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Alumnus honors his father, a longtime Marquette professor, with $2 million gift to advance research in biological sciences
President Kimo Ah Yun announced today that a $2 million gift from alumnus Nanda Alapati will advance undergraduate and graduate research in biological sciences.
From PMS to Menopause: Two new clinical studies strengthen the science behind one saffron extract
PMS and menopause represent distinct stages of a woman’s life, with different hormonal patterns and symptoms. Yet both are characterised by significant hormonal fluctuations that can influence interconnected biological pathways involved in emotional well-being, sleep, stress response and overall quality of life
How a photo of a person’s face could help predict whether they’ll survive cancer treatment
A simple selfie could hold surprising clues to your overall health and longevity, especially among people with cancer.
New Richland Lab Could Transform How Scientists Study Microbes and Boost Regional Jobs
The BriefGroundbreaking held Tuesday: PNNL officially began construction on the M2PC lab, a 30,800-square-foot facility funded by the U.S. Department of Energy's Office of Science that will study soil microbes to improve crop productivity and develop new biotechnology applications. The facility will be open to researchers from around the nation and the world.Research timelines could shrink dramatically: The facility's automation and AI capabilities could reduce experiments that currently take six months to just 72 hours, allowing scientists to explore more possibilities faster than ever before.New jobs coming to the Tri-Cities: The project is expected to create positions for automation engineers, AI experts, roboticists, technicians, and skilled craftspeople, with the facility opening in 2029.RICHLAND, Wash. — Pacific Northwest National Laboratory broke ground Tuesday on a first-of-its-kind facility that could accelerate scientific discoveries about the microscopic organisms living in soil—organisms that may hold the key to growing more food and developing new energy technologies.The Microbial Molecular Phenotyping Capability, or M2PC, represents a significant investment in automation and artificial intelligence to speed up research that traditionally takes years to complete. The 30,800-square-foot facility will house more than 100 connected automated instruments designed to study microbes at a pace and scale never before possible.Reshaping Agriculture's FutureThe M2PC facility will not put a new tool directly into a farmer's hands tomorrow morning, but it is actively reshaping the commercial pipeline to solve agriculture's biggest headache with biologicals: inconsistent field performance. For years, PNNL researchers have explored how microbes work and how they might help produce useful materials, advance energy technologies, and address challenges involving critical materials and minerals. But those experiments have been limited by what researchers could accomplish by hand."They can be used to provide nutrients to a plant so that the plant would grow more. So, like increasing your crop productivity, for example," said Douglas Mans, PNNL's Associate Laboratory Director for Integrated Discovery Sciences.PNNL's own research shows soil microbes can help plants access nutrients and withstand drought—benefits that could prove crucial as farmers face growing environmental pressures. The M2PC facility will allow scientists to identify and optimize useful microbes faster than ever before, accelerating the development of biological solutions that actually work consistently in the field.What Makes M2PC UniqueThe Microbial Molecular Phenotyping Capability differs from traditional research labs because it operates as a first-of-its-kind, AI-enabled autonomous laboratory designed to shrink experimental timelines from years down to months or weeks. The M2PC lab will connect more than 100 automated instruments to grow microbes, prepare samples, measure their behavior, and link observations to the molecular processes behind them. Artificial intelligence will help analyze results and guide the next experiments, allowing scientists to explore more questions faster.Deb Gracio, PNNL Director, emphasized the transformative potential during Tuesday's groundbreaking ceremony: "Research that has taken years will become possible in months and hopefully in weeks."That acceleration is already being demonstrated. PNNL's smaller automated lab, called the Anaerobic Microbial Phenotyping Platform or AMP2, completed three experimental cycles in just 72 hours—a process that normally would have taken about six months."That normally would have taken us about six months … and we were able to do that in 72 hours," Mans said.The AMP2 laboratory is not being closed or replaced. Instead, the current 1,800-square-foot laboratory serves as an active prototype and precursor for the much larger M2PC facility. AMP2 will continue operating as a separate lab designed to run anaerobic experiments—those conducted in the absence of oxygen—while M2PC will focus on aerobic research.Broader Applications Beyond AgricultureWhile improving crop productivity is one important application, the M2PC facility is designed to support research into multiple areas critical to national priorities. The lab will advance research into biofuels, manufacturing materials, and energy technologies. It will also help researchers understand how microbes respond to environmental changes and how to design biological systems for biotechnology applications.As a flagship component of the Department of Energy's Genesis Mission, M2PC represents a significant investment in using artificial intelligence and automation to accelerate U.S. scientific discovery. Dorothy Koch, Associate Director of the DOE Office of Science Biological and Environmental Research program, highlighted the facility's importance during the groundbreaking."M2PC will accelerate biological discovery and design," Koch said, noting that the facility is expected to conduct a minimum of 500 strain experiments per week, 100 microbiome experiments per week, and take a million measurements per month.Economic Opportunity for the RegionBeyond the scientific breakthroughs, the M2PC project represents significant economic opportunity for the Tri-Cities region. The facility will require hiring automation engineers, AI experts, technicians skilled in operating robotics, and specialized craftspeople to build and maintain the sophisticated equipment."We're anticipating that type of hiring," Mans said when asked about job creation.PNNL has already begun recruiting talent nationally and internationally for positions related to the smaller AMP2 lab, bringing automation engineers from cities like Boston and San Francisco to work in the region. The M2PC facility is expected to accelerate that trend."This capability won't really exist anywhere else in the world," Mans said, suggesting the facility could become a draw for scientific talent seeking to work on cutting-edge biotechnology research.Timeline and Next StepsThe M2PC facility is expected to open in 2029. Between now and then, construction crews will level and prepare the ground, while the building takes shape. Simultaneously, Ginkgo Bio Works, the automation contractor, will build the facility's automation components off-site so they can be installed as the building is completed.In the interim, PNNL researchers and the broader scientific community will begin planning the first experiments to be conducted in the facility, ensuring research is lined up and ready to begin as soon as the doors open.The groundbreaking ceremony included representatives from the Department of Energy, PNNL leadership, and elected officials at the federal, state, and local levels, underscoring the project's significance to the region and the nation's biotechnology future. News The U.S. Department of Energy Secretary tours Pacific Northwest National Laboratory Dan Hanson, Apple Valley News Now News Beyond DNA: Scientists Explore New Frontiers in Biology Research Dan Hanson, Apple Valley News Now News TRIDEC optimistic that Hanford, PNNL will see funding in national budget Robert Desaulniers News Big picture science: monitoring the Yakima River Basin News PNNL research could shape the future of fighting fentanyl COPYRIGHT 2026 BY APPLE VALLEY NEWS NOW. ALL RIGHTS RESERVED. THIS MATERIAL MAY NOT BE PUBLISHED, BROADCAST, REWRITTEN OR REDISTRIBUTED.
Understanding Intelligence Across Artificial and Biological Systems
Recently I started a new peer-reviewed journal at the crossroads of Artificial Intelligence and Cognition research. The journal, titled "AI and Brain", is published by Scilight Press, a young
Could AI Use a Simple Photo of Your Face to Reveal Clues About Your Health?
A new AI model can estimate biological age and predict cancer survival outcomes using a simple photo of a patient’s face, though more research is needed before doctors will be able to use it to help them decide on treatments.
Lil Jon recalls learning man who raised him isn’t his biological father
The rapper writes about the experience in his new memoir, “I Only Shout So You Can Hear Me.”
Advancing Women's Health to Improve Outcomes in All Phases of Life
The Executive Order (“EO”) makes it federal policy to prioritize turning women’s health research into better clinical care at every life stage, and it directs HHS, through NIH, to set up a new Women’s Health Division within 90 days. In coordination with the NIH Office of Research on Women’s Health, the Division will focus on, among other things, understudied women’s health conditions, greater inclusion of women and girls in clinical trials and grant recipients’ adherence to NIH's policy on sex as a biological variable. The EO also creates a White House Women’s Health Task Force, co-chaired by the Secretary of HHS and the Assistant to the President and Chief of Staff and composed of officials from other departments and agencies.
AI facial health recognition tools help physicians assess age and survival risk to guide personalized treatment
Mass General Brigham researchers trained a new AI foundation model on more than 40 million facial images, and used it to develop AI tools to estimate biological age and directly predict survival risk in patients with cancer
CBIH Announces Expanded Research Strategy at the Intersection of Endocannabinoid Science and Biological Medicine
Houston, Texas--(Newsfile Corp. - October 19, 2026) - Cannabis Bioscience International Holdings, Inc. (OTC Pink: CBIH), a public company trading on the OTC Markets under the ticker symbol CBIH, announced an expansion of its scientific research strategy focused on the intersection of endocannabinoid biology, precision medicine, and the development of intellectual property with potential biomedical applications."We are witnessing a new era in the history of medicine: an era in which human biology
Your age may not tell the whole story about your health, but your blood could
Researchers analyzed plasma metabolites from 18,476 individuals aged 1 to 96 years and developed two metabolomic aging measures to assess biological aging, chronic disease, and mortality risk. Accelerated metabolomic aging was associated with greater risks of chronic disease and death, while a separate mortality-linked measure provided additional information about health status and disease burden beyond conventional clinical assessments.
AI-Generated Images Threaten Citizen Science Data
AI-Generated Images Threaten Citizen Science Data Experts warn AI manipulation risks distorting biological records, citing manipulated mantis and bird photos on platforms like iNaturalist
Plague is stoppable. The next health threat may not be.
The word plague is scary. Centuries ago, the Black Death killed tens of millions of people and changed the course of history. Plague still kills people around the world, and the word still evokes catastrophe. New fears of plague surfaced on October 2, when a lab worker in Irkutsk, Russia, died of pneumonia. Reports suggested that she may have contracted plague through a laboratory exposure. Understandably, people were alarmed. On October 7, the World Health Organization called for the Russian Federation to be transparent about what it knew. WHO issued an update on October 10. Russian authorities told WHO that testing did not identify plague and that investigations found no laboratory release. WHO said confidence in its risk assessment remained limited and that further clinical, epidemiological, and laboratory information was needed. The cause of the woman’s illness remains unknown, and WHO says a laboratory-associated exposure cannot be excluded. As I explained in a recent interview, this incident is very unlikely to lead to a pandemic. Plague is still active, including in the U.S., which sees a handful of cases each year. But it is a disease we can prevent and treat. Plague doesn’t spread readily, and it responds to antibiotics. The standard response—isolate the patient, trace contacts, and administer antibiotics and monitor for symptoms among contacts for seven days—works. We have even planned for antibiotic-resistant plague. At CDC, we developed a playbook for antibiotic-resistant plague and ran exercises on how to find and stop it. CDC guidance anticipates engineered resistance and recommends two different classes of antibiotics if there’s reason to suspect it. There is no evidence that resistance—or even confirmed plague—is involved in this incident. We have thought through how to address plague, but we’re not ready for the next major health threat that emerges from a lab or from animal spillover to humans. What should concern people is how little stands between the world and the next pathogen to get loose. Since peak COVID, epidemic preparedness has fallen off the political agenda, but the risk is greater than ever. More labs handle dangerous pathogens with more ways to make those pathogens deadlier, and more people live and work in close contact with animals. There are actions we can take now: We need better lab safety in every country. The number of labs that work with dangerous pathogens has increased worldwide over two decades, but there’s no enforceable international standard and no inspection regime; the Biological Weapons Convention, fifty years on, still has no verification mechanism. Labs that study dangerous germs need strong safety systems, training, and oversight. We need to reduce spillover events. Three in four emerging human infections start in animals, and there’s a lot we can do to reduce spillover risk, but the world is doing very little of it. Live-animal markets are one place to act. For instance, closing live-bird markets helped control H7N9 influenza in China. Reducing opportunities for people to encounter infected animals can prevent infections before they become outbreaks. In The Formula for Better Health, which is now out in paperback along with the hardcover, Kindle, and audiobook versions, I argue that labs do too many risky experiments with too many dangerous pathogens in too many institutions, and that every experiment should first answer one basic question: Is the likely benefit greater than the risk? Spillover risk can also be reduced: In the book, I discuss how Brazil cut its deforestation rate by 70% from 2004 to 2012 while increasing agricultural production and reducing risky contact between people and forest animals. We need faster detection and response. Delay costs lives. Strong surveillance, good labs, and trained responders can turn a single case into a small cluster of infections instead of an epidemic. Resolve to Save Lives has worked for nearly a decade to help countries find and stop outbreaks faster. The 7-1-7 target, which Resolve to Save Lives developed with partners in Uganda and elsewhere, provides a clear standard: detect within 7 days, notify within 1 day and complete all essential early response actions within 7 days. In Uganda’s Kasese district, for example, a review of a measles outbreak using 7-1-7 identified shortages of accessible funds, fuel, and vehicles that delayed the response. District leaders established funds they could access quickly. When, a few months later, the Crimean-Congo hemorrhagic fever appeared, the district detected it in three days, notified authorities in one, and mounted an effective response in two. Only one case was confirmed, and the patient survived. Because funds were available before the emergency, authorities were prepared and able to act. This kind of preparation can’t wait until the next crisis begins. Plague is an old disease we that know how to stop. The next threat may be harder to recognize, harder to treat, and easier to spread. Safer labs, less risk of spillover, and faster outbreak detection and response need sustained investment now, while we still have time to prevent the next emergency. Share
How lost fibre in sugar impacts health and how we can get it back
The loss of fibre in sugar has led to numerous diseases; the solution may lie in redesigning food and restoring beneficial biological signals.
'I won't trust AI': Readers share mixed reaction to AI tools that calculate people's biological ages
Scientists have developed AI tools to measure a person's true "biological age." Live Science asked readers whether they would be comfortable using these tools.
NASA’s SpaceX CRS-35 Mission to Launch Health Research
NASA experiments focused on human and plant health and drug-resistant organisms will travel to the International Space Station aboard SpaceX’s 35th. This research supports astronaut health during long-duration missions through four investigations from the agency’s Biological and Physical Sciences division.
NASA’s SpaceX CRS-35 Mission to Launch Health Research
NASA experiments focused on human and plant health and drug-resistant organisms will travel to the International Space Station aboard SpaceX’s 35th. This research supports astronaut health during long-duration missions through four investigations from the agency’s Biological and Physical Sciences division.
Characterizing the patient experience: The role of patient‑reported outcomes
Biological endpoints are essential, but on their own, they cannot tell the full story. To truly understand the value of a treatment and care surrounding it, we must also seek to understand how patients and carers experience it. This is where patient-reported outcomes (PROs) and observer‑reported outcomes (reflecting the perspectives of non-clinical caregivers) are becoming more prominent in clinical research.
Flahy uses knowledge graphs to support AI-powered healthcare
Flahy uses knowledge graphs to connect biological and clinical data, supporting personalized decisions in AI-powered healthcare.
Scientists make stunning discovery that could help explain why life exists
Scientists have discovered that the universe's fundamental physical constants may be finely balanced to make life possible. Even tiny changes to these constants could make liquids too thick or too thin for essential biological processes, potentially preventing life as we know it. Surprisingly, these life-friendly conditions existed billions of years before living cells appeared. The findings raise intriguing questions about why the laws of physics seem so well suited to life.
What Killed Europe’s Ancient Wild Cattle? Scientists Find a Disturbing Answer
The fate of Scandinavia’s aurochs warns conservationists worldwide that curbing hunting alone may not save species facing depleted genetic diversity and fragmented habitats. The cattle on today’s farms descend from aurochs, wild animals that once roamed much of Europe, Asia, and northern Africa. They disappeared from Scandinavia thousands of years before the species became extinct
DOE, NIH, and Biohub Partner to Build Foundational Data for Predictive Biological AI Models
WASHINGTON and SAN FRANCISCO, Oct. 9, 2026 — The Department of Energy’s (DOE) Office of Science, the National Institutes of Health (NIH), and Biohub signed a Memorandum of Understanding (MOU) to advance the frontier of Artificial Intelligence (AI) in biology, deepen our understanding of human health and disease, and accelerate breakthroughs in medicine and biotechnology. […]
Democratic Senate candidate responds to anti-trans attacks pushed by Republicans
Dr Annie Andrews voices opposition to ‘biological men ... in women’s sports’ in response to Republican attacks
Would you trust AI to calculate your true 'biological age'?
Scientists have developed various AI tools to measure people's biological ages. Would you use one?
Life Is Asymmetric. The Scientists Who Figured Out Why Won the 2026 Nobel Prize in Chemistry
Henri Kagan and Kensō Soai designed chemical reactions producing only one of the two mirror-image forms of a molecule—an important finding for the synthesis of pharmaceuticals and other biological substances.
Biohub launches $1.8 billion AI biology initiative in major science push
Biohub, Google, Meta and the U.S. government are investing $1.8 billion to build AI-ready biological data for disease research.
Biological aging offers clues to long-term health after Fontan surgery
Our birthdays tell us how long we have lived, but not necessarily how our bodies are aging. Biological age reflects the condition and function of our cells and tissues, shaped by genetics, lifestyle, ...
Scientists discover 57 new marine species lurking in the depths of the South Atlantic
A group of scientists in Argentina discovered dozens of new species in the South Atlantic Ocean, shedding new light on one of the world’s most biologically dynamic regions.
Scientists discover 57 new marine species lurking in the depths of the South Atlantic
A group of scientists in Argentina discovered dozens of new species in the South Atlantic Ocean, shedding new light on one of the world’s most biologically dynamic regions.
Scientists discover 57 new marine species lurking in the depths of the South Atlantic
A group of scientists in Argentina discovered dozens of new species in the South Atlantic Ocean, shedding new light on one of the world’s most biologically dynamic regions.
Scientists discover 57 new marine species lurking in the depths of the South Atlantic
A group of scientists in Argentina discovered dozens of new species in the South Atlantic Ocean, shedding new light on one of the world’s most biologically dynamic regions.
Scientists discover 57 new marine species lurking in the depths of the South Atlantic
A group of scientists in Argentina discovered dozens of new species in the South Atlantic Ocean, shedding new light on one of the world’s most biologically dynamic regions.
Scientists discover 57 new marine species lurking in the depths of the South Atlantic
A group of scientists in Argentina discovered dozens of new species in the South Atlantic Ocean, shedding new light on one of the world’s most biologically dynamic regions.
Could the future “afterlife” be digital rather than spiritual? Science fiction is starting to look plausible
For most of human history, the idea of continuing after death belonged mainly to religion, philosophy and personal belief. Technology is now creating a very different possibility: a version of you that continues speaking, answering questions and interacting with family long after your biological life has ended. This would not be an afterlife in the spiritual sense. Today’s systems cannot preserve consciousness or prove that a person’s mind survives death. What they can increasingly preserve is d
Collaborating with Canadian Scientists on Marine Carbon Dioxide Removal Research
I first met Dr. Helen Gurney-Smith in fall 2024, when Dr. Shannon Meseck and I drove just beyond the U.S.-Canada border to the St. Andrews Biological Station in New Brunswick. We went there to study larval sea scallop respiration when exposed to near-future temperature and pH. This past winter, Dr.
Research Shows These 10 Diets Are Linked to Healthier Aging
A new study found that many different diets can slow biological aging.
Yale School of Medicine On the Science of Childhood Anxiety, Say, Anxiety Disorders Are the Most Common Mental Health Challenges In Youth
Credit: Matt Bradbury October 5, 2026 - By Isabella Backman - Anxiety disorders are the most common mental health challenges in youth. Left untreated, they can disrupt the lives of both children and their families. The good news is that with intervention, most children will overcome these conditions. Across Yale School of Medicine, scientists are working to understand anxiety at every level, from common anxious behaviors to molecular biomarkers in the brain. They are using their findings to develop and disseminate new evidence-based treatments for childhood anxiety. Today, the go-to treatment for childhood anxiety disorders is cognitive behavioral therapy (CBT). This is a form of psychotherapy that teaches children skills for confronting anxious thoughts and helps them practice managing situations that cause anxiety. While it is the gold-standard treatment backed by considerable scientific evidence, up to 50% of children will not see sufficient benefit from CBT alone. Wendy Silverman, PhD, Alfred A. Messer Professor in the Child Study Center, co-directs the Anxiety and Mood Disorders Program alongside Eli Lebowitz, PhD, associate professor in the Child Study Center. One of their main interests is learning how to improve outcomes beyond CBT. “We’re developing cutting-edge, research-based knowledge that can reduce the suffering that anxiety causes children and their families,” says Silverman. Changing parent behavior YSM experts are investigating how to improve CBT outcomes for children by involving the parents. Silverman’s research has uncovered two main components of parent intervention that improve childhood anxiety: not enabling children to completely avoid the things that make them anxious and taking steps to enhance their autonomy. Parents may unintentionally reinforce their child’s anxiety by allowing them to avoid what makes them anxious. They also may unintentionally limit the children’s sense of autonomy by being overly intrusive. “One of the things that we take pride in is that we’ve focused on trying to understand what parents need to do, and to test our ideas and see if changing the parents’ behaviors is enhancing the effects of CBT,” Silverman says. “Our findings thus far suggest that they do." As much as CBT can be helpful, it can also be challenging to get one’s child to do the necessary steps for CBT to work. This is one important reason why Lebowitz created a novel intervention program for parents named Supportive Parenting for Anxious Childhood Emotions (SPACE). Existing intervention programs often teach parents to act as therapists for their child, such as training them on how to practice breathing exercises. “It makes sense, but this doesn’t work very well in practice,” says Lebowitz. “And part of the reason, I think, is that it’s not easy to get your kid to do things, especially if they’re not excited about doing it.” SPACE is unique because it focuses entirely on parent involvement and changing parental behavior—children are not involved in the sessions. For example, parents learn how to use supportive messages that convey confidence that their child can tolerate and manage distress. “It might sound like a parent saying to a child, ‘I get that this is really hard for you, but I know that you can handle it,’” Lebowitz says. The program also works with parents to identify the ways in which they are accommodating anxious behaviors. “We’ll pick one thing that parents are doing that is an accommodation and help them make a detailed plan for how they’re going to change that,” Lebowitz explains. Treating Anxiety in Children and Adolescents Much of the existing research on SPACE has focused on parents of children under age 14. Ongoing studies are now exploring its use with parents of older teens. “Both anxiety and accommodation can interfere with normative developmental shifts during the teen years, including increased autonomy and individuation from parents,” says Rebecca Etkin, PhD, associate research scientist in the Child Study Center. “In this sense, SPACE may be particularly well-suited for anxious teens and their parents. We want to see whether it is effective during this distinct developmental window.” Unfortunately, many families in need of CBT face barriers, including limited availability of services and geographic constraints. One way to improve access is digital interventions. Silverman and her team are developing an evidence-based digitized intervention program for parents that they can access directly from their computer or smart phone. “The work we’re doing will be one of the very few parent interventions that is digitized and importantly tested for effectiveness,” she says. Creating interventions for anxiety-related challenges Silverman and Lebowitz recently received a generous gift to develop and test other interventions that help parents reduce other child anxiety-related behavioral and emotional difficulties, such as restrictive eating and unexplained somatic symptoms. One of these projects in particular focuses on understanding the risks of social media and its potential benefits, including offering a sense of connection. “A lot of research has focused on the idea that social media is harmful and the less of it the better,” says Lebowitz. “But we actually see is that this is not quite right—there are negatives, but there are also positives. So, we’re trying to get a little bit more nuanced of a picture.” The team is working with teens with social anxiety and their parents over an extended period to better understand their social media habits and how their anxiety levels affect engagement with different platforms. The teens will answer questions sent to an app on their phones about mood and social media usage in an effort to capture emotional responses as they unfold. “We hope to develop interventions that can help make the best of social media while protecting against the more problematic effects,” Lebowitz says. The brain’s role in anxiety Researchers are also testing therapies to address anxiety at the neurological and molecular levels. In collaboration with Dylan Gee, PhD, professor of psychology in Yale's Faculty of Arts and Sciences, and Hilary Blumberg, MD, John and Hope Furth Professor of Psychiatric Neuroscience at Yale School of Medicine, Lebowitz and Silverman are using brain imaging to identify changes in a child’s brain before and after parents enroll in SPACE. In one study, children viewed anxiety-inducing images while undergoing magnetic resonance imaging (MRI); the researchers conducted scans with and without the children’s parents nearby. Before SPACE, children’s brains were better able to activate the regulatory circuitry needed to turn off an anxious response when their parents were nearby. But after SPACE, children could activate this circuitry even without the parent around. “As parents work on gradually reducing some of their accommodations, you can see a child get better at regulating their own fear system in the brain,” Lebowitz says. “It’s remarkable.” Research into the molecular underpinnings of anxiety can also inform new childhood anxiety treatments. In a recent study, Lebowitz, Silverman, and Flora Vaccarino, MD, Harris Professor in the Child Study Center, discovered that a protein known as fibroblast growth factor 2 (FGF2) could be protective from the toxic effects of stress. FGF2 levels in children and their parents were linked to the children’s risk of developing anxiety and depression, the study showed. The findings could help explain why some children who are exposed to early life trauma such as poverty or abuse are more prone to developing mental health disorders. And FGF2 could be a target for treatment. “This is very novel because it starts to give a clue to what is the molecular chain that connects those lived experiences to the actual psychological outcomes,” Lebowitz says. New ways to study and treat childhood anxiety Michael Crowley, PhD, associate professor in the Child Study Center, collaborates with Silverman and Lebowitz to study the role that attention plays in development and maintenance of childhood anxiety. There is a large body of research that shows that anxious children, like anxious adults, are prone to focus on threatening stimuli such as angry faces compared with neutral faces. This has led to innovative interventions that involve attention retraining. The idea is that if experts train children to look away from threatening stimuli, it may reduce their anxiety—especially children with social anxiety who are most prone to attend to threats. The researchers have just completed a clinical trial for attention retraining with 10- to 14-year-olds with social anxiety disorders and are currently analyzing the findings. Besides this innovative attention retraining research, as Crowly notes, “I like to design tasks that are engaging to kids,” Crowley says. “My goal is to assess something without the kids knowing what we are assessing.” With this goal in mind, Crowley has created a virtual game, named Boom, to study threat processing in children with anxiety disorders. The game is similar to that of hot potato—the child and three digital players take turns virtually passing a ball to each other’s gloves. At some point, the ball turns into a bomb, and as the bomb lands in each player’s glove, the outline of the glove turns yellow. The goal is to avoid having the bomb go off in your glove. What isn’t obvious is that the game is designed to measure different types of threatening stimuli, both ambiguous and direct. In the game, the direct threat occurs as the bomb is traveling towards your glove. The ambiguous threat is the yellow outlined glove as it is unknown where the bomb will travel next. While children play the game, Crowley’s team measures their brain activity using electroencephalography (EEG). The researchers have discovered that in kids with anxiety, the brain reacts more strongly to ambiguous threats than it does in their peers, but less strongly to direct threats. They believe that the initial abnormally large brain response to not knowing where the bomb is going impairs the brain's ability to properly respond when the threat is actually traveling the child’s way. “The brains of children with anxiety are unable to differentiate between threats you need to do something about and those that are not your problem.” Michael Crowley, PhD, develops innovative games for studying anxiety in children and adolescents.Credit: Matt Bradbury Based on these insights, Crowley hopes to study whether interventions like attention training could restore appropriate threat processing. Crowley’s team is also working on a test called the Balloon Risk Avoidance Task, which evaluates risk-taking and avoidance behaviors. It features a digital balloon that is full of air and about to burst. Kids have six seconds to let air out of the balloon. The more air they let out, the less risk they face that the balloon will pop. But at the same time, the balloon becomes less valuable as it deflates. “The more air you keep in the balloon, the more points you get,” Crowley explains. So far, the researchers have found that when the balloons pop unexpectedly, teens with social anxiety show distinct brain responses. Studying these responses can help psychologists understand the underlying pathways driving the various manifestations of anxiety. The genetics of anxiety When Thomas Fernandez, MD, associate professor in the Child Study Center and of psychiatry, was still in training, there was a lot of excitement about understanding the genetics associated with autism spectrum disorder. Since then, scientists have identified around 250 genes associated with autism. The genetic contribution to anxiety disorders, on the other hand, has historically received less attention. Anxiety is less heritable than autism, but the genetic contribution for anxiety disorders that emerge in childhood may be higher than for anxiety disorders overall. While scientists estimate the heritability of anxiety disorders in general to be around 30% to 50%, some studies suggest higher heritability for certain childhood-onset anxiety presentations. “I saw firsthand how researchers in the field went about finding vulnerability genes for autism,” Fernandez says. “So, we’re using a very similar playbook for childhood anxiety.” “I saw firsthand how researchers in the field went about finding vulnerability genes for autism. So, we’re using a very similar playbook for childhood anxiety.” Thomas Fernandez, MD Associate Professor In the Child Study Center and in Psychiatry Now, Fernandez and Emily Olfson, MD, PhD, assistant professor in the Child Study Center, are studying children and their parents to identify genetic changes that are present in the child but not the parents, known as “de novo mutations.” “All of us have some de novo mutations—maybe about 50 to 100 sprinkled throughout the genome,” Olfson says. “But when they occur within the coding regions of genes, they can be really disruptive.” Previous research shows that people with autism have higher rates of damaging de novo mutations than the general population. In 2022, Olfson, Lebowitz, Silverman, and Fernandez published a study on 68 children and their families that found that children with anxiety had similarly high levels of these mutations. Studying de novo mutations can help point the researchers to where they should be looking for genes associated with anxiety. “The end game is using the genes to steer us toward the right part of biology that we can then target to come up with better treatments,” Fernandez says. Building on those findings, the team is now studying more families to better understand how these de novo mutations, along with other genetic and environmental factors, shape pediatric anxiety disorders. They recently received a National Institutes of Health grant to enroll 750 new families over the next five years. Olfson is the principal investigator, with co-investigators Lebowitz, Fernandez, Silverman, and Shuangge Steven Ma, PhD, department chair and professor of biostatistics at Yale School of Public Health. Neurodevelopment, Risk Genes, and Mental Health Conditions - The Olfson Lab Joel Gelernter, MD, Foundations Fund Professor of Psychiatry, is interested in how different anxiety disorders differ genomically. “We are studying social phobia, panic disorder, and generalized anxiety disorder, working to understand why people differ in their risk to these specific anxiety disorders and evaluating various risk factors,” he says. Gelernter was recently involved in one of the largest studies to date of the genomics underlying anxiety disorder. The study included around 122,000 people with anxiety disorders and around 730,000 without. It found that some genetic differences associated with anxiety were linked to signaling that helps reduce overactivity in the nervous system. Many anxiety medications available today work by targeting this process. “It’s nice when the biology that you get out of a large genome-wide study ratifies things that we already know because that can help increase confidence in further findings from the study,” Gelernter says. Uncovering the neurobiology of psychiatric disorders John Krystal, MD, Robert L. McNeil, Jr. Professor of Translational Research and chair of the Department of Psychiatry, is interested in the neurobiology of psychiatric disorders, including post-traumatic stress disorder (PTSD), of which anxiety is a major symptom. In the late 1980s, Krystal’s team discovered that the drug yohimbine activated symptoms in patients with PTSD. “This was the first time we could link a specific biological mechanism to the symptoms of PTSD,” Krystal says. At the time, he adds, this finding was highly controversial. “A lot of people felt that PTSD was a purely psychological syndrome that didn’t have an underlying biology.” Since then, Krystal has dived deep into understanding the neurobiology of PTSD to learn how to better treat it. His team is evaluating the use of ketamine and psychedelics. These would be among the first treatments to be developed specifically for PTSD. They may also be applicable for other disorders including anxiety disorders, Krystal adds. An important gap in PTSD treatment is the absence of biological tests that inform how to best help patients manage their PTSD symptoms. A doctor doesn’t diagnose cancer based on how they feel. Rather, they use tests of the biology of the cancer to determine the best course of treatment. “And we can’t do that in any psychiatric disorder other than Alzheimer’s disease,” Krystal says. “But now we are building a foundation for this approach to the treatment of anxiety disorders for the first time.” Source: Yale School of Medicine
Rethinking discovery: how powerful screening tools are redefining the search for new medicines
In medicine discovery, identifying the right biological target has always been a critical and complex step. Today, the rise of powerful screening tools is fundamentally reshaping this process, creating a step-change in how we move from scientific hypotheses to transformative medicines. Advances in high-throughput screening, genomics and AI-driven analytics are enabling scientists to interrogate disease biology at unprecedented scale, bringing forward opportunities that were previously beyond reach.
MedX Health Appoints Monaderm as a Representative for SkinSecure™ Across Europe for Beauty and Aesthetics Research
MISSISSAUGA, Ontario, October 05, 2026--MedX Health Corp. (TSXV: MDX), a data-driven skin health analytics company, today announced the appointment of Monaderm, the Monaco-based skin measurement specialist, as a key European sales agent for SkinSecure™, expanding the commercial reach of its non-invasive, objective biological skin measurement technology, which maps collagen, melanin and hemoglobin non-invasively in living skin in a single 30-second capture, across the European cosmetics and skin
Scientists discover 57 new marine species lurking in the depths of the South Atlantic
A group of scientists in Argentina discovered dozens of new species in the South Atlantic Ocean, shedding new light on one of the world’s most biologically dynamic regions.
AI’s Real Gift to Science
Advanced models can help researchers sort through mountains of biological data.
Proposition 134
Colorado voters will decide whether to designate athletic teams and sports from elementary all the way to college as male-only or female-only and require schools to ensure athletes are assigned to teams based on their biological sex.
Scientists Found a “Third State” Of Being Between Life and Death
Frog and human cells can reorganize after removal from their host, raising open questions about biological death and potential uses in regenerative medicine.
How sex chromosomes influence lifelong health beyond determining biological sex
A new review published in Science brings together growing evidence that the X and Y chromosomes do more than determine biological sex. They also shape how cells function, age and respond to disease.
This AI Scientist Can Design Experiments, Run Them in the Lab and Learn From the Results
The system can propose biological questions, design experiments and send robots to test them.
Research station will explore how Bloedel's nature affects our health
The University of Washington Center for Nature and Health is set to begin installation of a biological research station aimed to explore the connection between human health and physiological response to nature.
Here’s the newest faculty members of LSU’s College of Science
Three assistant professors have joined LSU’s College of Science this semester. Carl Procko, Ping Wang and Keegan Kirk brought their research expertise, including plant responses, adaptations and numerical analysis. Procko, assistant professor of biological sciences, works with the adaptations of plants in relation to their environments. He mentioned his interest in unusual plants, including carnivorous...
Proposition 134: Colorado voters asked to ban transgender kids from gendered sports
The measure would require that kids from kindergarten through college play on school sports teams that match their biological sex, not their preferred gender
Microsoft Pushes AI Deeper Into Scientific Discovery With Quine
AI can already help scientists make sense of large amounts of data. Microsoft Research is now testing whether it can play a bigger role in deciding what scientists should investigate next. Its new experimental system, Quine, brings together biological data, computational models and research tools to make predictions that researchers can put to the test […]
Discovering a Design Argument Based on Biological Information
Charles Thaxton, along with Walter Bradley and Roger Olsen, wrote what arguably was the first official book of the intelligent design movement.
This simple diet change could slow your biological age in just four weeks, study suggests
A simple change to the balance of your diet could reduce your biological age in just four weeks, according to a new study
An AI model has found a new ‘CRISPR-like’ biological system. Here’s what it means for science
After coding, mathematics and chatbots, AI companies are setting their sights on the messy world of biology.
Hands-on science can be cool
After spending many long days conducting experiments to find a new way to combat bacterial infections in crops, Misha Hegde and Mia Soleil Maurer have been rewarded with international recognition and access to top research facilities. But these are not typical scientists. They are 16-year-old German high school students.“Our supervisor told us that in order to start a project, you need to begin with either a question or a problem,” says Misha, adding that she and Mia had read about antibiotic resistance in certain plants being treated for bacterial infections. “We found out that antibiotics overuse is very common in agriculture,” explains Mia. “Our aim was to create an alternative to antibiotics and to try to raise awareness of the problem of overusing antibiotics.”Their subsequent research has focused on harnessing bacteriophages, the natural predators of bacteria, to eliminate pathogens threatening food crops treated with antibiotics. At the Schuldorf Bergstraße Jugend forscht MakerLab in Seeheim-Jugenheim, located in the German state of Hesse, they discovered a novel phage that infects the Rhizobium rhizogenes bacterium, which causes the hairy root disease that can reduce yields of tomatoes, carrots, soya beans and other food staples.The students believe their method could curb antibiotic use, while protecting plants from infections without disturbing the natural soil microbiome. “The application of phages is host-specific, so they would only kill the targeted pathogen or disease-causing bacteria,” explains Mia. It may also offer environmental benefits, since applying antibiotics can contaminate groundwater.Getting to this point has not been easy. The childhood friends admit to feeling frustrated when their trials did not yield the expected results. “We spent six months on our first experiment, just doing the same thing over and over and over again, to the point where we thought, is it even worth it? Why are we doing this?” Misha says. “You just need to be brave enough to take that first step and keep going.”The benefits of inquiry-based learningTheir determination has paid off. In 2025, the pair won first prize in biology at Jugend forscht, Germany’s national competition for young people interested in science, technology, engineering and mathematics. They were also among the winners of the German Research Foundation Europa-Preis, which is awarded to selected national winners at Jugend forscht, and took third place in the 2025 European Union Contest for Young Scientists.The Jugend forscht Foundation opens doors for young people to connect with scientists as well as industry professionals. Jessica Bönsch, executive director of the Foundation, sees Misha and Mia as prime examples of how young people can develop a deeper understanding of science through their own research projects. “The experience of working on your own research question is very important,” she explains, adding that “inquiry-based learning engages with real-life problems in a way that can be more motivating than traditional classroom teaching.”The Jugend forscht Foundation offers financial support through sponsor pools in Germany’s federal states. Some projects are developed in cooperation with student research centres, university labs or informal collaborative learning areas called makerspaces. Other activities start as hands-on “garage projects” and can grow within the Jugend forscht network and infrastructure.The Jugend forscht Foundation is also a partner of Science Comes to Town, an EU initiative to strengthen public awareness about science and create bridges between researchers and communities. The EU-financed project involves universities, research institutions and other stakeholders in three host cities — Brest (France), Kiel (Germany) and Split (Croatia).“It's so important for people not to live in a bubble, because I think science can be very scary if you misunderstand it,” Mia says of SCTT. The initiative’s aim of raising awareness about science is “absolutely amazing,” Misha adds. “I think it's the best way to kind of make science digestible for the public. In a world where misinformation in science is getting more radical, more dangerous, becoming more of a threat to the trust in scientific infrastructure and foundations, we need such programmes.”Misha and Mia also believe that SCTT can help break down gender stereotypes in science by encouraging young women to study and pursue careers in scientific fields. Both students have benefited from female mentors and encouragement they had when they were much younger. Mia’s love of science began with a class trip to a lab, while Misha — with a smile on her face — says she wanted to study history until “a teacher kind of coerced me into joining a school science club.”Recognition beyond EuropeIn May, Misha and Mia were among the finalists at the Regeneron International Science and Engineering Fair held in Phoenix, Arizona, and involving nearly 1,700 pre-university students from over 60 countries. “It was very crazy because there were so many people and so many teenagers interested in science,” Mia recalls. The event was also challenging. “It was eight hours of continuously presenting your project,” adds Misha.Attending the fair was a chance for the young women to see first-hand the value of international collaboration as well as how research cultures differ. “America is a bit more willing to take risks, and I think that's something we can learn about here in Europe,” Misha explains. However, she continues, “I think Europe has the talent, has the innovation and has the resources” to be competitive.Misha and Mia plan to continue their phage experiments in the new school year, inspired by the project’s hands-on nature and the support they receive from their supervisors. They have also attracted the interest of professional scientists and received invitations to leading research facilities, including the Centre for Synthetic Microbiology, jointly run by the University of Marburg and the Max Planck Institute for Terrestrial Microbiology in Germany. “It is so cool that we can do something to try to move the world in our school and at this age,” Mia says.After completing secondary school, Mia plans to study microbiology and pursue a career in medical research, focusing on Ebola and other infectious diseases. “This has been my dream for so long,” she says. Her friend Misha is interested in biological research with a focus on medicine. “I've gotten addicted to the process of going to the lab, planning out experiments, then failing, trying again,” Misha says. “I think there's just so much to be discovered, so much to be done.”The students' names and photos were published with the permission of their parents.Science|Business, which connects policymakers, academics and industry through its news reporting, analysis and events, is an SCTT partner.
Troy Clarkson To Deliver Falmouth Forum Season Opener
Author and columnist Troy Clarkson will present the first talk of the Marine Biological Laboratory’s 2026-27 Falmouth Forum series.
Could Proteins Become the Next Tool in Forensic Science?
Researchers reviewed how forensic proteomics uses mass spectrometry to analyze proteins in hair, bone, fingerprints, and body fluids. The approach can recover biological and contextual information when DNA is limited.
Merck Life Science Expands Bengaluru Manufacturing with €13 Million Investment
Merck Life Science is expanding its manufacturing capabilities in Bengaluru with an investment of approximately €13 million, strengthening the company’s ability to supply critical materials to customers across India and the wider Asia-Pacific region. The expansion at Merck Life Science’s Jigani site in Bengaluru will introduce biological buffer manufacturing alongside the facility’s established chemistry capabilities. The investment is designed to enable faster and more reliable access to critical materials used by customers across research, diagnostics, biotechnology and biopharmaceutical manufacturing. The development further advances Merck Life Science’s “in-region, for-region” approach, under which the company is expanding manufacturing capabilities closer to the markets and customers it serves. By adding biological buffer production in India, the Jigani expansion will broaden the site’s manufacturing capabilities while strengthening Merck Life Science’s regional supply infrastructure for the rapidly developing life sciences sector across India and Asia-Pacific. The company said the expansion reflects both the contribution of its teams and its collaboration with government and industry stakeholders. Merck Life Science acknowledged the support of India’s Department for Promotion of Industry and Internal Trade (DPIIT), the German Embassy New Delhi, and Invest India in helping strengthen life science manufacturing capabilities in the region. The investment comes as India continues to expand its role across pharmaceutical, biotechnology, diagnostics and biomanufacturing value chains, increasing demand for dependable regional access to materials supporting research and manufacturing operations. The Bengaluru expansion reinforces Merck Life Science’s focus on building manufacturing capacity within Asia-Pacific and supporting customers through a more regionalised supply network.
Justice Kagan rejects surrogate’s request for intervention in custody dispute
The baby’s biological parents said that high court intervention would only cause chaos and confusion.
Justice Kagan rejects surrogate’s request for intervention in custody dispute
The baby’s biological parents said that high court intervention would only cause chaos and confusion.
Biological sciences professor earns national award for advancing diversity and inclusion in entomology
Dr. Chelsea Cook, assistant professor of biological sciences in Marquette University's Klingler College of Arts and Sciences, has received the 2026 Distinguished Achievement Award in the Promotion of Diversity and Inclusion in the Field of Entomology from the Entomological Society of America.
Supreme Court Order Gives Parents Custody of Baby in Surrogacy Fight
A surrogate refused to have an abortion after the fetus was diagnosed with a serious heart problem. She asked the justices to block a court order giving custody to the biological parents.
From paleo to intermittent fasting: are any diets actually good for us?
As diet trends proliferate on social media, it can be hard to work out which are backed by science and which should be ignored. From paleo to keto, raw food to intermittent fasting, each attracts a tribe of ardent followers. Now Daniel Lieberman, professor of biological sciences at Harvard University, has written a book to try to cut through the noise. In Fed Up, he uses his background as an evolutionary anthropologist to scrutinise the evidence, turning himself into a guinea pig in the process and trying various diets. In this podcast, he tells Ian Sample which one has remained part of his routine
Virtual SUD support platform Nosis launches to address lifestyle, diet needs
Nosis, a platform supporting substance use disorder (SUD) recovery, is launching from stealth in all 50 states. | The virtual startup leverages labs with health coaches and dietitians to address the biological and metabolic health needs of individuals in recovery.
For the first time, scientists watch sound jump between quantum states
Stanford researchers have recorded the first real-time quantum jumps of sound, watching single phonons abruptly vanish from one energy state to another. The breakthrough could open new paths for quantum computing, error correction, highly sensitive biological sensors, and next-generation sound-based devices.
Is 50 the new 60?
Subscribe TL;DR: Younger generations are showing signs of worse health compared to earlier-born cohorts at the same age This backward “drift” is showing up both in mortality risk and chronic disease Worsening trends in obesity and diabetes are the most consistent signals Taking the long view, we’ve made astonishing gains in health and life expectancy in the last century. Global average life expectancy has more than doubled from 32 years in 1900 to 73 years in 2024. (But don’t forget, there were still old people when life expectancy was 32). As people lived longer, they also generally lived healthier along the way. It turns out that avoiding things that can kill you early, like malnutrition and lots of childhood infections, also keeps you healthier later in life. In a classic 2004 paper, Finch and Crimmins proposed that cohorts of children who benefited from fewer early life infections had less lifetime exposure to inflammation and cardiovascular disease later in life, accelerating mortality improvements at older ages. Poor nutrition in the womb has also been linked to a higher risk of later chronic disease. The upshot is that improvements in childhood health can pay dividends many decades later. The combination of better living conditions (nutrition, sanitation) and medical advances (antibiotics, vaccines, blood pressure meds, etc) meant that people’s healthy lifespan generally expanded, even as they lived longer. Aging researchers call this best-case scenario “compression of morbidity”—meaning we delay the onset of disease and disability even faster than the years of life we are adding. During my 20+ year research career, we could generally bank on the idea that younger generations would not only live longer but also keep getting healthier along the way. “60 is the new 50” as they say… Enter “Generational Health Drift” Sadly, this expectation of steady progress may be changing. You’ve probably heard that US life expectancy gains have slowed to a crawl in the past couple of decades. Mortality improvements are also slowing (though less dramatically) in many other high-income countries (you can read more about that in a review paper I wrote here). Mortality is a very blunt health measure, but it is often a good barometer for the broader population health trends happening underneath. And we are now seeing that younger generations may be in worse health at similar ages compared to earlier born cohorts. My collaborator Prof. George Ploubidis at University College London coined this worsening health in more recently born cohorts “generational health drift.” “Generational health drift” is bad news on multiple fronts. Most obviously, we don’t want our health progress to go backward. But the timing is also bad, since our populations are aging. In demographic terms, “population aging” means that the proportion of the population at older ages (i.e >65 years) is increasing. Fun demography fact: Current population aging is not due to the recent declines in the birth rates making the news, but declines in fertility decades ago, after the “baby boom.” As baby boomers reach older ages, the smaller cohorts behind them mean the percentage of older adults will increase. For example, the share of the population age 65 and older in the US increased from 12.4% in 2004 to 18.0% in 2024. This story of population aging was written long ago. Many worry that population aging will put pressure on health care and pension systems. But if people reach older ages in better health than in years past, those fiscal pressures would be less dire than projected. Healthy older people can also continue to contribute to society in many valuable ways, including paid work, caregiving, community service….even high political office 🤷. On the flip side, if younger generations reach retirement age in worse health and with more disabling conditions, this could magnify the societal challenge of population aging. Evidence for worsening generational health A recent paper that I LOVED in the Proceedings of the National Academy of Sciences by Dr. Leah Abrams and colleagues examined which birth cohorts (aka generations) were behind worsening US mortality. Behold the Lexis diagram (cue swooning demographers). Calendar time is on the x-axis, age on the y-axis. Birth cohorts can be followed over time as they age on the diagonal lines moving up and to the right. This figure plots the year-on-year % change in all-cause mortality at a given age. Green shading indicates mortality improvements over time, white is stagnation, and gray shading indicates worsening mortality. Following the diagonal line for those born in 1950, you can see a noticeable shift from green to gray that follows this cohort for most of their lives. This gray shading shows generally worsening mortality for the 1950 to 1959 birth cohorts compared to their predecessors across all ages. Concerningly for my GenX and elder millennial peeps, there was also a deterioration in mortality for birth cohorts born in the 1970s and 1980s, visible as dark gray areas at ages 30 to 45 during the 2010s. While some of these mortality changes reflect specific shocks such as the opioid epidemic, most deaths still occur from major causes of death such as cardiovascular disease and cancer. For cancer, the gray in the top left corner of the figure below reflects the legacies of smoking for older cohorts, followed by a period of green with improvements in cancer mortality as smoking rates declined. But the white/gray shading in the bottom right corner highlights a stagnation and reversal of the cancer trends, with cohorts born around 1970 to 1985 experiencing worsening cancer mortality. This deterioration was most noticeable for colon cancer mortality, possibly linked to obesity or dietary factors. Not just dying more, but less healthy along the way. A recent paper by Dr. Laura Gimeno of University College London (of which I am a co-author), found evidence that more recently born cohorts in Great Britain have stagnating or worsening health. A stylized picture of what“generational health drift” might look like: The review paper found: Rates of childhood overweight and obesity were highest among Gen Z. Rates of diabetes in the 40s almost doubled from 3.1% among the Baby Boomers to 5.9% in Generation X. Gen Z reported higher rates of poor mental health in adolescence compared to earlier-born groups. These UK results are consistent with studies showing worsening health across generations in the US as well. A 2021 US study found that more recently born cohorts had worse biological markers (like blood pressure and blood sugar) than earlier generations at the same age. A separate 2022 study of Americans aged 50 and over found that more recently born generations had a higher number of chronic diseases, with younger age of disease onset. A 2024 Lancet paper found that in the US, women born in 1945 had 33% obesity prevalence at age 50, rising to 48.2% for women born in 1970 turning 50. So what’s going on, and can we turn it around? We don’t have a definitive answer for what’s causing the deteriorating health of younger cohorts, but circumstantial evidence points to worsening trends in obesity and diabetes in both the US and UK. Remember that cohort trends reflect lagged effects of early environments, and younger generations have faced both earlier onset and more severe obesity across their lifetimes. Despite these very concerning trends, the future is not set in stone. We’ve reversed poor generational health trends before: drops in smoking are a major reason cancer and heart disease deaths fell so dramatically in recent decades. GLP-1 drugs may finally turn the tide against rising rates of obesity and diabetes, though it is still early days. But things could also get worse…for example from a return to higher levels of childhood infectious diseases that can have a lasting impact on health. See for example: [ ](https://jenndowd.substack.com/p/dont-you-forget-about-measles-the) [ Don’t You Forget About Me(asles): The Virus That Erases Immune Memory ](https://jenndowd.substack.com/p/dont-you-forget-about-measles-the) Jenn Dowd, PhD · March 24, 2025 [ Read full story ](https://jenndowd.substack.com/p/dont-you-forget-about-measles-the) Even as an optimist, emerging data on the “generational health drift” has my full attention. For most of my research career, we took it for granted that each generation would be healthier than the last. But if present trends continue, **50 could be the new 60….**and Gen Z celebrities will soon look older than Paul Rudd :). Stay well, Jenn Share the Health! If you found this post useful, please share it with a friend. Share
Polystyrene nanoplastics may threaten reproductive health and offspring development
Plastic pollution is increasingly being recognized as more than an environmental problem. Tiny plastic particles can enter living organisms, circulate through biological systems, and potentially reach reproductive tissues.
Business Group on Health taps BioRadar to boost workforce readiness for emerging threats
Biological threat intelligence is increasingly becoming a workforce and business issue, not just a public health concern. | Biological threat intelligence is increasingly becoming a workforce and business issue, not just a public health concern. Emerging threats—infectious disease outbreaks, pandemics and potential bioterrorism events—can cause workforce and operational disruptions.
Business Group on Health taps BioRadar to boost workforce readiness for emerging threats
Biological threat intelligence is increasingly becoming a workforce and business issue, not just a public health concern. | Biological threat intelligence is increasingly becoming a workforce and business issue, not just a public health concern. Emerging threats—infectious disease outbreaks, pandemics and potential bioterrorism events—can cause workforce and operational disruptions.
The 5 daily habits that science says can slow biological aging
Five daily habits that research links to slower biological aging, covering exercise, sleep quality, diet, stress management and social connection
Transformative Biological and Environmental Frontiers: Synthesizing the 2026 Tang Prize Science Laureates
The Tang Prize in Sustainable Development and Biopharmaceutical Science honors pivotal scientific advances that improve global health, restore damaged ecosystems, and deliver transformative medical treatments. The 2026 science laureates, Professor Susan Solomon for Sustainable Development, along with Dr. Steven A. Rosenberg, Dr. Michel Sadelain, and Dr. Carl H. June for Biopharmaceutical Science, demonstrate how disciplined
DNA Has a Four-Letter Alphabet. Scientists Just Expanded It to Eight
Researchers showed how a natural bacterial enzyme can accurately transcribe DNA containing four extra genetic letters. Life uses a four-letter DNA alphabet, but could its genetic machinery read a larger one? Researchers at the University of California San Diego have shown that RNA polymerase, the enzyme that copies DNA instructions into RNA, can accurately transcribe
The Big Holes in Wearable Heart Rate Variability And Readiness Scores
On September 9th, Apple announced it was revamping its Apple Watch Health Sensing System, rolling out a Readiness score (0 to 10), and increasing the frequency of heart rate variability (HRV) outputs 24-fold. This can be viewed as upping its competition with various other consumer wearable sensors. These “readiness scores” as a composite of multiple metrics, with heart rate variability (HRV) being front and center for most. The majority of Americans are now using wearable sensors, which equates to well over 100 million adults. HRV and Readiness scores are increasingly being marketed as a measurement of autonomic nervous system health, a digital marker for future disease, a clock for biological age, and a holistic metric to promote healthspan and even longevity. (Apple also introduced a new longevity tab and “Health Age”.) None of this has been proven. In this edition of Ground Truths I am going to review what we know about heart rate variability and readiness scores. Heart Rate Variability HRV is the variation in normal heart cycle timing. The variability of the heart rate, the barely perceptible millisecond changes in time between consecutive heart beats (see R-R intervals in the Figure below, left panel), is due to interplay between the sympathetic and parasympathetic (vagal nerve) inputs. Distinct from heart rate, individuals with the same heart rate can have very different HRVs. It is a rough reflection of the autonomic nervous system (ANS) activity, inadequate to say whether a person’s ANS function is abnormal. For more than three decades, heart rate variability (HRV) has been measured and several studies have found an association of low HRV and clinical outcomes, particularly a link with higher all-cause and cardiovascular mortality. There have also been less well established links of low HRV to risk of early cognitive impairment, dementia, mental illness, Type 2 diabetes and substance abuse. An important reminder is that HRV is a surrogate marker without any established cause-and-effect relationship. If you increase your HRV, that doesn’t mean it will improve health outcomes. In fact, there is no hard evidence for that. All that work linking to health outcomes was done with electrocardiogram (ECG) derived HRV. Now, in the era of consumer wearables, this is getting assessed differently, by optical pulse (yes, the lights you see) plethysmography (PPG) or what is called pulse rate variability (PRV). They are not the same, as shown below (right panel) and only concordant when the delay between the ECG and pulse is kept constant, which basically means at rest. I should mention there’s also what I will call MPV, a mattress mechanical movement sensor, a derived heart rate variability, that companies like Eight Sleep use, even further away from directly measuring HRV. HRV has not one uniform measurement but many different types of quantification, such as RMSSD, the magnitude of difference between successive R-R intervals of normal sinus beats (N-N) or SDNN, the standard deviation of NN intervals, both in milliseconds. SDNN is one of the so-called frequency domain HRVs (others are LF, HF, LF/HF). Different wearable sensors use different metics; Apple has relied on SDNN and nearly all of the others use RMSSD, which is generally considered the more accurate metric. There’s also the different length of time measured, such as for a matter of minutes, all day, or an overnight’s sleep. Short measurements are especially problematic since they don’t capture enough of respiratory modulation and other factors that influence HRV. Share Ground Truths How well does HRV correlate with PRV? There are very limited studies, especially independently done. One that is commonly cited was conducted by Air Force researchers in only 13 healthy adults assessing Oura ring 3 and 4, Whoop 4.0, and Garmin Fenix 6 and showed a correlation coefficient of 0.88 to 0.97 and a mean absolute percentage error from 6 to 10%. The correlation is not a perfect 1.0, but there’s at least a fairly high level of correlation. HRV is supposed to increase during the night due to takeover of the parasympathetic nervous system, and higher during deep sleep. A recent example of my 1 week, all day “HRV,” and one during sleep is shown below. As you can see, the N of 1 data are inconsistent for the same days from different sensors (Oura, AppleWatch, Fitbit Air, and Eight Sleep) by patterns, absolute numbers, and comparison with prior days and weeks. The largest study in over 8 million Fitbit users (the old version, not Google Fitbit Air, introduced in May 2026) gives you a sense of the effect of age, sex, and the 2 different main HRV (here PRV) metrics, with RMSSD on the left and SDRR (=SDNN) on the right below. That study, from data collected in 2018, is a major outlier, since all the more recent ones are tiny with respect to sample size. Many of the companies have not had independent evaluation of their HRV, such as Eight Sleep, but have published a low standard error on their website. There are some other published studies on the correlation between HRV and PRV, but they are all small and only in healthy adults. A scoping review emphasized the lack of study in underrepresented individuals, including the aged, people of color (which affects the PPG signal), and individuals who are underweight or obese. Add the typical adult age 60 plus with one or more chronic diseases. For example, one study in over 900 adults found poor correlation of HRV and PRV, non-uniformly underestimated across many chronic diseases (cardiovascular, endocrine, neurological, respiratory, and others), concluding PRV is “an invalid surrogate for HRV.” A recent systematic review of 43 studies comparing HRV and PRV found reasonable pooled absolute standardized error (HRV as gold standard) but only 10 of the studies provided quantitative synthesis in ideal conditions. Their main conclusion was similarly cautious: “PPG-derived HRV [PRV] should not be regarded as universally interchangeable with ECG-derived HRV across all devices, populations, and recording contexts.” Factors Affecting HRV and PRV That gets me to the long list of factors that affect HRV (and PRV) besides the device, the type of measurement (RMSSD, SDNN or others), the person’s signal, the sensor site, the duration of data capture, if weighting by sleep stage is used, how artifact is processed and corrected. And this list is not complete!: Oura puts out data from their community of users (who input data) on what affects their overnight HRV. The factors currently provided are: no alcohol (increase 8%), melatonin (increase 2%, float tank (increase 2%), wine (decrease 4%), and party (decrease 14%) in overnight HRV. Must be some big parties! Subscribe What is a PRV measurement good for? It has been falsely characterized as an index of “autonomic balance” and a specific indicator of stress. A 2018 review of the studies available for HRV and its relationship to stress, not using any of the current wearables, found that stress can lower HRV. But so can many other factors. The non-specificity of the signal, indexed to the table above, is striking. Evidence from a UK Biobank study of over 46,000 participants with actual HRV looked at genetically predicted HRV, a genetic risk score, that failed to show the expected HRV-mortality link, indicating that _HRV is likely not causa_l, but rather a reflection of person’s physiologic state. A review of consumer wearable HRV data from 5 longitudinal studies showed that nighttime PRV was not associated with perceived stress, and surprisingly higher HRV, in the largest cohort (N=717 participants), was correlated with higher stress. An Oura ring cohort of 525 first-year college students found a link between overnight PRV and perceived stress, but that was also seen with resting heart rate, sleep, and respiratory rate. Several very small studies have examined the relationship of HRV and athletic injuries or guiding training with mixed, and predominantly negative results. HRV biofeedback training with paced breathing had no significant effect on reducing stress or raising HRV, as demonstrated with sham controlled trials. When HRV for multiple days showed a decline in conjunction with body temperature, the Oura ring published data for prediction of Covid. The WHOOP company sponsored an observational study, published in 2026, of 30,000 users for 72 weeks, without a control group, that reported reduced alcohol intake (5.8 % points) by self-report. That doesn’t tell us much, and particularly about the merits of HRV for behavioral change. If you use the same device and conditions as longitudinal trends for multiple (at least 2-3) weeks that may be the one way to get something useful from the measurements. Data for overnight sleep with minimal motion and using RMSSD is the best proxy for real HRV. The reason to look at trends rather than any given night is that it more likely represents something, even though you won’t know with certainty what the “it” is. Keep in mind there are no data, no peer-reviewed evidence, to show that HRV fluctuation in-person has any correlation with health outcomes. Share Readiness Scores These are proprietary scores that integrate different metrics for each of the wearables: no algorithms have been disclosed. They are unvalidated against health outcomes. In a review of 14 composite health scores of readiness and recovery, HRV contributed 86% to the scores, followed by reading heart rate (79%), physical activity and sleep duration (both at 71%). That review noted the substantial variability in measurement protools and lack of standardization. Sleep staging is notoriously inconsistent and inaccurate by these sensors, which adds further to the HRV uncertainties for what the scores, which use sleep stage data, mean. Only resting heart rate has been shown consistently across devices to be extremely accurate. I’ve made a Table to summarize what we know about which metrics are included, the scores, any peer-reviewed studies that compared the readiness score with health outcomes, and the corresponding (if any, NA-not available) citation. You will note that some companies do not use the term “readiness," such as WHOOP for recovery, and Garmin, which has 2 different scores, one of which is Body Battery. Eight Sleep uses the term “Fitness Score.” They all include HRV; Apple includes a new metric they call “Recovery HRV” which among other components uses 7-days of sleep, but it is unclear what this means or how it is differentiated from other scores (there are clearly no data for outcomes). We have no knowledge of how the different components are weighted or whether any of these scores are better than resting heart rate, HRV alone, physical activity, or any other single metric. Since none of these are standardized, they are not interchangeable, so if you get a 90 for Oura that has no relationship to a 90 on a Google Fitbit Air. Notably, the company can update its algorithm for readiness score at any point without notification to device users. Without any useful evidence of actionability for these scores or established relationship with health outcomes, it is hard to make a case for their value. At the Apple recent announcement they showed their Readiness score (0-10) on the watch (Figure below) but there are no published data on this score, not even on their website. It’s available only on their new Watch Series 12 or Ultra 4 [of course, ;-)]. That exemplifies the problems with these scores, lack of data and evidence for being meaningful to promote health. Perhaps the best study (which isn’t saying much) is the WHOOP Recovery for golfer performance, because it did correlate with an objective outcome, even though there was no control group and the authors were all from the company. Among the 389 pro golfers, an absolute 10-per cent point increase in Recovery score was associated with about 0.5 fewer strokes per round. But that’s hardly a health outcome! WHOOP is also conducting a study in over 2,700 runners to see if their recovery score will be linked to less injuries and improved performance, but that is not yet published and has no control group or randomization. Putting This in Context For two decades I’ve been enthusiastic about the potential for digital health and particularly wearable biosensors. Over the years, we’ve seen some great progress for their ability to promote physical activity and accurately detect atrial fibrillation (the first FDA cleared deep learning AI for consumers). That work was the subject of rigorous research. But there are holes in the data and evidence for other metrics. One notable one is the “VO2 max” story that I wrote about earlier this year. At that time many subscribers asked me to cover heart rate variability, which I finally got to here. When I dived into the research and publication for HRV and readiness scores, I expected to find at least some that were of high quality and demonstrated their utility by linkage to health outcomes. To my surprise, I found none. The wearable sensor measurements for HRV (PRV) are, for the most part, accurate, but that validation work has only been done in small studies of healthy adults and does not take into account the long list of factors, from the device, software side, and the user side, that affect HRV measurements. Moreover, this metric chiefly relies on optical sensing and, as we have learned for heart rate PPG sensing, may be less accurate in people of color. Keep in mind that all of the health outcome association evidence comes from ECG-derived HRV; none are from wearable sensor data. I will repeat the key point: there's no peer-reviewed evidence to show that in-person HRV fluctuation—or efforts to raise your HRV— has any correlation with health outcomes. For those of you who look at your HRV on awakening, or even 2+ week trends of it being low, I hope this context helps to relieve any anxiety. Yes, low HRV (not PRV) has been shown to increase risk of some diseases as summarized above. But efforts to raise your HRV—a surrogate metric— has not been established for improving any health outcomes. HRV does not have any evidence of causality (the genetic evidence actually goes against this possibility). In this summary, I have not included data for other wearable sensors such as Polar, Samsung, Withings, Suunto, Amazfit, Coros, Ultrahuman, or additional mattress sensors. These are beyond my first-hand experience, and as far as I know from my in-depth review none have any peer-reviewed published data that differ from the 6 sensors I’ve reviewed here. From the points I’ve gone over above, we’re not ready for readiness scores. Besides being proprietary, they are predominantly based on metrics that have their own issues. It’s compounding the problem, like building a house without a solid foundation that has never undergone a rigorous inspection, and then selling it. Like I mentioned for PRV, you can look at trends over weeks rather than any single day, to get a handle, but even that may not be helpful. There’s simply no evidence that these scores meaningfully relate to health outcomes. I’d emphasize they might, but that requires doing prospective or randomized studies to prove it. None exist. There’s great promise for HRV/PRV utility_. For example**,**_ Prof Maiken Nedergaard, who discovered the brain glymphatics that are essential in eliminating metabolic waste products from the brain during sleep, has posited that HRV could be a non-invasive marker for neuromodulator oscillations, brain-body regulatory circuits, and brain clearance. That would be extremely useful, but like everything else on HRV and readiness scores it requires solid research and validation. The lay media isn’t helping much to get the story straight. Earlier this year The Economist published a piece entitled “The most useful indicator of your overall health” which ordained HRV as an “accumulated stress score.” That’s akin to the false assertion about VO2max: “V02 max is the singular most powerful marker for longevity.” As I’ve summarized here, that is not established. The fact is that so many things can lower HRV, including physical exercise (especially an intense workout), reduced sleep quality, stress, the list above, no less the device, signal, and software. Whatever fluctuations observed have not been correlated with any health outcome. Sadly, “datamaxxers” are widely using HRV and readiness scores that have never been validated to mean anything. We already know that for some people using the sensors for sleep metrics, it can induce “orthosomnia,” an obsession to get high sleep quality, with associated high levels of anxiety. In an experiment done by a company to promote sleep quality for its employees, “For those employees who did use the trackers, many reported feeling perfectly rested until their tracker told them they had had a terrible night. Others were told that they had slept like a baby when they had actually been lying awake worrying about the quality of their sleep. “ The same problem can result from preoccupation with HRV or readiness scores, with anxiety that would lead to further reduction in both. It you are using a wearable like >100 million American adults, it’s OK to look at these data, but contextualized with the major caveats reviewed here. If you are one to require evidence that HRV or readiness scores are linked to health outcomes, you may not even want to look. The companies make it hard to turn them off! Let me end with the companies that make and sell wearables. Apple’s doubling down on HRV (24-fold more reporting and heart rate very 5 seconds) and introduction of a Readiness score tells us that consumers have bought into these metrics and they are joining the club. However, all of this is occurring with a backdrop of tens millions of users, claims about the data that are not backed up by adequate evidence, marketing way out in front of whatever limited data exists, and not being transparent about their readiness score algorithms. The companies can well afford to do the research that is needed to connect these metrics with health outcomes show, once and for all, that increasing HRV or using readiness scores promotes our health. If they believed and invested in the products they are selling, we’d not be in this position of not knowing. That’s essentially where we are with HRV and readiness scores. Perhaps someday this will change and we’ll have good reason to embrace them. NB: I wrote this post. No AI. I have no conflicts of interest with any of its content. Loading... Ground Truths has 215,000 subscribers from every US state and 214 countries. There are over 300,000 followers of Ground Truths so more than 90,000 folks who can easily convert to be free subscribers. Your subscription to these free essays and podcasts makes my work in putting them together worthwhile. If you’re not a subscriber, please join! If you found this interesting PLEASE share it! Share Ground Truths The proceeds from all voluntary paid subscriptions go to support our summer internship program. It enabled us to accept and support a record number of 62 summer interns that joined us in 2026! These are high school, college and medical students selected from thousands of applicants. We couldn’t do this expanded program without the funds coming in through Ground Truths. Thank you!
Science Vs on the 49ers Substation: Anatomy of a Hatchet Job
In August, Pablo Torre Finds Out and Science Vs released an episode about my theory that electromagnetic fields from the electrical substation beside the 49ers facility may be contributing to the team’s run of soft-tissue injuries. As the originator of the theory, I was also a subject of the episode. I sat was interviewed by Wendy Zukerman and Rose Rimler of Sciene Vs. I sent them research, connected them with scientists, and spent hours digging through the City of Santa Clara’s and Silicon Valley Power’s records to help clarify critical details. Both Wendy and Rose came off as affable and professional, showing curiosity during the interviews, with Wendy going out of her way to question the “conspiracy theory” framing itself. Then they titled the episode We Solve the 49ers Viral Conspiracy Theory. I was familiar enough with their catalog that I never expected them to agree with my theory, but I did expect them to give it a fair hearing and to deliver their findings honestly. On both counts they came up short. They were not directly dishonest in anything they said, but rather in what they left out, in how what remained was cut, and in the picture painted by those two things in combination. They asked me to recorded the interview on my phone for better audio quality, and I held on to my copy for reference later. That turned out to be a fortuitous decision. Here is the raw audio of my first interview, unedited*. Only my side was recorded, so their questions aren’t on it, but you can generally infer them from the answers, and every claim I make below about what I said can be checked against my statements in this clip. (Note: Wendy had connection trouble at the beginning of the interview and was cutting in and out, which accounts for the false starts.) 0:00 -1:19:13 Audio playback is not supported on your browser. Please upgrade. Science Vs is a fun show. It is pitched at roughly a high-school understanding of science, for an audience that is skeptical, Snopes-oriented, and worried about misinformation. Take a claim circulating online, interview a supporter of the claim, interview consensus scientists, and then tell people which side of the line it lands on. I have listened to their episodes on raw milk, seed oils, 5G and other contested issues in the wellness space. I have problems with all of them, but each at least made an honest attempt to represent the actual range of scientific opinion by talking to credentialed scientists with differing perspectives. Dissenting researchers were heard from, answered, and often given a chance to respond. This episode did not do that. This article is not a relitigation of the science. I have written extensively about that already. This post is for the record. It is simply an accounting of what was wrong with their episode. Contents Is there a power plant next to the 49ers practice facility? — the clearest single example of getting something objectively wrong For the record — a high-level overview of all of the problems with their investigation Draw your own conclusions — why they had to make this episode at all What they left out about childhood leukemia — the exposure threshold, and playing games with statistics to minimize sick children What they left out about the mechanism — the body of literature they refused to cover, and evidence for the mechanism used against it The scientists Science Vs interviewed and did not air — four credential scientists who support myhe theory, recorded and cut, or not even called How they misrepresented me and my case — an answer severed from its question, and three telling edits How you would actually study the injuries — it doesn’t actually matter which team is the most injured, overall The theory: magnetic fields, oxidative stress, and collagen Since the episode never states my theory, here it is below. Those who are familiar with my work can skip this section. Electrical equipment produces magnetic fields, and those fields induce faint electrical currents in anything that passes through them, including people. My argument goes further than induced current. Mitochondria — the structures that generate a cell’s energy — run on continuous flows of electrons and protons, and those flows carry faint electromagnetic fields of their own. Maxwell’s principle of superposition shows that when two fields share the same space, they add together. An external field does not need to be strong to alter an internal field, it only needs to be present. The electron transport chain inside the mitochondria leaks a small fraction of its electrons by design, and those become reactive oxygen species — free radicals, which healthy cells use as signals. External magnetic fields cause the rate of leakage to change, increasing free radicals. When free radicals accumulate faster than the cell’s antioxidant systems can clear them, the result is oxidative stress. Oxidative stress is a recognized driver of chronic illness, including cardiovascular disease, neurodegeneration, diabetes and cancer, and it is in every medical school curriculum. One of its ordinary effects in connective tissue is that it switches on matrix metalloproteinases — MMPs, the enzymes that break collagen apart — while suppressing new collagen synthesis. Tendons are made of collagen. An athlete loading his soft tissue heavily six days a week is already creating oxidative stress in the tendons, so the addition of magnetic field exposure compounds the damage and inhibits repair, making him more susceptible to injury when enormous force lands on a tendon in a fraction of a second. That is the theory. We know that EMF causes oxidative stress, and we know that oxidative stress degrades collagen. The only thing missing is a study showing that direct connection. I have never claimed certainty that the substation is contributing to the elevated injury rate. I do believe it is likely, and I believe it warrants caution, and that a revenue machine like a major NFL team can easily afford to remove the exposure out of precaution. Is there a power plant next to the 49ers practice facility? Here is the clearest single instance of the problem with this episode. It requires no knowledge of electromagnetic fields at all. This story first came to me through Jon Feliciano, a former 49er, in an interview on Willard & Dibs on 95.7 The Game. Asked about why the 49ers are always injured, he said players used to joke that it was the power plant behind the practice fields. Wendy Zukerman corrects him on air. “It’s important to say that it’s not a power plant near the 49ers site.” Torre then asks her to explain the difference between a substation and a power plant. Her answer: a power plant generates electricity and transmits it to a substation, which converts the voltage into something your house can use and sends it on to your home or your business. There are two problems with that. The first is that there is a power plant on that site. The Gianera Generating Station is a natural-gas-fired peaker plant owned by Silicon Valley Power, and it has been there since 1986. I have published aerial photographs of the location from 1987 in which the gas plant is the only thing standing, before the practice facility was even there. I even mentioned the gas plant in my first interview. (Feliciano has since gone on record about this issue, and it is clear he had the substation in mind rather than the gas plant.) The second is that her definition describes a distribution substation, and the facility beside the 49ers is not that. It is the Northern Receiving Station, which takes in bulk power from outside the city’s grid and delivers it to distribution substations. Silicon Valley Power’s own map distinguishes receiving stations from substations, and Rose Rimler even reads the label out loud in the episode when she walks through that map on air. A few minutes before the map segment, Zukerman tells Torre: “like I said, we fact check everything.” Well, maybe not everything. I made a mistake On the morning of July 6th, at 10:20, I sent Rose and Wendy two studies. During the interview I had been asked which human studies show oxidative stress from electromagnetic fields, and I had not been able to name one on the spot. Rose emailed asking for the studies, I quickly searched for a couple, and I wrote that I thought these were the most relevant from that search. Unfortunately, I was busy and did not read either one closely at first. I picked them because they were topically relevant — one on substation workers, one on power plant workers. Neither were great studies, and their problems go past the ones raised in the episode. That was careless on my part. There is context that did not make the episode, though. Before that email I had been on a Zoom call with Rose talking about EMF and oxidative stress, and I pointed her to Dr. Henry Lai at the University of Washington, who has spent years aggregating the literature on this question. His tallies show that roughly 90% of studies since the late 1990s find oxidative effects from electromagnetic field exposure — hundreds of studies, systematically counted. Rose told me she was already aware of his work. So when she asked for studies, I understood her to have the aggregate view already and that she would report anything within that context. Not reading those two carefully was still a mistake, but the larger mistake was assuming the episode would be based on a thorough review of the actual body of literature, rather than on whatever I happened to send that morning. The second email At 1:49 that same afternoon — three hours and twenty-nine minutes after the first — I sent them a second email that I had been preparing for a while. It was a structured document in six numbered sections, written in response to a request they had made two weeks earlier, laying out my entire argument with citations attached to every link in the chain. The episode aired on August 13th, five weeks later, and not a single item from the second email is in it. Here is how it opens: The full email is included at the bottom of this post in Appendix B. Nearly 1,500 words in total. It contains two named mechanisms with the physics behind them. Occupational studies in humans. The literature on oxidative stress and collagen. A section addressing the strongest counter-evidence against my own theory, which I raised myself. And a closing section stating plainly what the theory cannot yet show. My entire argument, in writing, with detailed citations for every claim, provided to them five weeks before broadcast, and none of it made it into the episode. That is the single largest omission, but it is not an isolated one. The whole episode is riddled with similar problems, and the conclusion they came to is not merely a difference of opinion about the scientific evidence. Through omission and through strategic editing, Science Vs misinformed its audience — about what the evidence shows, about what I argued, and about who they spoke to. That is a notable outcome for a show whose stated purpose is correcting misinformation. For the record I am not going to tell you that Science Vs set out to discredit me, or that they had come to their conclusion before they reported the story, or that they used misleading editing to make me look like a man retreating from his own theory. I cannot know what was in anyone’s head, and I am not going to pretend otherwise, either. What I can tell you is what is on the record. They asked me for evidence and aired the weakest thing I sent. They interviewed three scientists who supported my theory and aired none of them. They discussed childhood leukemia without ever saying the exposure level at which it appears. And they took an answer I gave weeks before Ken Karipidis, the one EMF scientist who was put on air, was interviewed, and placed it directly after his critique, where it comes off as a major concession. A friend of mine who has worked as a journalist for thirty years read that last one and called it sleazy. I agree with her. Those are just the four issues that are impossible to defend as pure editorial decision, but they are not the only issues. The most glaring issues stem from what they left out: The exposure level at which the childhood leukemia association actually appears — three to four milligauss, a number the episode never states despite it being much lower than what I measured. The mechanism itself: The episode gets as far as “oxidative stress could weaken collagen,” which leaves it sounding like speculation, rather than a known pathway. The second email, and all the studies in it. Dr. Paul Héroux at McGill, whose work my proposed mechanism rests on, whose contact details I supplied, and who was never called. Dr. Beatrice Golomb at UC San Diego, who runs a research group on oxidative stress and mitochondrial function and has specific expdertice in collagen, interviewed and not aired. Dr. David Carpenter at Albany, the most prominent academic voice on the harm from magnetic field exposure, interviewed and not aired. Dr. Joel Moskowitz at Berkeley, interviewed and not even credited. The specific, testable condition I put in writing that would make me abandon the theory. My own unprompted statement of the theory’s evidentiary gap. My caveats about my own measurements. My ranking of EMF as one factor among several rather than the only one. The new equipment installed at those facilities between 2010 and 2014, and the sharp rise in system load from 2013 onward. But that is not all. What they kept, they selectively edited to serve a narrative that was not served by the raw transcripts of the interviews. A description of thousands of commercial routers in a workplace, reduced to the Wi-Fi in your house. My own acknowledgment, multiple times, that "I'm not a scientist" clipped in an episode that spends considerable energy pointing out that I am not a scientist. And a qualification I volunteered about my own measurements, cut from my answer and delivered later by their EMF expert as a correction. Together their edit produce a portrait of a wellness guy with Wi-Fi phobia and two bad studies, backing away from his theory the moment a “real” scientist looked at it. A practice facility where nothing changed because no new substation was built. Injuries written off as random because the 49ers were not quite the single most injured team in the league over the period in question. That portrait is false even though almost no individual statement made in the episode is. Draw your own conclusions At the top of the episode, Pablo Torre says his show had been flooded with requests to investigate the substation — that it was the thing they were asked to look into over and over again. Neither show went hunting for this story. It arrived from their own audience, in volume, and it could not be waved off. A thread I posted on X reached twenty-two million people. A guy with a gaussmeter and a brand-new Substack obligated a Pultizer prize winning program to spend an hour on a question about player health, that is considered fringe enough that most media operations won’t touch it. Pablo Torre Finds Out could not ignore it. So Science Vs came in and ran a “debunking” operation instead of an investigation. Everything below is what had to be left on the cutting room floor to deliver the “debunking”. They could not ignore it. So they tried debunked it instead. The demand was strong enough to force an episode, and since the episodes release the 49ers have sustained more injuries, including season ending ones, and interest has only grown. Demand from fans and playets is strong enough to force a better investigation from someone else. An omission is not a lie until you find out what was omitted. What follows is the detailed record so you can see the full picture. Draw your own conclusions. I have drawn mine. I am going to keep publishing. A note about Pablo Torre Finds Out After the episode aired I posted publicly, calling out Pablo Torre Finds Out for concerns I had about the integrity of their investigation, and about an interview directly with Pablo Torre which had been offered but never happened. I have since spoken with a producer at PTFO. The offer had rested on a misunderstanding about where things stood between us, and it fell away as the Science Vs part of the production widened past the science. He apologized for the miscommunication and I accepted. The producer also confirmed to me that they did essentially hand off the entire investigation to Science Vs for narrative purposes — so Pablo would be genuinely curious or potentially surprised by their findings — while still taking responsibility for what went out under their name. I appreciated the candor and the accountability, and I am comfortable with where we left things. So this post is not about PTFO. My disagreement is with Science Vs. What they left out about childhood leukemia Childhood leukemia appears at three milligauss. They gave no number at all. 1. They built an EMF ruler, then discussed childhood cancer without it. The sequence on air went like this: First I measured almost 9 mG, then I measured up to 50 milligauss. Torre reacts with concern — “that sounds high.” Cut to Karipidis: the public limit is 2,000 milligauss. Torre reacts again — “What happens at 2,000?” Karipidis explains that nothing happens at 2,000, that safety factors are built in. Then: at more than 50,000 milligauss you get flickers of light in the retina, and higher still, nerve stimulation. The listener now has a ruler (their ruler) to measure these numbers with. Fifty is nothing by their ruler. Then the episode turns to childhood leukemia and states, accurately, that there is a real association — but tellingly, they never give the exposure level at which that association appears. Childhood leukemia appears at three milligauss. They conveniently left that out. The pooled analyses that produced the World Health Organization’s carcinogen classification found roughly a doubling of childhood leukemia risk above three to four milligauss. That is the number that belongs in that segment, and it is more than ten times below the reading that had just been dismissed as trivial. I gave them that number myself, on tape, in the interview. Describing my own threshold, I said my comfort level for long-term chronic exposure is three to four milligauss, but preferably one. 2. Six children in thirteen million. The episode reports that these fields might explain one to four percent of childhood leukemias, then reframes it as a German estimate of perhaps six cases among thirteen million children. Torre, to his credit, is uncomfortable. What never gets explained is why that number is small. Almost no children lives above three milligauss in Europe. Fewer than two children in a hundred, in the Italian data. So even if the risk to those children doubles, the number of additional cases across an entire country stays small — not because the hazard is small, but because hardly anyone is exposed to it. Count the whole population and the few who are exposed disappear. And the reason hardly anyone is exposed is that siting rules keep housing away from transmission lines. In Europe, at least. The Dutch government has a standing precautionary policy against building new homes in any zone where the annual average magnetic field exceeds 4 milligauss — the same number the episode never mentioned. Denmark and Norway treat 4 milligauss as the level that triggers a look at mitigation. That is five hundred times below the ICNIRP figure quoted on air. The United States has no federal equivalent. That is evidence of infrastructure siting policy working. It is not evidence that there is no hazard. It is evidence that we already act as though there is one. If you listen to the raw audio you will hear that my proposed solution is EMF exposure is to build better infrastructure. What they left out about the mechanism 3. They accused me of cherry-picking, and then cherry-picked themselves. On air, Zukerman tells Torre that people who worry about electromagnetic fields dismiss the studies showing null results and collect the ones showing harm, and that this is why you have to be careful not to cherry-pick. They had two papers I had rattled off in a hurry, and a second email containing a carefully chosen set. They ran the two weakest, graded them on air, and presented the result as the state of the evidence for not only my theory, but the whole question of oxidative stress from magnetic fields. That is cherry-picking from my emails. The bigger picture is what they did with the literature as a whole. Zukerman acknowledges it exists, dismisses it, and disposes of it in a single stroke. You can go online right now, she tells Torre, and find scores of studies showing these fields increase oxidative stress. The issue, she says, is that they are not studies in people. Many of them are in people. The occupational studies in my second email are in people. That email had been in her inbox for five weeks. She waved off the literature on a factual claim that the documents in her possession contradict. (I have written separately about the evidentiary standard at work here). The effect was that they essentially baited me: ask the subject to supply the evidence, take the weakest thing he sends, and let that stand as a proxy for the whole argument. Wendy has been doing this show for ten years and clearly knows how to extract what she needs for her desired narrative. 4. They presented the collagen-improvement research as a gotcha, but I had already addressed it. The episode treats the existence of studies showing that EMF can improve collagen as a surprise that undercuts me, but I had pre-emptively addressed that five weeks earlier in the email they ignored. Those studies use measured, high-intensity pulsed dosing. The mechanism by which they work is oxidative signalling. The cell reads a controlled rise in reactive oxygen species as a warning, upregulates its antioxidant defenses, mounts a repair response, and the therapy stops before the system is overwhelmed. The key point is that it induces an oxidative response, which means those studies are actually evidence for my proposed mechanism, not against it. A field that produces a therapeutic effect cannot be biologically inert (which is the implication when they say “Nothing happens at 2,000 milligauss). Chronic ambient exposure is the same pathway with no off switch, and it is most consequential during the evening and while sleeping, when the body is in repair mode and the exposure does not stop. Section 5 of my email is titled What about the study showing improved collagen synthesis. I raised the counter-evidence myself, explained why I did not think it refuted the theory, and wrote that I was disappointed the question had not come up in the interview. That is worth holding against the cherry-picking charge in the item above: the studies they presented as inconvenient for me were studies I had gone out of my way to put in front of them. 5. Section 1 of my email stated a critical argument that was never put to the expert directly responsible for it. My email says the exposure limits exist to prevent acute effects and do not address chronic exposure at all, and that my dispute is with the entire framework. Zukerman gestures at this once. After Karipidis gives the 2,000 milligauss figure, she tells Torre that I would object because those levels do not capture “more subtle effects.” That is not my argument, and “subtle” is doing a lot of work here. My argument is that the limits are built to prevent acute effects — nerves firing, muscles twitching, etc — and were not designed to address chronic exposure at all. In fact, ICNIRP’s own documents state as much themselves. Mine is a structural objection to what the standard measures, reduced as a concern about subtlety, it becomes a matter of degree, rather than a categorical difference. They interviewed Ken Karipidis, vice chair of ICNIRP — the body that writes those limits. He was asked what the limit is, but he was never asked how it applies to chronic exposure. The scientists Science Vs interviewed and did not air 6. They interviewed four officials of the standards body. The episode credits roughly a dozen researchers. Four of them are associated with ICNIRP. Ken Karipidis is the vice chair. Rodney Croft chaired ICNIRP from 2020 to 2024 and led the development of its current guidelines. Dan Baaken is ICNIRP’s scientific secretary. Frank de Vocht sits on the Main Commission. One of them speaks in the episode. Their institution’s position is more than adequately represented — the 2,000 milligauss figure, the safety factors, the assurance that nothing happens below the line. 7. The four who were left out. Dr. Beatrice Golomb is Professor of Medicine at UC San Diego — a physics undergraduate degree, a PhD in biology, an MD. She directs a research group whose stated focus is the relationship between oxidative stress, mitochondrial function and health. That is the mechanism the episode spent its first half dismissing. Her published work includes the fluoroquinolone case series behind the FDA’s black box warning on an antibiotic class that ruptures tendons, where the accepted mechanism is oxidative stress and mitochondrial toxicity — the back half of my chain, already on a drug label. She is in the credits. She is not in the episode. She has told me she finds my theory biologically plausible, and that she has a recording of her interview. Dr. David Carpenter directed the Institute for Health and the Environment at the University at Albany for decades and is the most prominent academic voice arguing these fields cause harm. Childhood leukemia is the reason these fields carry a WHO classification at all, and Carpenter is the person you call if you want that case made by someone who has spent a career on it. He is in the credits. He is not in the episode. He has told me that when he was interviewed they could not have been less interested in what he had to say. Dr. Joel Moskowitz directs the Center for Family and Community Health at UC Berkeley’s School of Public Health. He told me directly that they interviewed him and that he thought it went well. He does not appear in the episode, and unlike Golomb and Carpenter, he does not even appear in the credits. Dr. Paul Héroux at McGill is the researcher whose work provides the foundation for the oxidative stress mechanism my theory rests on. I gave Rose his email address and phone number. He was never interviewed. They never even called him. 8. “He’s not a scientist.” The episode leans hard on the fact that I am not a credentialed scientist. Zukerman says it. Torre repeats it. “At all.” Having built a segment on that, they then left out the physicist-biologist-physician, the professor of public health, the director of a university environmental health institute, and the McGill researcher whose work the primary mechanism comes from. They spent the episode telling their audience I am not a scientist, and then kept four actual scientists who support the theory off because their argument does not survive otherwise. How they misrepresented me and my case 9. They played my words as a response to an interview I had never heard. Near the end of the hour, Zukerman says she went to me and told me the evidence was lacking. Then she plays me saying I am not wedded to it being an EMF, that I have staked my reputation on it needing more study, and that I am not certain of anything. That segment was placed immediately after Karipidis had finished taking the cherry-picked papers apart. It plays as a man folding under expert scrutiny. Commenters have used it against me since, but it is incorrect. Here is the sequence as it happened. I was interviewed. Karipidis was interviewed weeks later. I was never told what he said, or even who he was. I was never asked to respond to it. I did not know his name until the episode aired. That is not a simple editing decision. That is a quote from one interview, moved to follow a critique from a different interview it was not a response to, so that it would land as a concession. A friend of mine who has spent thirty years as a journalist read that sequence and called it sleazy. She is right. The full passage is reproduced in Appendix A, and it is worth reading. What airs is the preamble. Four paragraphs later I say “to directly answer your question” — and that answer, about what would change my mind if the team relocated, is not in the episode. Neither is the sentence two paragraphs on, where I say the EMF might turn out to be ten percent of the problem. I will say the underlying point again, though, because I meant it and I still do. I am not wedded to my theory that magnetic fields from the substation are contributing to the 49ers injuries. I could be wrong. What I am wedded to is the process of scientific inquiry, and the fact that we should be cautious around these exposures and we need more independently funded studies. 10. Three telling edits. They cut “I’m not a scientist” mid-sentence. What I said: “...and I am not certain of anything. I’m not a scientist. To me, I find the mechanisms compelling. I will go back to the fact that I got into this not because of the 49ers, but because of clients I was working with who suffer from EDS...” What aired: “...and that I am not certain of anything. I’m not.” The clip ends on the first two words of the sentence in which I say I am not a scientist, in an episode that spends considerable energy establishing that I am not a scientist. The full sequence is in Appendix A. They cut my own description of my work. Asked what I do, I said I run a wellness business, that I am focused on writing software to help people navigate environmental stressors, that environmental health is my focus, and that I also do independent journalism and research. What aired is the wellness business and the environmental health, with the software and the journalism removed from my own answer. The software engineering does come up later — narrated by them, as a hacker who grew up to write firmware — but my current work, in my own words, arrives as “wellness guy.” Thousands of commercial routers became home Wi-Fi. What I described: working at a wireless networking company surrounded by thousands of Wi-Fi routers, and a stress-induced health collapse afterward that working in that environment contributed to. What aired: Wi-Fi, the kind you have at home — reinforced by a clip of Christian McCaffrey talking about turning his router off at night. Three cuts, and every one of them makes me seem less credible. That is not a coincidence. 11. I gave them my own caveats and the test that would disprove me. In the first email I wrote that a well-designed chronic, ambient-level exposure study in tendon showing no collagen degradation, run over many months, would undercut my confidence in the theory. That is a specific, testable condition, stated in advance and in writing. There was a second interview, weeks later, which was not used in the episode, but in that I asked again for the falsification criterion to be included. What the episode presents instead is a man saying “we need more study,” which reads as a hedge, an open-ended request for the benefit of the doubt. It is the opposite of a hedge. Section 6 of my second email says, unprompted, that as far as I am aware there is not a single study showing EMF-driven oxidative stress degrading collagen in a human in vivo or in human tendon in a lab. I wrote that because it is true and because it is the first thing anyone should check. Under their standard it becomes the hinge of the entire first half, framed as something they had to surface without my cooperation. I had handed it to them five weeks earlier. And in the interview I said that my 25 to 50 milligauss readings were taken at knee level, and that these fields attenuate quickly, so by the time it reaches your head it is not that high anymore. That did not air either. The qualification arrives later, from Karipidis, as a correction. How you would actually study the injuries 12. They measured the wrong thing. The episode spends its final act on whether the 49ers are the most injured team in the NFL, finds no clean ranking, and lands on “injuries are random”. That is the wrong test. You would define the exposure — measured field levels at the facility — and the outcome narrowly: soft-tissue injuries, not a single MSK injury count that a broken finger and a ruptured Achilles both land in. Then you would compare the 49ers to themselves before and after the exposure changed, and compare that change against every other team over the same window. That controls for league-wide shifts in rules, turf and training load. It is a difference-in-differences design, and it is standard. I sent them that argument on July 28th, in writing, along with the fact that in eleven of the past twelve seasons the 49ers had finished top ten in Adjusted Games Lost. And by the episode’s own reporting, the 49ers are second in games lost to injury over the past decade, with FTN’s Aaron Schatz confirming that once you adjust for starters they come out second worst in the league — after having been one of the healthiest teams for years before that. A finding like that is where an investigation starts, not where it stops. 13. I did a lot of substation research for the episode that was never aired. I had reported that the substation next to the facility was expanded in 2014. That was wrong, and Rose Rimler and I sorted it out together. They gave me credit on air, which I appreciated, but framed it as a concession on my part to something they had found. In fact I had been investigating it myself, was uncertain before they asked, but was waiting for clarification from Silicon Valley Power. The uncertainty centered around a substation named “Esparanca” that was proposed right behind the facilities as part of the stadium construction, but now appears to never have been built. I spent days in Silicon Valley Power’s records, and did eventually reach Silicon Valley Power for confirmation and indentified the mistake myself. I also gave them highly detailed documents on what we do know about those facilities: new equipment installed between 2010 and 2014, and load growth across the system with an inflection around 2013–2014, with the Northern Receiving Station carrying the highest capacity in the system and sitting closest to the data center corridor. None of that is in the episode. I have a separate piece about it coming out soon. *I cut 2 seconds from the raw audio to remove personal information that had no connection to anything in the episode. Appendix A: the passage the clip was taken from This is the sequence from my first interview, in full. The episode uses one fragment of it. It’s tricky because my understanding is that there’s something like a 15-year half-life on collagen remodeling issues. They’re going to get a new crop of players. What I really need, though, is for the injuries to be broken down so we can see the soft tissue injuries. Right now, they’re categorized as MSK injuries, but let’s say we can actually identify them more specifically. Is that right? He was able to do that? Oh, cool. I wasn’t able to find that information. Interesting — I didn’t know that data existed. I tried so hard to get it, and I didn’t know it was available. Maybe you could connect me with that person. That would be amazing. I’m not wedded to it being an EMF, honestly. I’m not. I would say that, to a certain extent, I’ve staked my reputation on the fact that it needs more study. It’s important to look into it, and I am not certain of anything. I’m not a scientist. To me, I find the mechanisms compelling. I will go back to the fact that I got into this not because of the 49ers, but because of clients I was working with who suffer from EDS, Ehlers-Danlos Syndrome, a tendon hypermobility issue. This condition is documented to be partially caused by oxidative stress. I’ve worked with them to mitigate their EMF exposure and have seen people improve. I think it’s a bigger story. In a way, the 49ers represent an occupational cluster with specific exposure risks. If someone would conduct a study on this, I believe we could learn a lot. Perhaps we would discover that it’s like, okay, maybe it’s 10% of the problem. I don’t know the exact number, but I think either way, conducting the study would provide valuable insights. To directly answer your question, it’s challenging for me because it’s part of a bigger story. If the 49ers move and stop having injuries, I might conclude that it was related to the substation. However, if they move and still experience injuries, I would want to analyze the nature of those injuries. Are they primarily soft tissue injuries? I don’t think it’s necessarily a case closed, but the story might lose traction at that point regardless. Three things are worth noting. The aired fragment stops immediately before the sentence in which I say I am not a scientist — the cut described in item 10. It also stops four paragraphs before the words “to directly answer your question.” What the episode plays is the throat-clearing. The actual answer, about what would change my mind, never airs. And two paragraphs in, I say the EMF might turn out to be ten percent of the problem. That is the ranking the episode says I never gave. Appendix B: the full email, July 6th, 1:39 PM Hi Rose, You asked me to send you some studies a couple of weeks ago. I apologize for the delay. I have been incredibly busy. I also wanted to give you a chance to dig in yourself, and get your own perspective before I influenced you too much with mine. That said, I do want to make sure that the actual argument is abundantly clear, so here it is! One note before I begin, there are really two separate questions here: Does the substation cause the soft-tissue injuries? That was my specific claim, and what the podcast is about. Is the theory biologically sound? Can 50/60 Hz fields at these levels do anything biological below the safety limits? Question two is why people have been calling me a conspiracy theorist. The regulatory and advisory bodies (ICNIRP, etc) maintain that anything below their exposure limits is biologically inert, and that position is broadly accepted within the mainstream, but the actual science paints a different picture. To defend my theory I’ve had to defend a much larger claim: that the advisory bodies have the biology wrong. I can’t honestly answer question 1 without first addressing that. Here’s is a simplified outline of my theory, with links to studies: 1. Advisory body thresholds for biological effects The ELF magnetic-field limits (ICNIRP’s ~2,000 mG public / 10,000 mG occupational) exist to prevent acute effects from exposure. If a magnetic field is strong enough, it makes nerves fire and muscles contract. Muscles twitch. You can see faint flashes of light in your vision. People can even feel tingling or even a shock. That happens due to Faraday’s law, which states that a time-varying magnetic field induces an electric field inside the body via the creation of Eddy currents.The standards assume that those currents do nothing below the twitch threshold. They do not consider chronic effects at all. My argument is that they are biologically active and do have chronic effects. 2. There are multipe ELF-EMF mechanisms for inducing oxidative stress. This is basic biophysics. Below are the two primary mechanisms. Simplest first. Dr. Paul Héroux of McGill has the most intuitive explanation, which rests on Maxwell’s principle of superposition: because Maxwell’s equations are linear, two sets of electromagnetic waves sharing the same space simply add together. In the interview I pictured a pebble dropped into a pond, sending out clean ripples. Then a boat motors past at distance, sending larger waves, and where they meet the ripples, the two add together and the original pattern gets distorted. In our cells, the mitochondria run on continuous currents of electrons and protons that carry their own faint electromagnetic fields. An external field from a substation, by the principle of superposition, adds to those internal currents and shifts the pattern. The electron transport chain in the mitochondria leaks a fraction of its electrons by design as reactive oxygen species (ROS), which act as signalling molecules in a healthy cell. Distorting that field increases that electron leakage, creating oxidative stress. A tiny electromagnetic interference results in a large downstream effect. https://www.sciencedirect.com/science/article/pii/S2405844025006474 The more complex pathway is Dimitris Panagopoulos’s Ion Forced-Oscillation / Voltage-Gated Ion Channel (IFO-VGIC) mechanism. Weak, polarized, low-frequency fields force the ions (calcium, potassium, sodium) next to an ion channel’s voltage sensor to oscillate; because that force scales with the inverse cube of the distance involved, fields far below the stimulation threshold can still force the channel open, disrupting the cell’s ion balance and driving ROS overproduction (Nitric oxide and superoxide interact and produce peroxynitrite, a highly unstable cytotoxin that breaks down into free radicals). https://www.researchgate.net/publication/366088934 https://www.spandidos-publications.com/ijo/59/5/92 https://www.mdpi.com/1422-0067/22/18/10041 https://www.frontiersin.org/journals/public-health/articles/10.3389/fpubh.2025.1585441/full https://pmc.ncbi.nlm.nih.gov/articles/PMC3772193/ 3. Evidence of oxidative stress, in vivo, in humans from ELF-EMF There are many studies, and the strongest are occupational, which applies to the 49ers situation. 115 power-plant workers vs. 145 office controls. Serum malondialdehyde (MDA, the standard lipid-peroxidation marker), superoxide dismutase, and catalase were all significantly higher in the exposed group, and the markers rose with increasing field exposure. https://journals.sagepub.com/doi/abs/10.3233/WOR-203244 A follow-up where they reversed the oxidative stress in power plant workers. A double-blind randomized controlled trial: 91 power-plant workers given vitamin E, vitamin C, both, or placebo for 90 days. The antioxidant groups showed reduced lipid peroxidation and raised antioxidant capacity versus controls. https://pubmed.ncbi.nlm.nih.gov/32191586/ A spot-welder study: 46 welders occupationally exposed at 50 Hz, showed significantly altered red-blood-cell antioxidant enzyme activity and concluded ELF-MF “might act as an oxidative stressor… even at the recommended levels of exposure.” https://pubmed.ncbi.nlm.nih.gov/18504600/ A substation-specific study found oxidative stress and DNA damage https://pubmed.ncbi.nlm.nih.gov/24460415/ 4. Oxidative stress degrades collagen This half isn’t controversial at all. Oxidative stress activates the matrix metalloproteinases (MMPs) that break collagen down and suppresses its synthesis. Here are three example studies: Siwik et al. 2001: Oxidative stress raises MMPs and lowers collagen synthesis in cardiac fibroblasts. https://pubmed.ncbi.nlm.nih.gov/11121376/ Fisher et al. 2009: Collagen fragmentation drives oxidative stress and elevates MMP-1 in aged human skin. https://pmc.ncbi.nlm.nih.gov/articles/PMC2631323/ Varani et al. 2006: Decreased collagen production in oxidatively aged skin. https://pubmed.ncbi.nlm.nih.gov/16723701/ 5. What about the study showing improved collagen synthesis I’m glad you asked this question, and I’m bummed we didn’t get to it in the interview because it is a great question, and very important to understand. Superficially it may appear to be a refutation of my theory, but I would argue that it actually supports the underlying argument. That study used a short, high-intensity pulsed dose: therapeutic-PEMF, the same type of field used clinically to stimulate bone and tissue healing. The reason this works is because it triggers the very same biological pathways that can lead to oxidative stress. The exposure still stimulates ROS production, but done at a controlled dosage, for a limited duration it has a different effect. The cell reads the ROS as a warning signal and it upregulates its antioxidant defenses, and mounts a repair/proliferation response. The therapy is then stopped before the cell gets overwhelmed. That is essentially a hormetic response: a small dose of a stressor producing a beneficial adaptation. Two things follow: At the very least, this means the field is biologically active, which by itself undercuts the regulatory claim that these fields are inert below their thresholds. There is a wealth of literature on PEMF (pulsed EMF) bone regeneration and calcium channel signalling (which is the second mechanims in section one). Here is one. https://www.nature.com/articles/srep13856 At best, it leads us straight to my actual concern, which is that under chronic, chaotic and unregulated exposure, the cell’s antioxidant capacity gets overwhelmed, resulting in oxidative stress. There are plentiful examples of things that are beneficial at controlled doses, but harmful at uncontrolled doses. Excecise is one obvious, uncontroversial example. Botox is perhaps a more interesting example. 6. What about a study that shows EMF causing collagen degradation in humans? As far as I am aware there is not a single study showing EMF-driven oxidative stress degrading collagen in a human, in vivo, or in human tendon in a lab. There are studies involving isolated fibroblasts though, which secrete collagen. The most relevant one showed that human fetal scleral fibroblasts exposed to 50 Hz ELF-EMF showed a significant decrease in collagen synthesis and that MMP-2 expression was upregulated, which is the exact mechanism I described in section 2. https://pmc.ncbi.nlm.nih.gov/articles/PMC3626379/ That’s it! Thanks again for the interview. Best, Peter Anthony Cowan Environmental Health · Wellness Tech · Researcher & Journalist Publisher & Editor, Living Energy Bio: petercowan.comSocial: X · Instagram · TikTokApp: sunlightis.lifePhone: [redacted]
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