Taurine supplements have been considered promising for delaying ageing, but that may not be the caseShutterstock / Eugeniusz Dudzinski The amino acid taurine was once thought to decline with age, and animal research suggested that taurine supplements could delay ageing. But a new study shows that the decline doesn’t happen consistently. In fact, taurine levels tend to increase in people over time, suggesting that low levels of the nutrient aren’t a driver of ageing. Previous research has shown that taurine concentrations decline in men as they age and that people with higher taurine levels at 60 years old tend to have better health outcomes. This, along with evidence that taurine supplements extend lifespan in mice and monkeys, suggested that low taurine contributes to ageing.Advertisement The trouble is that taurine fluctuates in response to other factors too, such as illness, stress and diet – therefore, declines in this key amino acid may not be due to ageing. Maria Emilia Fernandez at the National Institute on Aging in Maryland and her colleagues analysed taurine levels in 742 people between 26 and 100 years old. The participants, about half of whom were women, didn’t have underlying health conditions and provided three to five blood samples between January 2006 and October 2018. On average, taurine levels were almost 27 per cent higher in women at 100 years old than at 26 years old and rose about 6 per cent in men between the ages of 30 and 97. Similar results were seen in 32 monkeys that underwent three to seven blood draws between 3 and 32 years of age. Between 5 and 30 years of age, taurine levels rose 72 per cent in female monkeys and 27 per cent in male monkeys, on average. Together, these findings indicate that taurine levels are not a reliable indication of ageing. What’s more, taurine levels also varied widely between people and even within individuals over time, suggesting that other environmental factors influence them, says Fernandez. Get the most essential health and fitness news in your inbox every Saturday. Sign up to newsletter However, some people may still benefit from taurine supplementation, says Fernandez, pointing to studies that show it helps regulate blood sugar in people with type 2 diabetes or obesity. But whether it can delay ageing in otherwise healthy people is an open question. Vijay Yadav at Rutgers University in New Jersey says he and his colleagues are currently conducting a clinical trial of taurine supplementation in middle-aged adults. “We hope to finish the trial by the end of 2025,” he says. “Hopefully it will generate sufficiently rigorous data to show whether or not taurine supplementation delays the pace of ageing in humans or increases health and fitness.” Journal reference:Science DOI: 10.1126/science.adl2116 Article amended on 5 June 2025We corrected Vijay Yadav's affiliationTopics:

IBM and Roche are teaming up on an AI solution to a challenge faced by millions worldwide: the relentless daily grind of diabetes management. Their new brainchild, the Accu-Chek SmartGuide Predict app, provides AI-powered glucose forecasting capabilities to users. The app doesn’t just track where your glucose levels are—it tells you where they’re heading. Imagine having a weather forecast, but for your blood sugar. That’s essentially what IBM and Roche are creating.AI-powered diabetes managementThe app works alongside Roche’s continuous glucose monitoring sensor, crunching the numbers in real-time to offer predictive insights that can help users stay ahead of potentially dangerous blood sugar swings.What caught my eye were the three standout features that address very specific worries diabetics face. The “Glucose Predict” function visualises where your glucose might be heading over the next two hours—giving you that crucial window to make adjustments before things go south.For those who live with the anxiety of hypoglycaemia (when blood sugar plummets to dangerous levels), the “Low Glucose Predict” feature acts like an early warning system, flagging potential lows up to half an hour before they might occur. That’s enough time to take corrective action.Perhaps most reassuring is the “Night Low Predict” feature, which estimates your risk of overnight hypoglycaemia—often the most frightening prospect for diabetes patients. Before tucking in for the night, the AI-powered diabetes management app gives you a heads-up about whether you might need that bedtime snack. This feature should bring peace of mind to countless households.“By harnessing the power of AI-enabled predictive technology, Roche’s Accu-Chek SmartGuide Predict App can help empower people with diabetes to take proactive measures to manage their disease,” says Moritz Hartmann, Head of Roche Information Solutions.How AI is speeding up diabetes researchIt’s not just patients benefiting from this partnership. The companies have developed a rather clever research tool using IBM’s watsonx AI platform that’s transforming how clinical study data gets analysed.Anyone who’s been involved in clinical research knows the mind-numbing tedium of manual data analysis. IBM and Roche’s tool does the heavy lifting—digitising, translating, and categorising all that anonymised clinical data, then connecting the dots between glucose monitoring data and participants’ daily activities.The result? Researchers can spot meaningful patterns and correlations in a fraction of the time it would normally take. This behind-the-scenes innovation might do more to advance diabetes care and management in the long run than the app itself.What makes this collaboration particularly interesting is how it brings together two different worlds. You’ve got IBM’s computing prowess and AI know-how pairing up with Roche’s decades of healthcare and diabetes expertise.”Our long-standing partnership with IBM underscores the potential of cross-industry innovation in addressing unmet healthcare needs and bringing significant advancements to patients faster,” says Hartmann.“Using cutting-edge technology such as AI and machine learning helps us to accelerate time to market and to improve therapy outcomes at the same time.”Christian Keller, General Manager of IBM Switzerland, added: “The collaboration with Roche underlines the potential of AI when it’s implemented with a clear goal—assisting patients in managing their diabetes.“With our technology and consulting expertise we can offer a trusted, customised, and secure technical environment that is essential to enable innovation in healthcare.”What this means for the future of healthcare techHaving covered healthcare tech for years, I’ve seen plenty of promising innovations fizzle out. However, this IBM-Roche partnership feels promising—perhaps because it’s addressing such a specific, well-defined problem with a thoughtful, targeted application of AI.For the estimated 590 million people (or 1 in 9 of the adult population) worldwide living with diabetes, the shift from reactive to predictive management could be gamechanging. It’s not about replacing human judgment, but enhancing it with timely, actionable insights.The app’s currently only available in Switzerland, which seems a sensible approach—test, refine, and perfect before wider deployment. Healthcare professionals will be keeping tabs on this Swiss rollout to see if it delivers on its promise.If successful, this collaboration could serve as a blueprint for how tech giants and pharma companies might work together on other chronic conditions. Imagine similar predictive approaches for heart disease, asthma, or Parkinson’s.For now, though, the focus is squarely on using AI to improve diabetes management and helping people sleep a little easier at night—quite literally, in the case of that clever nocturnal prediction feature. And honestly, that’s a worthwhile enough goal on its own.(Photo by Alexander Grey)Want to learn more about AI and big data from industry leaders? Check out AI & Big Data Expo taking place in Amsterdam, California, and London. The comprehensive event is co-located with other leading events including Intelligent Automation Conference, BlockX, Digital Transformation Week, and Cyber Security & Cloud Expo.Explore other upcoming enterprise technology events and webinars powered by TechForge here.

Our columnist tried Dexcom’s Stelo wearable to see if the data could help her live—and eat—healthier.

Human organs could be bioprinted for transplants within 10 years, according to Lithuanian startup Vital3D. But before reaching human hearts and kidneys, the company is starting with something simpler: regenerating dog skin. Based in Vilnius, Vital3D is already bioprinting functional tissue constructs. Using a proprietary laser system, the startup deposits living cells and biomaterials in precise 3D patterns. The structures mimic natural biological systems — and could one day form entire organs tailored to a patient’s unique anatomy. That mission is both professional and personal for CEO Vidmantas Šakalys. After losing a mentor to urinary cancer, he set out to develop 3D-printed kidneys that could save others from the same fate. But before reaching that goal, the company needs a commercial product to fund the long road ahead. That product is VitalHeal — the first-ever bioprinted wound patch for pets. Dogs are the initial target, with human applications slated to follow. Šakalys calls the patch “a first step” towards bioprinted kidneys. “Printing organs for transplantation is a really challenging task,” he tells TNW after a tour of his lab. “It’s 10 or 15 years away from now, and as a commercial entity, we need to have commercially available products earlier. So we start with simpler products and then move into more difficult ones.” Register Now The path may be simpler, but the technology is anything but. Bioprinting goes to the vet VitalHeal is embedded with growth factors that accelerate skin regeneration. Across the patch’s surface, tiny pores about one-fifth the width of a human hair enable air circulation while blocking bacteria. Once applied, VitalHeal seals the wound and maintains constant pressure while the growth factors get to work. According to Vital3D, the patch can reduce healing time from 10–12 weeks to just four to six. Infection risk can drop from 30% to under 10%, vet visits from eight to two or three, and surgery times by half. Current treatments, the startup argues, can be costly, ineffective, and distressing for animals. VitalHeal is designed to provide a safer, faster, and cheaper alternative. Vital3D says the market is big — and the data backs up the claim. Vital3D’s FemtoBrush system promises high-speed and high-precision bioprinting. Credit: Vital3D Commercial prospects The global animal wound care market is projected to grow from $1.4bn (€1.24bn) in 2024 to $2.1bn (€1.87bn) by 2030, fuelled by rising pet ownership and demand for advanced veterinary care. Vital3D forecasts an initial serviceable addressable market (ISAM) of €76.5mn across the EU and US. By 2027-2028, the company aims to sell 100,000 units. Dogs are a logical starting point. Their size, activity levels, and surgeries raise their risk of wounds. Around half of dogs over age 10 are also affected by cancer, further increasing demand for effective wound care. At €300 retail (or €150 wholesale), the patches won’t be cheap. But Vital3D claims they could slash treatment costs for pet owners from €3,000 to €1,500. Production at scale is expected to bring prices down further.  After strong results in rats, trials on dogs will begin this summer in clinics in Lithuania and the UK — Vital3D’s pilot markets. If all goes to plan, a non-degradable patch will launch in Europe next year. The company will then progress to a biodegradable version. From there, the company plans to adapt the tech for humans. The initial focus will be wound care for people with diabetes, 25% of whom suffer from impaired healing. Future versions could support burn victims, injured soldiers, and others in need of advanced skin restoration. Freshly printed fluids in a bio-ink droplet. Credit: Vital3D Vital3D is also exploring other medical frontiers. In partnership with Lithuania’s National Cancer Institute, the startup is building organoids — mini versions of organs — for cancer drug testing. Another project involves bioprinted stents, which are showing promise in early animal trials. But all these efforts serve a bigger mission. “Our final target is to move to organ printing for transplants,” says Šakalys. Bioprinting organs A computer engineer by training, Šakalys has worked with photonic innovations for over 10 years.  At his previous startup, Femtika, he harnessed lasers to produce tiny components for microelectronics, medical devices, and aerospace engineering. He realised they could also enable precise bioprinting.  In 2021, he co-founded Vital3D to advance the concept. The company’s printing system directs light towards a photosensitive bio-ink. The material is hardened and formed into a structure, with living cells and biomaterials moulded into intricate 3D patterns. The shape of the laser beam can be adjusted to replicate complex biological forms — potentially even entire organs. But there are still major scientific hurdles to overcome. One is vascularisation, the formation of blood vessels in intricate networks. Another is the diverse variety of cell types in many organs. Replicating these sophisticated natural structures will be challenging. “First of all, we want to solve the vasculature. Then we will go into the differentiation of cells,” Šakalys says. “Our target is to see if we can print from fewer cells, but try to differentiate them while printing into different types of cells.”  If successful, Vital3D could help ease the global shortage of transplantable organs. Fewer than 10% of patients who need a transplant receive one each year, according to the World Health Organisation. In the US alone, around 90,000 people are waiting for a kidney — a shortfall that’s fuelling a thriving black market. Šakalys believes that could be just the start. He envisions bioprinting not just creating organs, but also advancing a new era of personalised medicine. “It can bring a lot of benefits to society,” he says. “Not just bioprinting for transplants, but also tissue engineering as well.” Want to discover the next big thing in tech? Then take a trip to TNW Conference, where thousands of founders, investors, and corporate innovators will share their ideas. The event takes place on June 19–20 in Amsterdam and tickets are on sale now. Use the code TNWXMEDIA2025 at the checkout to get 30% off. Story by Thomas Macaulay Managing editor Thomas is the managing editor of TNW. He leads our coverage of European tech and oversees our talented team of writers. Away from work, he e (show all) Thomas is the managing editor of TNW. He leads our coverage of European tech and oversees our talented team of writers. Away from work, he enjoys playing chess (badly) and the guitar (even worse). 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The probability of any American having dementia in their lifetime may be far greater than previously thought. For instance, a 2025 study that tracked a large sample of American adults across more than three decades found that their average likelihood of developing dementia between ages 55 to 95 was 42%, and that figure was even higher among women, Black adults and those with genetic risk. Now, a great deal of attention is being paid to how to stave off cognitive decline in the aging American population. But what is often missing from this conversation is the role that chronic stress can play in how well people age from a cognitive standpoint, as well as everybody’s risk for dementia. We are professors at Penn State in the Center for Healthy Aging, with expertise in health psychology and neuropsychology. We study the pathways by which chronic psychological stress influences the risk of dementia and how it influences the ability to stay healthy as people age. Recent research shows that Americans who are currently middle-aged or older report experiencing more frequent stressful events than previous generations. A key driver behind this increase appears to be rising economic and job insecurity, especially in the wake of the 2007-2009 Great Recession and ongoing shifts in the labor market. Many people stay in the workforce longer due to financial necessity, as Americans are living longer and face greater challenges covering basic expenses in later life. Therefore, it may be more important than ever to understand the pathways by which stress influences cognitive aging. Social isolation and stress Although everyone experiences some stress in daily life, some people experience stress that is more intense, persistent or prolonged. It is this relatively chronic stress that is most consistently linked with poorer health. In a recent review paper, our team summarized how chronic stress is a hidden but powerful factor underlying cognitive aging, or the speed at which your cognitive performance slows down with age. It is hard to overstate the impact of stress on your cognitive health as you age. This is in part because your psychological, behavioral and biological responses to everyday stressful events are closely intertwined, and each can amplify and interact with the other. For instance, living alone can be stressful—particularly for older adults—and being isolated makes it more difficult to live a healthy lifestyle, as well as to detect and get help for signs of cognitive decline. Moreover, stressful experiences—and your reactions to them—can make it harder to sleep well and to engage in other healthy behaviors, like getting enough exercise and maintaining a healthy diet. In turn, insufficient sleep and a lack of physical activity can make it harder to cope with stressful experiences. Stress is often missing from dementia prevention efforts A robust body of research highlights the importance of at least 14 different factors that relate to your risk of Alzheimer’s disease, a common and devastating form of dementia and other forms of dementia. Although some of these factors may be outside of your control, such as diabetes or depression, many of these factors involve things that people do, such as physical activity, healthy eating and social engagement. What is less well-recognized is that chronic stress is intimately interwoven with all of these factors that relate to dementia risk. Our work and research by others that we reviewed in our recent paper demonstrate that chronic stress can affect brain function and physiology, influence mood and make it harder to maintain healthy habits. Yet, dementia prevention efforts rarely address stress. Avoiding stressful events and difficult life circumstances is typically not an option. Where and how you live and work plays a major role in how much stress you experience. For example, people with lower incomes, less education or those living in disadvantaged neighborhoods often face more frequent stress and have fewer forms of support—such as nearby clinics, access to healthy food, reliable transportation or safe places to exercise or socialize—to help them manage the challenges of aging As shown in recent work on brain health in rural and underserved communities, these conditions can shape whether people have the chance to stay healthy as they age. Over time, the effects of stress tend to build up, wearing down the body’s systems and shaping long-term emotional and social habits. Lifestyle changes to manage stress and lessen dementia risk The good news is that there are multiple things that can be done to slow or prevent dementia, and our review suggests that these can be enhanced if the role of stress is better understood. Whether you are a young, midlife or an older adult, it is not too early or too late to address the implications of stress on brain health and aging. Here are a few ways you can take direct actions to help manage your level of stress: Follow lifestyle behaviors that can improve healthy aging. These include: following a healthy diet, engaging in physical activity and getting enough sleep. Even small changes in these domains can make a big difference. Prioritize your mental health and well-being to the extent you can. Things as simple as talking about your worries, asking for support from friends and family and going outside regularly can be immensely valuable. If your doctor says that you or someone you care about should follow a new health care regimen, or suggests there are signs of cognitive impairment, ask them what support or advice they have for managing related stress. If you or a loved one feel socially isolated, consider how small shifts could make a difference. For instance, research suggests that adding just one extra interaction a day—even if it’s a text message or a brief phone call—can be helpful, and that even interactions with people you don’t know well, such as at a coffee shop or doctor’s office, can have meaningful benefits. Walkable neighborhoods, lifelong learning A 2025 study identified stress as one of 17 overlapping factors that affect the odds of developing any brain disease, including stroke, late-life depression and dementia. This work suggests that addressing stress and overlapping issues such as loneliness may have additional health benefits as well. However, not all individuals or families are able to make big changes on their own. Research suggests that community-level and workplace interventions can reduce the risk of dementia. For example, safe and walkable neighborhoods and opportunities for social connection and lifelong learning—such as through community classes and events—have the potential to reduce stress and promote brain health. Importantly, researchers have estimated that even a modest delay in disease onset of Alzheimer’s would save hundreds of thousands of dollars for every American affected. Thus, providing incentives to companies who offer stress management resources could ultimately save money as well as help people age more healthfully. In addition, stress related to the stigma around mental health and aging can discourage people from seeking support that would benefit them. Even just thinking about your risk of dementia can be stressful in itself. Things can be done about this, too. For instance, normalizing the use of hearing aids and integrating reports of perceived memory and mental health issues into routine primary care and workplace wellness programs could encourage people to engage with preventive services earlier. Although research on potential biomedical treatments is ongoing and important, there is currently no cure for Alzheimer’s disease. However, if interventions aimed at reducing stress were prioritized in guidelines for dementia prevention, the benefits could be far-reaching, resulting in both delayed disease onset and improved quality of life for millions of people. Jennifer E. Graham-Engeland is a professor of biobehavioral health at Penn State. Martin J. Sliwinski is a professor of human development and family studies at Penn State. This article is republished from The Conversation under a Creative Commons license. Read the original article.

Let’s start with one unambiguous fact: More children are diagnosed with autism today than in the early 1990s. According to a sweeping 2000 analysis by the Centers for Disease Control and Prevention, a range of 2–7 per 1,000, or roughly 0.5 percent of US children, were diagnosed with autism in the 1990s. That figure has risen to 1 in 35 kids, or roughly 3 percent.The apparent rapid increase caught the attention of people like Robert F. Kennedy Jr., who assumed that something had to be changing in the environment to drive it. In 2005, Kennedy, a lawyer and environmental activist at the time, authored an infamous essay in Rolling Stone that primarily placed the blame for the increased prevalence of autism on vaccines. (The article was retracted in 2011 as more studies debunked the vaccine-autism connection.) More recently, he has theorized that a mysterious toxin introduced in the late 1980s must be responsible. Now, as the nation’s top health official leading the Department of Health and Human Services, Kennedy has declared autism an “epidemic.” And, in April, he launched a massive federal effort to find the culprit for the rise in autism rates, calling for researchers to examine a range of suspects: chemicals, molds, vaccines, and perhaps even ultrasounds given to pregnant mothers. “Genes don’t cause epidemics. You need an environmental toxin,” Kennedy said in April when announcing his department’s new autism research project. He argued that too much money had been put into genetic research — “a dead end,” in his words — and his project would be a correction to focus on environmental causes. “That’s where we’re going to find an answer.”But according to many autism scientists I spoke to for this story, Kennedy is looking in exactly the wrong place. Three takeaways from this storyExperts say the increase in US autism rates is mostly explained by the expanding definitions of the condition, as well as more awareness and more screening for it.Scientists have identified hundreds of genes that are associated with autism, building a convincing case that genetics are the most important driver of autism’s development — not, as Health Secretary Robert F. Kennedy Jr. has argued, a single environmental toxin.Researchers fear Kennedy’s fixation on outside toxins could distract from genetic research that has facilitated the development of exciting new therapies that could help those with profound autism.Autism is a complex disorder with a range of manifestations that has long defied simple explanations, and it’s unlikely that we will ever identify a single “cause” of autism.But scientists have learned a lot in the past 50 years, including identifying some of the most important risk factors. They are not, as Kennedy suggests, out in our environment. They are written into our genetics. What appeared to be a massive increase in autism was actually a byproduct of better screening and more awareness. “The way the HHS secretary has been walking about his plans, his goals, he starts out with this basic assumption that nothing worthwhile has been done,” Helen Tager-Flusberg, a psychologist at Boston University who has worked with and studied children with autism for years, said. “Genes play a significant role. We know now that autism runs in families… There is no single underlying factor. Looking for that holy grail is not the best approach.”Doctors who treat children with autism often talk about how they wish they could provide easy answers to the families. The answers being uncovered through genetics research may not be simple per se, but they are answers supported by science.Kennedy is muddying the story, pledging to find a silver-bullet answer where likely none exists. It’s a false promise — one that could cause more anxiety and confusion for the very families Kennedy says he wants to help. Robert F. Kennedy Jr. speaks during a news conference at the Department of Health and Human Services in mid-April to discuss this agency’s efforts to determine the cause of autism. Alex Wong/Getty ImagesThe autism “epidemic” that wasn’tAutism was first described in 1911, and for many decades, researchers and clinicians confused the social challenges and language development difficulties common among those with the condition for a psychological issue. Some child therapists even blamed the condition on bad parenting. But in 1977, a study discovered that identical twins, who share all of their DNA, were much more likely to both be autistic than fraternal twins, who share no more DNA than ordinary siblings. It marked a major breakthrough in autism research, and pushed scientists to begin coalescing around a different theory: There was a biological factor.At the time, this was just a theory — scientists lacked the technology to prove those suspicions at the genetic level. And clinicians were also still trying to work out an even more fundamental question: What exactly was autism? For a long time, the criteria for diagnosing a person with autism was strictly based on speech development. But clinicians were increasingly observing children who could acquire basic language skills but still struggled with social communication — things like misunderstanding nonverbal cues or taking figurative language literally. Psychologists gradually broadened their definition of autism from a strict and narrow focus on language, culminating in a 2013 criteria that included a wide range of social and emotional symptoms with three subtypes — the autism spectrum disorder we’re familiar with today.Along the way, autism had evolved from a niche diagnosis for the severely impaired to something that encompassed far more children. It makes sense then, that as the broad criteria for autism expanded, more and more children would meet it, and autism rates would rise. That’s precisely what happened. And it means that the “epidemic” that Kennedy and other activists have been fixated on is mostly a diagnostic mirage. Historical autism data is spotty and subject to these same historical biases, but if you look at the prevalence of profound autism alone — those who need the highest levels of support — a clearer picture emerges. (There is an ongoing debate in the autism community about whether to use the terminology of “profound autism” or “high support needs” for those who have the most severe form of the condition.) In the ’80s and ’90s, low-support needs individuals would have been less likely to receive an autism diagnosis given the more restrictive criteria and less overall awareness of the disorder, meaning that people with severe autism likely represented most of the roughly 0.5 percent of children diagnosed with autism in the 1990s. (One large analysis from Atlanta examining data from 1996 found that 68 percent of kids ages 3 to 10 diagnosed with autism had an IQ below 70, the typical cutoff for intellectual disability.)By 2025, when about 3 percent of children are being diagnosed with autism, about one in four of those diagnosed are considered to have high-support needs autism, those with most severe manifestation of the condition. That would equal about 0.8 percent of all US children — which would be a fairly marginal increase from autism rates 30 years ago. Or look at it another way: In 2000, as many as 60 percent of the people being diagnosed with autism had an intellectual disability, one of the best indicators of high-support needs autism. In 2022, that percentage was less than 40 percent.As a recently published CDC report on autism prevalence among young children concluded, the increase in autism rates can largely be accounted for by stronger surveillance and more awareness among providers and parents, rather than a novel toxin or some other external factor driving an increase in cases.Other known risk factors — like more people now having babies later in their life, given that parental age is linked to a higher likelihood of autism — are more likely to be a factor than anything Kennedy is pointing at, experts say. “It’s very clear it’s not going to be one environmental toxin,” said Alison Singer, founder of the Autism Science Foundation and parent of a child with profound autism. “If there were a smoking gun, I think they would have found it.”While Kennedy has fixated on vaccines and environmental influences, scientists have gained more precision in mapping human genetics and identifying the biological mechanisms that appear to be a primary cause of autism. And that not only helps us understand why autism develops, but potentially puts long-elusive therapies within reach. It began with an accident in the 1990s. Steven Scherer, now director of the Center for Applied Genomics at the Hospital for Sick Children in Toronto, began his career in the late 1980s trying to identify the gene that caused cystic fibrosis — in collaboration with Francis Collins, who went on to lead the Human Genome Project that successfully sequenced all of the DNA in the human genome in the early 2000s. Scherer and Collins’s teams focused on chromosome 7, identified as a likely target by the primitive genetic research available at the time, a coincidence that would reorient Scherer’s career just a few years later, putting him on the trail of autism’s genetic roots.After four years, the researchers concluded that one gene within chromosome 7 caused cystic fibrosis. Soon after Scherer helped crack the code on cystic fibrosis in the mid-1990s, two parents from California called him: He was the world’s leading expert on chromosome 7, and recent tests had revealed that their children with autism had a problem within that particular chromosome.That very same week, Scherer says, he read the findings of a study by a group at Oxford University, which had looked at the chromosomes of families with two or more kids with autism. They, too, had identified problems within chromosome 7.“So I said, ‘Okay, we’re going to work on autism,’” Scherer told me. He helped coordinate a global research project, uniting his Canadian lab with the Oxford team and groups in the US to run a database that became the Autism Genome Project, still the world’s largest repository of genetic information of people with autism.They had a starting point — one chromosome — but a given chromosome contains hundreds of genes. And humans have, of course, 45 other chromosomes, any of which conceivably might play a role. So over the years, they collected DNA samples from thousands upon thousands of people with autism, sequenced their genes, and then searched for patterns. If the same gene is mutated or missing across a high percentage of autistic people, it goes on the list as potentially associated with the condition. Scientists discovered that autism has not one genetic factor, but many — further evidence that this is a condition of complex origin, in which multiple variables likely play a role in its development, rather than one caused by a single genetic error like sickle-cell anemia.Here is one way to think about how far we have come: Joseph Buxbaum, the director of the Seaver Autism Center for Research and Treatment at the Icahn School of Medicine at Mount Sinai in New York, entered autism genetics research 35 years ago. He recalls scientists being hopeful that they might identify a half dozen or so genes linked to autism.They have now found 500 genes — and Buxbaum told me he believed they might find a thousand before they are through. These genetic factors continue to prove their value in predicting the onset of autism: Scherer pointed to one recent study in which the researchers identified people who all shared a mutation in the SHANK3 gene, one of the first to be associated with autism, but who were otherwise unalike: They were not related and came from different demographic backgrounds. Nevertheless, they had all been diagnosed with autism.Researchers analyze the brain activity of a 14-year-old boy with autism as part of a University of California San Francisco study that involves intensive brain imaging of kids and their parents who have a rare chromosome disruption connected to autism. The study, the Simons Variation in Individuals Project, is a genetics-first approach to studying autism spectrum and related neurodevelopmental disorders. Michael Macor/San Francisco Chronicle via The Associated PressPrecisely how much genetics contributes to the development of autism remains the subject of ongoing study. By analyzing millions of children with autism and their parents for patterns in diagnoses, multiple studies have attributed about 80 percent of a person’s risk of developing autism to their inherited genetic factors. But of course 80 percent is not 100 percent. We don’t yet have the full picture of how or why autism develops. Among identical twins, for example, studies have found that in most cases, if one twin has high-support needs autism, the other does as well, affirming the genetic effect. But there are consistently a small minority of cases — 5 and 10 percent of twin pairs, Scherer told me — in which one twin has relatively low-support needs while the one requires a a high degree of support for their autism.Kennedy is not wholly incorrect to look at environmental factors — researchers theorize that autism may be the result of a complex interaction between a person’s genetics and something they experience in utero. Scientists in autism research are exploring the possible influence when, for example, a person’s mother develops maternal diabetes, high blood sugar that persists throughout pregnancy. And yet even if these other factors do play some role, the researchers I spoke to agree that genetics is, based on what we know now, far and away the most important driver.“We need to figure out how other types of genetics and also environmental factors affect autism’s development,” Scherer said. “There could be environmental changes…involved in some people, but it’s going to be based on their genetics and the pathways that lead them to be susceptible.”While the precise contours of Health Department’s new autism research project is still taking shape, Kennedy has that researchers at the National Institutes of Health will collect data from federal programs such as Medicare and Medicaid and somehow use that information to identify possible environmental exposures that lead to autism. He initially pledged results by September, a timeline that, as outside experts pointed out, may be too fast to allow for a thorough and thoughtful review of the research literature. Kennedy has since backed off on that deadline, promising some initial findings in the fall but with more to come next year.RFK Jr.’s autism commission research risks the accessibility of groundbreaking autism treatmentsIf Kennedy were serious about moving autism science forward, he would be talking more about genetics, not dismissing them. That’s because genetics is where all of the exciting drug development is currently happening.A biotech firm called Jaguar Gene Therapy has received FDA approval to conduct the first clinical trial of a gene therapy for autism, focused on SHANK3. The treatment, developed in part by one of Buxbaum’s colleagues, is a one-time injection that would replace a mutated or missing SHANK3 gene with a functional one. The hope is that the therapy would improve speech and other symptoms among people with high-needs autism who have also been diagnosed with a rare chromosomal deletion disorder called Phelan-McDermid syndrome; many people with this condition also have Autism spectrum disorder.The trial will begin this year with a few infant patients, 2 years old and younger, who have been diagnosed with autism. Jaguar eventually aims to test the therapy on adults over 18 with autism in the future. Patients are supposed to start enrolling this year in the trial, which is focused on first establishing the treatment’s safety; if it proves safe, another round of trials would start to rigorously evaluate its effectiveness.“This is the stuff that three or four years ago sounded like science fiction,” Singer said. “The conversation has really changed from Is this possible? to What are the best methods to do it? And that’s based on genetics.”Researchers at Mount Sinai have also experimented with delivering lithium to patients and seeing if it improves their SHANK3 function. Other gene therapies targeting other genes are in earlier stages of development. Some investigators are experimenting with CRISPR technology, the revolutionary new platform for gene editing, to target the problematic genes that correspond to the onset of autism.But these scientists fear that their work could be slowed by Kennedy’s insistence on hunting for environmental toxins, if federal dollars are instead shifted into his new project. They are already trying to subsist amid deep budget cuts across the many funding streams that support the institutions where they work. “Now we have this massive disruption where instead of doing really key experiments, people are worrying about paying their bills and laying off their staff and things,” Scherer said. “It’s horrible.” For the families of people with high-needs autism, Kennedy’s crusade has stirred conflicting emotions. Alison Singer, the leader of the Autism Science Foundation, is also the parent of a child with profound autism. When I spoke with her, I was struck by the bind that Kennedy’s rhetoric has put people like her and her family in. Singer told me profound autism has not received enough federal support in the past, as more emphasis was placed on individuals who have low support needs included in the expanding definitions of the disorder, and so she appreciates Kennedy giving voice to those families. She believes that he is sincerely empathetic toward their predicament and their feeling that the mainstream discussion about autism has for too long ignored their experiences in favor of patients with lower support needs. But she worries that his obsession with environmental factors will stymie the research that could yield breakthroughs for people like her child.“He feels for those families and genuinely wants to help them,” Singer said. “The problem is he is a data denier. You can’t be so entrenched in your beliefs that you can’t see the data right in front of you. That’s not science.”See More:

Researchers are trying to understand more about the biological and social differences that contribute to later diabetes diagnoses and worse outcomes in women.

The idea of using the body’s own organs as mini bioreactors to grow replacement tissue or even regenerate other organs might sound like something out of a science fiction movie, but it's already becoming reality in cutting-edge labs around the world.A collaboration between Wenzhou Medical University, Nanjing University, and the University of Macau has taken an unexpected turn in regenerative medicine by turning to the spleen, a lymphatic organ typically overshadowed by its more high-profile neighbors. Their findings, recently published in Science Translational Medicine, suggest that the spleen could be key to growing new, functional tissues within the body. And the implications are huge, particularly for diseases like type 1 diabetes.Reinventing the Spleen's PurposeRoughly the size of an avocado and tucked under the left side of the rib cage just above the stomach, the spleen’s usual responsibilities include filtering damaged blood cells and supporting the immune system. It’s often considered non-essential as many people live healthy lives without their spleen, if it was removed after injury or illness.But its seemingly simple structure might be exactly what makes it so powerful. With its sponge-like texture, nutrient-rich environment, and proximity to major blood vessels like those of the liver, the spleen turns out to be an ideal candidate for tissue cultivation.Insulin, Made in the SpleenIn this study, researchers set their sights on type 1 diabetes, a condition in which the immune system destroys insulin-producing pancreatic islet cells. Working with the spleens of primates (macaques), the team engineered microenvironments within the test organs to support human pancreatic islets.“We’re essentially converting the spleen into a high-performance bioreactor,” explained study co-author Lei Dong in a press release. “By enhancing extracellular matrix support, accelerating blood vessel growth, and suppressing immune attacks, we’ve created an ideal niche for transplanted cells to thrive.”After transplantation, the human islet cells matured inside the primates’ spleens and began producing insulin and C-peptide (a byproduct of insulin production) continuously for 28 days. It’s a critical proof of concept — showing that not only can the spleen host new tissue, but it can support it long enough to function effectively.This isn't the team’s first foray into reimagining the spleen’s capabilities. They already reprogrammed mouse spleens to perform liver functions, used gene editing to grow liver tissue without transplanting any cells, and even rebuilt thyroid tissue in animal models.Now, the next frontier is personal: using patient-specific induced pluripotent stem cells (iPSCs) to grow customized organs. “The spleen acts like a living bioreactor embedded in our bodies,” said Dong. “With minimally invasive B-ultrasound-guided delivery, we could one day cultivate custom-made organs on demand.”While the concept is promising, clinical use is still a few years away. However, after undergoing thorough safety testing, this work forces a re-evaluation of regenerative medicine and what we consider “non-essential.” The spleen, long overshadowed and often dismissed, might just be one of the body’s most underutilized resources — an internal bioreactor whose potential is only just starting to be realized.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:Science Advances: Transforming the spleen into a liver-like organ in vivoScience Translational Medicine: Islet transplantation in immunomodulatory nanoparticle–remodeled spleensHaving 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.

French fries at Steak 'n' Shake in Greenwood, Indiana. RFK Jr touted French fries while dining at a ... More Steak 'n' Shake.Missvain, Wikimedia Commons RFK Jr is not just bringing back infectious diseases like measles. Our top health official is working hard to back diet-related diseases like obesity, diabetes, and heart attacks. During his first three months in office, RFK, Jr. has made three big pronouncements about what Americans should eat. The first is important but for the wrong reasons. The second builds on the fallacies of the first. And the third goes against 60 plus years of scientific evidence. 1. Ultra-processed foods (UPFs) are poisoning us Something is poisoning the American people. And we know that the primary culprit is our changing food supply to highly chemical and processed food. RFK Jr, at his Senate Finance Confirmation Hearings, January 29, 2025 French Fries, with 13 Ingredients, would be considered an ultra-processed food.Open Food Facts RFK is not wrong if he is referring to ultra-processed foods (or UPFs). A recent study found that those who ate more UPFs were more likely to show early symptoms of Parkinson’s disease and a review study linked UPFs to higher risk of dying from heart disease, type 2 diabetes, obesity, and mental health outcomes including anxiety and sleeping difficulties. UPFs are made from multiple ingredients including additives like colorants, flavor enhancers, and preservatives. They contain high amounts of sugars, salt, and fats, which makes them hyper-palatable, or simply tasty. And they are cheap, readily available (witness the local gas station convenience store), and handy to eat. Unfortunately for the consumer, a review of studies with a combined population of over 1 million, found that for each 10% increase in UPF consumption, your risk of mortality increases by 10%. Why are UPFs unhealthy? Many people eschew the long list of “chemicals” on the ingredient labels of everything from Wheaties to Fritos. One type of ingredient--food dyes--can have negative health effects and are associated with hyperactivity in children. In fact, MAHA hopes to ban food dyes in UPFs like soft drinks and Fruit Loops. Yet I haven’t heard MAHA alerting us to the high levels of salt, sugar, and saturated fat in UPFs… all things that have been shown over and over to contribute to chronic diseases like high blood pressure, diabetes, and cancer.FI/FOOD Washington Post Studio DATE: 1/7/05 PHOTO: Julia Ewan/TWP Kellogg's Fruit Loops now have 1/3 ... More less sugar and 12 added vitamins and minerals. (Photo by Julia Ewan/The The Washington Post via Getty Images)The Washington Post via Getty Images Dr Kevin Hall, who worked as a nutrition researcher at NIH for 21 years, found that people on an ultra-processed diet consumed about 500 more calories per day, which could explain why UPFs are associated with type 2 diabetes and obesity. But what explains why UPF consumers gobble up more calories? Dr Hall thinks energy density might be the culprit. Simply put, a chocolate chip cookie packs a lot more calories into every bite than a banana. So eating that ultra processed chocolate chip cookie means eating more calories per bite compared to eating fruit and other less processed foods. Not to mention that the sugar, salt and fat taste good… making me want to eat 4 or 5 chocolate chip cookies instead of one banana. Cramer ton, North Carolina, Floyd & Blackie's bakery employee with tray of large M&M chocolate chip ... More cookies. (Photo by: Jeffrey Greenberg/Universal Images Group via Getty Images)Jeffrey Greenberg/Universal Images Group via Getty ImagesUndated: A bunch of ripe yellow Bananas. (Photo by Richard Whiting /Getty Images)Getty Images The preliminary results of Dr Hall’s recent study, which he posted on X, show that the high energy density and the irresistible taste of salt, sugar, and fat explain why people on high UPF diets eat more calories. But don’t expect to see the final results of this important study published anytime soon. Turns out Dr Hall took early retirement at 54 yrs old from his research position at NIH. Why? Because the MAHA administration forced him to withdraw his name from a paper on UPFs that mentioned “health equity”--or the difficulties some groups have accessing healthy food. The administration also took away the money Dr Hall needed to continue his UPF research, censored his media access, and even incorrectly edited his response to a NY Times inquiry. Just as we were on the brink of understanding why UPFs are making us sick, one of the world’s leading UPF scientists is out. Hard to see how lack of scientific information is Making Americans Healthy Again. 2. Eat Beef Tallow instead of Seed OilsWASHINGTON, DC - MARCH 31: Beef tallow french fries photographed for Food in Washington, DC on March ... More 31, 2025. (Photo by Scott Suchman for The Washington Post via Getty Images; food styling by Lisa Cherkasky for The Washington Post via Getty Images)The Washington Post via Getty Images While dining on fries and a double cheeseburger at Steak N Shake with Fox News’s Sean Hannity, Kennedy touted French fries cooked in beef tallow. Robert F. Kennedy Jr 10/21/24 @RobertKennedyJr Did you know that McDonald’s used to use beef tallow to make their fries from 1940 until phasing it out in favor of seed oils in 1990? This switch was made because saturated animal fats were thought to be unhealthy, but we have since discovered that seed oils are one of the driving causes of the obesity epidemic. …Americans should have every right to eat out at a restaurant without being unknowingly poisoned by heavily subsidized seed oils. It’s time to Make Frying Oil Tallow Again 🇺🇸🍔 Close-up of a large frozen ball of beef kidney fat during home rendering of beef tallow, Lafayette, ... More California, March 25, 2025. (Photo by Smith Collection/Gado/Getty Images)Gado via Getty Images To be sure, consuming a lot of seed oils raises health concerns, including that they contain few nutrients, are often highly processed, and some, like soybean oil, might contain unhealthy amounts of omega 6 acids. But, are seed oils worse than saturated animal fats? Seed oils, unlike animal fats, are mostly unsaturated. According to Dr. Christopher Gardner, director of nutrition studies at the Stanford Prevention Research Center who has been studying the role of fat in our diet since 1995, "Every study for decades has shown that when you eat unsaturated fats instead of saturated fats, this lowers the level of LDL cholesterol [bad cholesterol] in your blood. There are actually few associations in nutrition that have this much evidence behind them…To think that seed oils are anywhere near the top of the list of major nutrition concerns in our country is just nuts." And in a 2025 study, participants with the highest intake of butter, which similar to beef tallow is largely saturated animal fat, had a 16% less likely to die. About ⅓ of the deaths were due to cancer, about a third to cardiovascular disease, and a third other causes. The authors conclude: “Substituting butter with plant-based oils may confer substantial benefits for preventing premature deaths. These results support current dietary recommendations to replace animal fats like butter with non hydrogenated vegetable oils that are high in unsaturated fats, especially olive, soy, and canola oil.” (Note that olive oil, while plant-based, is not a seed oil since most of the oil comes from the fleshy part of the olive.) Still life featuring a collection of olive oil bottles, 2011. (Photo by Tom Kelley/Getty Images)Getty Images In short, if you have to choose between seed oils and animal fat, you are probably better off with seed oils, or even better, extra virgin olive oil (EVOO). But, you should avoid consuming too much of any sort of oil or fat, which brings us to the third RFK Jr pronouncement.RFK Jr and West Virginia Governor Morissey. Presidential Candidate Robert F. Kennedy, Jr. ... More Celebrates Hispanic Heritage Month In Los Angeles. Patrick Morrisey speaking at the 2017 CPAC in National Harbor, Maryland.Mario Tama, Getty Images; Gage Skidmore 3. Become a Carni-Bro At a public event to promote MAHA in West Virginia, RFK Jr body shamed Governor Patrick Morrisey for his weight. I’m going to put him on a really rigorous regime. We’re going to put him on a carnivore diet … Raise your hand if you want Governor Morrissey to do a public weigh-in once a month. And then when he’s lost 30 lbs I’m going to come back to this state and we’re going to do a celebration and a public weigh in with him. RFK, Jr. MAHA seems to be at the forefront of the next culture war: dump plant-based foods and become a “carni-bro.” Yet a comprehensive review of studies on foods and obesity concluded: High intakes of whole grains, legumes, nuts, and fruits are associated with a reduced risk of overweight and obesity, while red meat and sugar-sweetened beverages are associated with an increased risk of overweight and obesity. NEW YORK, NEW YORK - JULY 04: Spectators pose for a photo ahead of the 2023 Nathan's Famous Fourth ... More of July International Hot Dog Eating Contest at Coney Island on July 04, 2023 in the Brooklyn borough of New York City. The annual contest, which began in 1972, draws thousands of spectators to Nathan’s Famous located on Surf Avenue. (Photo by Alexi J. Rosenfeld/Getty Images)Getty Images How do UPFs compare to red meat? The only study I found comparing the two found people eating UPFs had an approximately 14% greater chance of dying whereas those who ate red meat had an approximately 8% chance of death over the same time period. (Those eating other types of meats like chicken and pork and fish did not have a greater chance of dying.) But this study was conducted with Seventh Day Adventists, whose meat consumption was way lower than the average American (while their UPF consumption was fairly typical of the US). People in West Virginia, whose governor is in fact rotund, are by far and away the biggest consumer of hotdogs in the US, at 481 hot dogs per person per year. In a recent UK study with a more typical population, every added 70 g of red meat and processed meat (like ham, hotdogs, bacon, and deli meats) per day was associated with a 15% higher risk of coronary heart disease and a 30% higher risk of diabetes. Because red and processed meat consumption is also associated with higher rates of cancer, the World Cancer Research Fund recommends limiting red meat to no more than three portions per week and avoiding processed meat altogether.TOPSHOT - An overweight woman walks at the 61st Montgomery County Agricultural Fair on August 19, ... More 2009 in Gaithersburg, Maryland. At USD 150 billion, the US medical system spends around twice as much treating preventable health conditions caused by obesity than it does on cancer, Health Secretary Kathleen Sebelius said. Two-thirds of US adults and one in five children are overweight or obese, putting them at greater risk of chronic illness like heart disease, cancer, stroke and diabetes, according to reports released recently at the "Weight of the Nation" conference. AFP PHOTO / Tim Sloan (Photo by Tim SLOAN / AFP) (Photo by TIM SLOAN/AFP via Getty Images)AFP via Getty Images Heart Disease: Still the leading killer According to the CDC, heart disease is the leading cause of death in the US, accounting for one in five deaths, or one death every 33 seconds. Heart disease cost the US about $252.2 billion from 2019 to 2020. And if you look at a map of where heart disease is more common, it looks uncannily like a map of MAHA supporters (including in West Virginia). .Heart Disease Death Rates, 2018–2020 for Adults, Ages 35+, by CountyCDC The first items in a list of CDC recommendations for preventing heart disease are all about food: Choose healthy meals and snacks high in fiber and limit saturated and trans fats, salt, and sugar. This sounds like a recipe for avoiding UPFs. But it could also be a recipe for substituting whole grains and fruit and vegetables for red and processed meats, which punch the double whammy of being meat and UPFs. Is RFK, Jr. Making America Healthy Again? Let’s celebrate Kennedy’s move away from UPFs, an important step toward improving Americans’ health. But why does our top health official publicly tout beef tallow, French fries, and double cheeseburgers, when we know that Americans’ consumption of saturated fat and meat lead to obesity, diabetes, cancer, and heart disease? Or has he weighed in on ultra-processed meats, like Slim Jim’s, which with sales at $3 billion last year is America’s fastest growing snack?NEW ORLEANS - OCTOBER 01: Amanda Barrett (L), 18-years-old, watches her mother Eve Barrett peel a ... More mold-covered layer of paint off a wall as the family sees what is left of their home in the Lakeview District October 1, 2005 in New Orleans, Louisiana. The people of New Orleans are still cleaning up over a month after Hurricane Katrina hit the area. (Photo by Ethan Miller/Getty Images)Getty Images It’s hard to understand what is going on in RFK’s brain. He gloms on to a limited number of studies suggesting health risks of eating seed oils, while ignoring saturated fats and even encouraging Americans to eat fast foods. He wants to rout out corruption in the food and pharmaceutical industry, yet uses his position to sell Make America Tallow Again hats and T-shirts. He says he believes climate change poses an existential threat, yet on his second day in office eliminated funding for research on heat waves, indoor mold after flooding, and other NIH climate change and health programs. And in his big May report on children’s health, he ignores the largest causes of death for those under 19--gun violence and accidents. Raise your hand if you want Secretary Kennedy to conduct a public truth-telling once a month.

Hinge Health, a digital physical therapy company, closed its first day of trading on the New York Stock Exchange on Thursday at $37.56, up about 17% over the $32 IPO price it set the previous day. That’s a good first-day result. But even with the pop, Hinge’s public valuation is significantly less than its last private market one. The 11-year-old company’s approximate market capitalization, excluding employee options, was about $3 billion, which is less than half of the $6.2 billion Hinge attained in its October 2021 Series E funding round, which was led by Tiger Global Management. Until recently, companies went to great lengths to avoid down-round IPOs. However, the stigma associated with going public below the last private valuation has lessened significantly if that valuation was during the heady 2020-2021 era. Companies whose IPOs are priced lower than their last private valuation by VCs include Reddit, which debuted last year at about $5.4 billion, roughly half its $10 billion valuation from 2021. Another example is ServiceTitan, whose IPO valued it at about $6.3 billion, below the $7.6 billion valuation it secured in a Series H round two years earlier. Hinge Health’s IPO raised $437 million, with about $237 million in proceeds going directly to the company and the remainder to its existing investors. The company’s largest outside shareholders are Insight Partners, which holds 19% of all stock, and Atomico, which has 15% of all shares. Other venture capital firms that own approximately 8% of Hinge’s shares include 11.2 Capital, Coatue, Tiger Global, and Bessemer Venture Partners, according to the company’s latest S-1 filing. Co-founders Daniel Perez and Gabriel Mecklenburg own 18.9% and 8.2%, respectively. The company aims to reduce musculoskeletal pain with the help of wearable sensors and computer vision technology remotely monitored by a clinical care team of physical therapists, physicians, and board-certified health coaches. Techcrunch event Join us at TechCrunch Sessions: AI Secure your spot for our leading AI industry event with speakers from OpenAI, Anthropic, and Cohere. For a limited time, tickets are just $292 for an entire day of expert talks, workshops, and potent networking. Exhibit at TechCrunch Sessions: AI Secure your spot at TC Sessions: AI and show 1,200+ decision-makers what you’ve built — without the big spend. Available through May 9 or while tables last. Berkeley, CA | June 5 REGISTER NOW Omada Health, another digital health company, filed to go public earlier this month. The 13-year-old startup offers virtual care between doctors’ visits for chronic conditions like diabetes and hypertension, and competes with Hinge Health in the musculoskeletal pain reduction space. Omada’s biggest shareholders include U.S. Venture Partners and Andreessen Horowitz, and was last valued in 2022 at just above $1 billion. Hinge Health’s primary competitor is Sword Health, which was valued at $3 billion about a year ago. At that time, Sword Health’s CEO, Virgilio Bento, told TechCrunch that the company might also pursue an IPO in 2025 if it grows as expected and the macroeconomic environment is favorable.