnn Manson, principal investigator of VITAL and chief of the Division of Preventive Medicine at Brigham and Women’s Hospital in a press statement.Telomeres — repetitive DNA sequences at the ends of chromosomes — protect genetic material during cell division. As we age, telomeres naturally shorten, a process linked to increased risk of age-related diseases and general cellular aging.While earlier small-scale studies offered mixed results, the VITAL Telomere sub-study stands out due to its size and rigor. It followed 1,054 participants aged 50 and older over four years, comparing those who took 2,000 IU of Vitamin D3 daily (a high dosage usually recommended for those with deficiency) with those who took a placebo. Telomere length was measured at the start, at two years, and at four years.The results? Vitamin D3 supplementation significantly slowed telomere shortening — effectively preserving the equivalent of close to three years of cellular aging compared to the placebo group.Why Aging Research Matters“Our findings suggest that targeted vitamin D supplementation may be a promising strategy to counter a biological aging process, although further research is warranted,” said study’s first author Haidong Zhu, a molecular geneticist at the Medical College of Georgia in the news release.Aging research often gets lumped in with science fiction-like efforts to stop aging or live forever, but its real goal is far more grounded: to improve health across the lifespan. Instead of chasing immortality, scientists aim to extend the health span — the number of years people live free of chronic disease and disability.By uncovering interventions like Vitamin D that can support healthier aging, researchers hope to help more people enjoy a higher quality of life well into their later years, without resorting to expensive or unproven treatments.This article is not offering medical advice and should be used for informational purposes only.Article SourcesOur writers at Discovermagazine.com use peer-reviewed studies and high-quality sources for our articles, and our editors review for scientific accuracy and editorial standards. Review the sources used below for this article:Cleveland Clinic: Vitamin D DeficiencyNational Institutes of Health, Office of Dietary Supplements: Vitamin D Fact Sheet for Health ProfessionalsHaving worked as a biomedical research assistant in labs across three countries, Jenny excels at translating complex scientific concepts – ranging from medical breakthroughs and pharmacological discoveries to the latest in nutrition – into engaging, accessible content. Her interests extend to topics such as human evolution, psychology, and quirky animal stories. When she’s not immersed in a popular science book, you’ll find her catching waves or cruising around Vancouver Island on her longboard.

On Tuesday, the Senate unanimously passed the No Tax on Tips Act, pushing one of President Donald Trump’s campaign promises one step closer to becoming law. The pledge to eliminate federal taxes on service and hospitality workers’ tips rallied voters in the 2024 election, so much so that even former Vice President Kamala Harris endorsed the idea in her campaign against Trump. Now, both Democrats and Republicans on Capitol Hill seem to want to make it a reality. It’s easy to see why “no tax on tips” has broad bipartisan support: It looks like a populist policy that gives lower-wage workers much-needed relief, and opposing it might make you seem out of touch with the working class. But as I wrote last year, “no tax on tips” would actually be more of a tax break for businesses that would cost the federal government an estimated $10 billion to $15 billion a year in tax revenue. In short, the policy incentivizes businesses to lower workers’ wages and make them rely more on tips. But that’s exactly the opposite of what workers — and tipped workers in particular — need. Tipped workers are underpaid. Some of them would certainly see their take-home pay increase if the federal government stops taxing them on tips, assuming that their wages stay the same. But tips can be volatile, and often vary by season, and a “no tax on tips” policy would make offseasons worse for tipped workers, who will likely be stuck with lower base pay. The reality is that the problem for tipped workers isn’t that their taxes are too high — it’s that their wages are far too low. Plus, not having their taxes tipped means workers might end up accruing less credit toward their Social Security. In fact, many underpaid workers won’t even see a difference from the policy. Some tipped workers — by some estimates more than a third of them — earn so little that they are already exempt from income taxes, which means that a “no tax on tips” law would do nothing to boost their take-home pay. More than that, “no tax on tips” doesn’t help out most low-wage workers: More than 95 percent of low- and moderate-wage workers don’t receive tips on a regular basis. So while Congress busies itself with flashy tax cuts that won’t go too far in helping low-wage workers, it might be better to focus on the root cause of tipped workers’ problem: the subminimum wage.What is the subminimum wage and why is it so low? The last federal minimum wage increase was in 2009, and it’s been the same since: $7.25 per hour. Many states have minimum wages that are higher than the federal level — but most also have a subminimum wage for tipped workers. That’s a carveout that allows employers to pay their workers less so long as they make up the difference in tips, and that wage is just $2.13 per hour. If a subminimum wage worker doesn’t make enough tips to reach the full minimum wage, the employer is required to pay the difference. These tiered minimum wages date back to the Fair Labor Standards Act (FLSA), passed in 1938. The legislation created a subminimum wage with the intention of encouraging employers to hire people “whose earning capacity is impaired by age or physical or mental deficiency or injury.” The idea was to ensure that job opportunities and work training programs would still be available for people with disabilities. But in 1966, Congress amended the FLSA to include a subminimum wage for workers who regularly receive tips, hoping this would lower payroll costs for service-sector businesses. This change fundamentally changed the culture around tipping: While customers used to give workers tips as a show of gratitude, tips became a necessity for workers in order to make ends meet. Since then, workers in the service and hospitality sectors in most places have been subject to a subminimum wage that has not increased since 1991. While tipped wages are often sold to workers as a benefit — in theory, there’s no limit to how much they can make if customers are generous — the reality is that their overall take-home pay, even including tips, is often not enough. For example, the median wage for waiters in 2024 was $33,760, according to the Bureau of Labor Statistics, and the bottom 10 percent of waiters earned about $18,000. For context, the standard deduction — that is, the portion of your income that is untaxed — is $29,200 for a married couple and $14,600 for an individual. “No tax on tips” might give waiters a small tax break, but it’s hardly enough to work as a meaningful solution to low wages.The movement to abolish the subminimum wageMany workers have grown frustrated with the tiered minimum wage system, leading to the creation of organizations like One Fair Wage, which advocates for getting rid of the subminimum wage — a measure that would likely help alleviate poverty. (At least eight states have eliminated the subminimum wage for tipped workers.) And because a handful of states have already abolished the subminimum wage in favor of one equal minimum wage for tipped and non-tipped workers alike, we can see how the former holds workers back.According to an analysis by the Center for American Progress, tipped workers have a higher poverty rate in states with a subminimum wage compared to states that have abolished it. In states with the subminimum wage, 14.8 percent of tipped workers live in poverty. By contrast, those same workers have a poverty rate of 11 percent in states that have gotten rid of the subminimum wage. The biggest problem with the “no tax on tips” idea is that it will likely only suppress wages, which will ultimately hurt workers in the long run. There are better ways Congress can help low-wage workers than eliminating taxes on tips, including by expanding the standard deduction — giving a meaningful tax cut to all low-wage workers, not just those who receive tips — or by finally getting rid of the subminimum wage. And they might consider increasing the minimum wage while they’re at it. After all, a raise is long overdue. This story is written for the Within Our Means newsletter. Sign up here.See More:

When CRISPR was first introduced as a gene-editing tool in 2012, the world was in awe of all the possibilities it held — eventually earning its discoverers the Nobel Prize in Chemistry in 2020. Now, after years of refining the technology and running clinical trials, gene-editing has taken a major leap toward personalized medicine.As Kiran Musunuru, professor of Translational Research in Penn’s Perelman School of Medicine, put it in a press statement, “The promise of gene therapy that we’ve heard about for decades is coming to fruition, and it’s going to utterly transform the way we approach medicine.”Musunuru and a team from the Children’s Hospital of Philadelphia and Penn Medicine have successfully treated a baby boy with a rare metabolic disorder using personalized CRISPR therapy. Their case study, published in The New England Journal of Medicine, demonstrates the powerful potential of precision gene editing for rare diseases.A Child Living With a Rare DiseaseIronically, rare genetic diseases aren’t as uncommon as they sound. In the U.S., about 1 in 10 people live with a rare disorder. What makes them “rare” is that each individual condition typically affects fewer than 2,000 people, making research and treatment development incredibly challenging.One of those affected is KJ. He was born with CPS1 deficiency, a urea cycle disorder caused by the absence of a key enzyme the body needs to eliminate ammonia — a toxic byproduct of protein metabolism. Since liver transplants aren’t viable until patients are older, this condition carries a 50 percent mortality rate in early infancy.Fortunately, Musunuru and Rebecca Ahrens-Nicklas, director of the Gene Therapy for Inherited Metabolic Disorders Frontier Program (GTIMD), had been studying this class of disorders for years and reached out to KJ’s family shortly after his diagnosis.“We thought it was our responsibility to help our child, so when the doctors came to us with their idea, we put our trust in them in the hopes that it could help not just KJ but other families in our position,” said his mother, Nicole Muldoon in the press release.CRISPR — Scissors for Your DNA In just six months, the researchers developed a personalized treatment. In February 2025, KJ received his first infusion — a dose of CRISPR components delivered to his liver using lipid nanoparticles.CRISPR (short for clustered regularly interspaced short palindromic repeats) acts like a smart pair of molecular scissors. In KJ’s case, it was custom-designed to find the faulty gene and fix the error — like correcting a typo in his DNA.After receiving multiple doses, KJ has shown significant improvement. He’s now able to eat more protein and recover from everyday childhood illnesses without the dangerous ammonia buildup that once threatened his life. Even better, he’s had no serious side effects from the treatment.“While KJ will need to be monitored carefully for the rest of his life, our initial findings are quite promising,” added Ahrens-Nicklas.Expanding Success to More PatientsThis breakthrough builds on years of foundational research and collaboration. For KJ and his family, the little boy's seemingly endless hospital stay now comes to end.“We’re so excited to be able to finally be together at home so that KJ can be with his siblings, and we can finally take a deep breath,” said his father, Kyle Muldoon, in the statement.“Years and years of progress in gene editing and collaboration between researchers and clinicians made this moment possible, and while KJ is just one patient, we hope he is the first of many to benefit from a methodology that can be scaled to fit an individual patient’s needs,” added Ahrens-Nicklas.This case offers a hopeful path forward — one where gene-editing may now fulfill its bright promise to save patients with no other treatment options.This article is not offering medical advice and should be used for informational purposes only.Read More: CRISPR Eliminates Targeted Tumors by 50 PercentArticle SourcesOur writers at Discovermagazine.com use peer-reviewed studies and high-quality sources for our articles, and our editors review for scientific accuracy and editorial standards. Review the sources used below for this article:Jackson Laboratory: What Is CRISPR?Karolinska Institutet: More and more people with unusual diseases are diagnosedNew England Journal of Medicine: Patient-Specific In Vivo Gene Editing to Treat a Rare Genetic DiseaseHaving worked as a biomedical research assistant in labs across three countries, Jenny excels at translating complex scientific concepts – ranging from medical breakthroughs and pharmacological discoveries to the latest in nutrition – into engaging, accessible content. Her interests extend to topics such as human evolution, psychology, and quirky animal stories. When she’s not immersed in a popular science book, you’ll find her catching waves or cruising around Vancouver Island on her longboard.

May 16, 20253 min readIn World First, Baby Receives Personalized CRISPR Gene-Editing TreatmentA CRISPR treatment seems to have been effective for a baby’s devastating disease, but it is not clear whether such bespoke therapies can be widely appliedBy Heidi Ledford & Nature magazine KJ Muldoon, a baby born with a genetic disease that affected his ability to metabolize proteins, has become the first person to receive a bespoke CRISPR treatment. Children's Hospital of PhiladelphiaA baby boy with a devastating genetic disease is thriving after becoming the first known person to receive a bespoke, CRISPR therapy-for-one, designed to correct his specific disease-causing mutation.Little KJ Muldoon, now nearly ten months old, is doing well after receiving three doses of a gene-editing treatment to mend a mutation that impaired his body’s ability to process protein, his parents told reporters this week. But it is too soon to use the word “cure”, says Rebecca Ahrens-Nicklas, a pediatrician at Children’s Hospital of Philadelphia in Pennsylvania, and one of Muldoon’s physicians. “This is still really early days,” she says. “We know we have more to learn from him.”To reach this point, an international team of clinicians and researchers in industry and academia, with support from US government funders and regulatory agencies, raced to develop Muldoon’s therapy in a mere six months. Yet, the drug that it developed, described in the New England Journal of MedicineOn supporting science journalismIf you're enjoying this article, consider supporting our award-winning journalism by subscribing. By purchasing a subscription you are helping to ensure the future of impactful stories about the discoveries and ideas shaping our world today.It’s an ambitious approach that researchers hope will inspire others to harness CRISPR to treat ultra-rare genetic diseases. “This truly is the future for all of these gene and cell therapies,” says Arkasubhra Ghosh, who studies gene therapy at Narayana Nethralaya Eye Hospital in Bengaluru, India, and who was not involved in the study. “It’s really exciting.”Early illnessDozens of people have received CRISPR-based therapies for genetic conditions such as sickle-cell anaemia, but those treatments were designed to be used in many people with the same disorder, regardless of the underlying mutations that caused it. By contrast, researchers tailored Muldoon’s therapy to correct a specific genetic sequence in his genome.Muldoon had inherited two mutations, one from each parent, that meant that he did not produce the normal form of a crucial enzyme called carbamoyl phosphate synthetase 1 (CPS-1). This compromised his ability to process the nitrogen-containing compounds produced when the body breaks down protein. As a result, his blood had high levels of ammonia, a compound that is particularly toxic to the brain.The best treatment for CPS-1 deficiency is a liver transplant, but it would be months before Muldoon became eligible. Meanwhile, each day brought added risk of brain damage or death: only about half of babies with severe CPS-1 deficiency survive long enough to receive a transplant.Ahrens-Nicklas decided to offer the family another option. She and her colleagues had been working with a CRISPR-based technique called base editing, which can make targeted, single-letter changes to DNA sequences. The team was developing ways to quickly and safely tailor a base-editing therapy to correct an individual’s particular mutations. Perhaps now it was time to try the approach in humans, she thought.With the approval of Muldoon’s parents, the researchers enlisted a lengthy roster of collaborators. The team quickly screened for the best base-editing approach and tested it in mice and monkeys. Companies donated proprietary expertise and components. The US Food and Drug Administration fast-tracked its evaluation of the treatment.Rapid deploymentIn just six months, Muldoon received his first dose — a “remarkable” achievement, says Waseem Qasim, a pediatrician at the University College London Great Ormond Street Institute of Child Health, who has used base editing to engineer immune cells to fight cancer.After that initial dose, Muldoon could safely eat the amount of protein recommended for his age, but still needed medications to keep his ammonia levels in check. With a second round of the therapy, the researchers were able to reduce the amount of medicines needed, but could not eliminate his need to take them.Muldoon has since received a third and final dose. His clinicians are carefully reducing his medication dosage, little by little, says Ahrens-Niklas.It’s unclear how this approach could be expanded to treat others with ultra-rare diseases: even when designed to treat hundreds of people, gene therapies and gene-editing therapies are notoriously expensive. “There’s no great answer to this,” says Qasim.For now, each milestone that Muldoon reaches is a tiny miracle to his parents. Earlier this week, his mother, Nicole, walked into his hospital room to find him sitting up by himself in his crib. “We never thought this was going to happen,” she says.This article is reproduced with permission and was first published on May 15, 2025.

Baby KJ after a gene-editing infusion with researchers Rebecca Ahrens-Nicklas and Kiran MusunuruChildren’s Hospital of Philadelphia A baby boy with a life-threatening genetic condition has become the first person to receive a bespoke CRISPR gene-editing treatment, giving a glimpse into what the future of medicine might look like. It’s the first time anyone has been given a gene-editing treatment designed to correct a disease-causing mutation found only in that individual, Rebecca Ahrens-Nicklas at the Children’s Hospital of Philadelphia, Pennsylvania, told a press briefing. “He’s showing some early signs of benefit,” she says, but it is too soon to tell how well the treatment worked. Advertisement The researchers published the details as soon as possible in the hope that it will inspire others, says team member Kiran Musunuru at the University of Pennsylvania. “We very much hope that showing that it’s possible to make a personalised gene-editing therapy for a single patient in several months will inspire others to do the same,” he says. “I don’t think I’m exaggerating when I say that this is the future of medicine,” he says. “This is the first step towards the use of gene-editing therapies to treat a wide variety of rare genetic disorders for which there are actually very few treatments currently in development at all.” The boy, KJ, inherited mutations in each of his two copies of a gene for a liver enzyme called CPS1. Without this enzyme, ammonia builds up in the blood when proteins, including ones we eat, are broken down, damaging the brain. More than half of children born with a CPS1 deficiency die, says Ahrens-Nicklas. Get the most essential health and fitness news in your inbox every Saturday. Sign up to newsletter She and Musunuru have been developing treatments for this kind of condition that target the liver, allowing them to rapidly create a base-editing therapy – a form of CRISPR – that corrects one of KJ’s two copies of the CPS1 gene. The team contacted US regulators early on. “They recognised that this was an unusual circumstance,” says Musunuru. “KJ was very, very sick, and there wasn’t time for business as usual. When we formally submitted our application to the FDA [Food and Drug Administration] when KJ was 6 months of age, the FDA approved it in just one week.” KJ was given a low dose of the treatment in February 2025 when he was 6 months old, followed by larger doses in March and April. He is now able to eat more protein than before, despite taking lower amounts of other medications to manage his condition. Ideally, children would be treated even earlier to prevent the long-term damage conditions such as CPS1 deficiency can cause. As New Scientist reported last year, Musunuru aims to one day edit human genes before birth. Other gene-editing therapies are designed to work for many people, regardless of the specific mutation causing their condition. For instance, the first ever approved gene-editing treatment, for sickle cell disease, works by turning on the production of fetal haemoglobin, rather than by correcting the mutations in adult haemoglobin that cause the condition. Despite being a “one-size-fits-all” treatment, it still costs £1,651,000 per course of treatment in England. KJ with his family after the treatmentChildren’s Hospital of Philadelphia Personalised treatments are likely to be even more expensive. Musunuru says he can’t put a number on KJ’s treatment, because the companies involved did much of the work for free. But the price will come down, he thinks. “As we get better at doing this, economies of scale will kick in and you can expect the cost to come down orders of magnitude,” he says. One reason personalised gene-editing treatments haven’t been developed before is that regulators have regarded therapies targeting different mutations in the same gene as separate, meaning companies would have had to restart the approval process from scratch for every different mutation. But there is now a move towards what is called a platform approach, where regulators will give broad approval to a therapy for a condition, whichever mutation is targeted. “Platform-based approaches, like genome editing with CRISPR – as we’re seeing with KJ’s treatment – offer a scalable way to treat even the rarest diseases,” says Nick Meade at the Genetic Alliance UK, a charity that helps people with rare diseases. “This at last makes treatment a realistic prospect for thousands of families.” Journal reference:New England Journal of Medicine DOI: 10.1056/NEJMoa2504747 Topics:crispr

A team of doctors and scientists have successfully treated a rare genetic condition with the first-ever personalized gene-editing therapy. Results of the groundbreaking treatment have been published in The New England Journal of Medicine, with an accompanying editorial by a doctor who had previously overseen the FDA's gene-therapy regulation efforts. The patient in this historic case was KJ, an infant born with CPS1 deficiency, which has about a 50 percent mortality rate within the first week. Patients that do survive can experience severe brain disease, mental and developmental delays, and potential liver transplants. His care team developed a personalized gene-editing treatment based on CRISPR, a technology for modifying human DNA. The successful gene repair for KJ combined years' worth of previous federally-funded medical research, including the discovery of CRISPR and human genome sequencing that allowed the mutation to be identified. This approach to gene editing could potentially be used in the future to aid patients with other genetic disorders, such as sickle cell disease, cystic fibrosis, Huntington’s disease and muscular dystrophy. A pair of CRISPR-based drugs have already received FDA approval for sickle cell disease treatments, but there is still a lot to potentially be explored in this field.This article originally appeared on Engadget at https://www.engadget.com/science/doctors-successfully-treated-a-baby-with-the-first-ever-personalized-gene-editing-therapy-202307902.html?src=rss

Science & technology | One of a kindFor the first time, a CRISPR drug treats a child’s unique mutationScientists hope more children will benefitPhotograph: Children's Hospital of Philadelphia May 15th 2025WITHIN DAYS after KJ was born in Philadelphia in August 2024 it was clear that something was wrong. He was not eating and slept too much. Blood tests revealed sky-high levels of ammonia, a toxic substance the body usually expels. Genome sequencing confirmed that he had a rare genetic disease called carbamoyl-phosphate synthetase 1 (CPS1) deficiency, which often kills in infancy, and for which no good neonatal treatment exists. Then one of his doctors suggested something radical: a gene-editing drug designed specifically for him.Explore moreThis article appeared in the Science & technology section of the print edition under the headline “One of a kind”From the May 17th 2025 editionDiscover stories from this section and more in the list of contents⇒Explore the editionReuse this content

Scientists have successfully treated a 9.5-month-old boy with an ultra-rare genetic disorder using the world's first personalized gene-editing therapy. The patient, identified as KJ, has CPS1 deficiency -- a condition affecting just one in 1.3 million babies that prevents proper ammonia processing and is often fatal. The breakthrough treatment, detailed in the New England Journal of Medicine, uses base editing technology to correct KJ's specific DNA mutation. The therapy delivers CRISPR components wrapped in fatty lipid molecules that protect them in the bloodstream until they reach liver cells, where they make the precise edit needed. After three infusions, KJ now eats normal amounts of protein and has maintained stable ammonia levels even through viral illnesses that would typically cause dangerous spikes. His weight has increased from the 7th to 40th percentile. Dr. Peter Marks, former FDA official, called the approach "one of the most potentially transformational technologies" because it could be rapidly adapted for thousands of other rare genetic diseases without lengthy development cycles. Read more of this story at Slashdot.