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Flu cases rise on west coast earlier than usual as US officials encourage vaccine
California flu test rate at 9.65%, higher than normal 1% rate for early October, amid mutation of H1N1 influenza A strain
Why doctors are urging women to redo early genetic tests for cancer risks
Advances in technology detect far more genetic mutations, which can be lifesaving information for a generation of women first screened years ago.
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
The genetic secret helping bats survive a deadly epidemic
We’re easing you into Halloween season with an episode about bats. There’s a silent serial killer decimating little brown bats as they hibernate. White nose syndrome has driven populations across the U.S. to almost the brink of extinction over the last decade. But recently, conservation biologist Giorgia Auteri and her team noticed several genetic mutations in the survivors. These mutations could explain how natural selection has shifted the existing population – and inform conservation efforts in the future.Interested in more animal science? Email us your question at shortwave@npr.org.Support public media with NPR+ and enjoy perks for over 25 podcasts like this one. This show’s perks include sponsor-free listening. Learn more at plus.npr.org.
The Next Bioweapon Could Attack Our Genes Instead of Our Bodies. I Promise You We’re Not Ready for That.
The most devastating weapons conceived by humanity cause cellular damage as a side effect. What would happen if the genetic mutation itself were the nefarious goal?
How to Watch: White Sox at Astros, Wild Card Series
Your broadcast guide this week, including every permutation of Game 3 start times!
Insurance Coverage Lags as Cancer Science, Treatment Move Forward
“Brain cancer” or “H4 G34-mutant”? As knowledge about genetics advances, some doctors say cancers should be defined by their mutations, not the tissues where they manifest.
Insurance Coverage Lags as Cancer Science, Treatment Move Forward
“Brain cancer” or “H4 G34-mutant”? As knowledge about genetics advances, some doctors say cancers should be defined by their mutations, not the tissues where they manifest.
[Science Through Covers] EGFR T790M mutation in US Southeast drives inherited lung cancer risk
Harvard Medical School team links 200-year-old founder effect to sharply higher lung cancer risk among non-smokers in southern Appalachia
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
Guardant Health (GH) Lands First FDA Cleared Breast Cancer Liquid Biopsy Role
Guardant Health (NasdaqGS:GH) received FDA approval for its Guardant360 CDx liquid biopsy as a companion diagnostic in advanced HR-positive, HER2-negative breast cancer. The decision makes Guardant360 CDx the first FDA approved liquid biopsy companion diagnostic for longitudinal ctDNA testing in breast cancer care. The approval is supported by clinical trial data where early detection of ESR1 mutations using Guardant360 CDx informed treatment changes for patients. The Guardant360 CDx breast...
This Rare Gene Drastically Raises Lung Cancer Risk in People Who Never Smoked
The gene is found predominantly in Southern Appalachia and may be one of the most powerful cancer-risk mutations ever found.
She Can’t Feel Pain or Anxiety. Her Genetic Mutations Hold the Key to Eliminating Human Suffering, Scientists Claim.
A life without pain seems miraculous. But denying this hallmark of human existence could come with its own set of challenges.
Harvard scientists design evolutionary traps to stop viral mutations
When a virus mutates, the world usually finds out the hard way. Variants of influenza and SARS‑CoV‑2 can slip past vaccines and antibody drugs before scientists fully understand what has changed.
The dirtiest places on an airplane; testing for a breast cancer gene mutation; the evolution of esophageal cancer; plus other stories with Vanderbilt Health sources
William Schaffner, MD, Professor of Preventive Medicine, was quoted by several news outlets about public health issues, including: WKRN News 2 (heat-related illness); NBC News (how bad will flu and COVID be this winter?); AAA’s The Extra Mile (the dirtiest places on an airplane); WKRN News 2 (again) (measles in Tennessee); and The Tennessean and Healthline (new COVID vaccines). Schaffner also spoke to the EMJ European Medical Journal for a Q&A interview. Tuya Pal, MD, Professor of Medicine, was quoted in a New York Times story about testing for a breast cancer gene mutation. Michael Gibson, MD, PhD, Professor of Medicine, was quoted in a MedPage Today story about the epidemiologic evolution of esophageal cancer. Medpage Today writer Shannon Fritz quoted Shravani Durbhakula, MD, Associate Professor of Pain Medicine, who answered questions about a street drug called cychlorphine. Becker’s Behavioral Health picked up the story. WSMV Channel 4 News reporter Diana Rocco interviewed Michael Caucci, MD, Associate Professor of Psychiatry and Obstetrics and Gynecology, for a story about postpartum psychosis and the trial of Lindsay Clancy.
GRN gene: When genetic information upends life
A family in Argentina has become an ideal case to study frontotemporal dementia. Across generations they transmit a mutation in the GRN gene, responsible for producing a protein essential to healthy brain cell function
Breakthrough Israeli cancer study finds mutations break DNA when it doesn’t bend
Weizmann Institute of Science and Rowan University researchers show that repair enzymes fail to fix gene structures of certain shapes, in discovery that may lead to new therapies
Mail-in voting, commutations and crime, politics of tariffs
Mail-in voting limits proceed, the Commutations Advisory Board meets and tariffs reemerge.
A hidden “on switch” in human DNA has finally been decoded
Researchers have used AI to uncover the DNA signature of a key genetic “switch” involved in turning genes on. After analyzing about 500,000 DNA sequences, the model identified the initiator in roughly 60% of human genes. The breakthrough could help predict the effects of harmful mutations and eventually contribute to decoding the broader genetic instructions that control gene activity throughout the body.
Ain’t Polis’ Peters commutation a pity?
I am hoping that, yet again, my long-suffering and very forgiving editor will pardon my rambling thoughts today, as there are too many open tabs on my computer that deal with issues I want to talk about (Ed: pretty used to this, so OK). Like a lot of journalists and columnists, I am on the […]
Judge criticizes Trump's Justice Department as he says he has no choice but to dismiss Jan. 6 seditious conspiracy case
The move Tuesday closes the book on the Jan. 6 cases that were wiped out with Republican President Donald Trump's sweeping pardons and commutations last year, freeing from prison people convicted of violent of assaults on police and other crimes.
Cancer may be breaking its own DNA to keep growing
Cancer cells rely on powerful genetic switches to keep growth genes running at full speed, but that intense activity can damage their own DNA. The resulting breaks are repeatedly repaired, sometimes with small mistakes that allow new mutations to accumulate. Researchers believe this self-inflicted damage may help tumors evolve while also creating a potential target for new treatments.
Can Humans Live Forever? Study Puts a Cap on Life Span at 194 Years
A new study suggests that DNA mutations may limit human life span to 146–194 years, even under favorable conditions. The findings could help broaden understanding of the aspects of aging that may ultimately prove impossible to reverse.
Why Did This Man Avoid Alzheimer’s? Scientists Reveal Their Astonishing Theory - Futura-Sciences
A Family Plagued by Early-Onset Alzheimer’s Doug Whitney inherited a rare genetic mutation that’s devastated much of his family: many relatives experienced significant cognitive decline as early as their 50s. Yet Doug himself has stayed mentally alert well past the age at which illness struck in the family. According to...
New Alzheimer's drug repairs DNA damage and reduces brain inflammation
A drug originally developed for spinal cord injury may offer a fresh approach to treating Alzheimer’s disease. In mouse studies, KCL-286 repaired dangerous DNA damage, reduced inflammation, and targeted multiple disease-related pathways instead of focusing on just amyloid or tau. Since it has already cleared an initial human safety trial, researchers believe it could move more quickly into Alzheimer’s clinical testing.
Colorado governor fires two clemency board members who spoke out about Tina Peters’ commutation
Colorado Gov. Jared Polis on Wednesday fired two members of the state’s clemency board after they spoke out against his controversial decision to grant clemency to Tina Peters – an election denier whose sentence was cut in half by the outgoing Democratic governor in May.
Fallout from USMNT loss to Turkey and previewing the Mbappe-Haaland clash
On today’s show, we look back at the United States’ final group stage match against Turkey and evaluate their readiness for the Round of 32. Manchester City insider Sam Lee joins us to preview the tournament’s first true superstar heavyweight clash as Kylian Mbappe and France square off against Erling Haaland and Norway in a battle for Group I supremacy. Plus, The Athletic’s Jay Harris is back in the studio to break down the latest bracketology, advancement percentages, and qualification permutations for Groups G, H, and I using The Athletic’s World Cup Tracker.
What do Canada and Switzerland need to qualify for the World Cup knockouts from Group B?
Discover all the permutations for how the teams in Group B can qualify for the knockout rounds
Long-lived families reveal a rare genetic clue to healthy aging
A study of long-lived families has identified rare genetic variants that may help people stay healthier for much longer as they age. One standout mutation appears to temper inflammation, potentially delaying disease and extending years of healthy living.
Long-lived families reveal a rare genetic clue to healthy aging
A study of long-lived families has identified rare genetic variants that may help people stay healthier for much longer as they age. One standout mutation appears to temper inflammation, potentially delaying disease and extending years of healthy living.
Scientists discover neurons must break their DNA to build the brain
As newborn neurons make their way through the developing brain, they must squeeze through incredibly tight spaces to reach their final destinations. Researchers discovered that this physical journey routinely causes some of the most severe forms of DNA damage—double-strand breaks—yet the young brain has evolved an impressive ability to repair the damage almost immediately.
This DNA repair gene went rogue and exposed a cancer weakness
Scientists have discovered that a gene normally considered a DNA-protecting "good guy" can become dangerous when cells make too much of it. The gene, EXO1, acts like molecular scissors that help repair DNA, but when overproduced it starts cutting DNA it shouldn't, creating damage linked to cancer.
Study identifies genetic cause for rare skin condition, points to new therapeutic option
The research highlights the value of studying rare genetic diseases to uncover fundamental immunological mechanisms.
Your DNA is changing all the time. Here’s why
We tend to think of the DNA strands that contain our genetic code as consistent, stable units. But in reality, the cells that make up our bodies are constantly replicating and changing. Even as you read this sentence, in fact, the genes within your cells are mutating. So, what causes these mutations and what’s the impact? Science writer Roxanne Khamsi examines the answers in her new book, Beyond Inheritance. Today on the show, she gets into how scientists examine these mutations, how they’ve shifted our understanding of disease and what the future of genetic therapy could entail.Interested in more biological and life sciences? Email us your question at shortwave@npr.org.Listen to every episode of Short Wave sponsor-free and support our work at NPR by signing up for Short Wave+ at plus.npr.org/shortwave.
Scientists Thought They Understood Evolution. They Were Wrong.
Beneficial mutations happen quite frequently, but the world changes too fast for them to stick.
Scientists finally crack an “undruggable” pancreatic cancer target and nearly double survival
For decades, pancreatic cancer has been one of the most lethal cancers, with few effective treatment options. A new drug, daraxonrasib, targets the KRAS mutation that fuels most pancreatic tumors—something many scientists once thought couldn't be done. In a major clinical trial, the treatment nearly doubled survival for patients with advanced disease and reduced the risk of death by 60%.
Scientists discover inherited traits that break Mendel’s Laws of genetics
A major mouse study found that some inherited traits are passed down through epigenetic changes that break the classic rules of genetics. Researchers discovered hundreds of cases where these chemical DNA marks behaved unexpectedly, including some that seemed to emerge out of nowhere. They also identified the first known naturally occurring paramutation in a mammal, hinting that environmental influences may play a larger role in inheritance than scientists realized.
Colorado elections clerk set to be released from prison Monday based on her sentence commutation
Former Colorado elections clerk and conspiracy theorist Tina Peters is set to be released from prison
Colorado elections clerk set to be released from prison Monday based on her sentence commutation
Former Colorado elections clerk and conspiracy theorist Tina Peters is set to be released from prison.
Scientists say evolution may work differently than we thought
A major research study is challenging one of evolution’s most influential ideas: that most genetic changes that become permanent are essentially neutral. Researchers at the University of Michigan found that beneficial mutations are actually far more common than scientists have long assumed. The puzzle is that these advantageous mutations rarely spread through entire populations. Their answer? Nature keeps changing the rules.
A mistaken commutation and an over-the-top reaction
It seemed an itch that Gov. Jared Polis just had to scratch. After months of hints and speculation, Polis put his signature on a commutation of the prison sentence of Colorado’s election-denying queen, former Mesa County Clerk Tina Peters. True, Peters’s break was one of 44 commutations and pardons announced en masse by Polis late […]
Scientists discover hidden weakness shared by hundreds of cancer mutations
Scientists have unveiled a powerful new tool called PerturbFate that could change how researchers tackle diseases driven by huge numbers of genetic mutations, including cancer and Alzheimer’s. Instead of trying to target every faulty gene individually, the system tracks how different mutations reshape cells over time and identifies the hidden “control hubs” where those pathways converge.
Colorado Democrats formally censure Gov Polis over Tina Peters commutation
Colorado Democratic Party formally censures Gov. Jared Polis for commuting Tina Peters' sentence in the Mesa County voting system breach case.
Scientists Discovered a Mutation in Our Genes from an Ancient Species
A rare look inside Homo erectus genes revealed a mutation that we still share.
Bennet: Gov’s election denier commutation ‘disqualifying’ for potential Senate pick
Scientists Discover Ancient “Language Switches” Hidden in Human DNA
Researchers have identified tiny genetic “switches” that appear to play a surprisingly large role in human language ability.
Lung Cancer Research Foundation Grants Team Science Award Focused on Understanding and Treating Lung Cancers with HER2 Mutations
/PRNewswire/ -- The Lung Cancer Research Foundation (LCRF) announces the first recipients of its LCRF | Boehringer Ingelheim Team Science Award on Innovative...
A Mutation Gave Humans the Gift of Speech. These Mice Have It, Too.
Scientists wanted to know why the chatter of Alston’s singing mice sounds so much like human conversation. What they found might change how we study both species.
Man destined to get Alzheimer’s saved by accidental heat therapy
Doug Whitney has a genetic mutation that means he should have developed Alzheimer’s disease decades ago, but his long-term work in hot engine rooms may have protected him in a similar way to sauna therapy
Scientists Discover Evolution’s 120-Million-Year-Old “Cheat Sheet”
A long-standing assumption about evolution is being challenged by new research showing that vastly different species can rely on the same genetic pathways to develop similar traits.
Your DNA has a secret “second code” that decides which genes get silenced
Not all parts of our genetic code are equal, even when they appear to say the same thing. Scientists have discovered that cells can detect less efficient genetic instructions and selectively silence them. A protein called DHX29 plays a key role in this process by identifying and suppressing weaker messages. This finding reveals a hidden layer of control in how genes are used.
How does mitochondrial DNA affect your health? - Salk Institute for Biological Studies
Highlights Salk scientists have created a platform to study mitochondrial DNA mutations that lead or contribute to human disease They generated a library of 155 mitochondrial DNA mutant cells, nearly the human level of mitochondrial DNA mutant diversity The platform and library will accelerate innovation in the mitochondrial disease therapeutic space LA JOLLA—Some of your most important life partners are the mitochondria that power all your cells. You and these little cellular powerhouses are in a 1.5-billion-year-old evolutionary relationship—but mitochondria brought some baggage. Mitochondria brought their own DNA with them when they joined with the bigger, more complex cells so long ago, and today that mitochondrial DNA influences human health.
Woman, 41, Admits She Feels ‘Like a Ticking Time Bomb’ After Learning She’s a Carrier for Fatal Huntington’s Disease
A woman said she feels like a 'ticking time bomb' after she learned she carries a gene mutation for Huntington's disease, a rare illness affects an individual's ability to move and think, as well as their mental health.
A gene mutation may trap the brain in the wrong reality in schizophrenia patients
A newly identified gene mutation may help explain why schizophrenia patients struggle to update their understanding of reality. The mutation disrupts a brain circuit involved in flexible decision-making, causing mice to stick with outdated choices even when conditions change. Researchers pinpointed the issue to a key thalamus–prefrontal cortex pathway. By reactivating this circuit, they were able to restore normal behavior—raising hope for future therapies.
Mouse study shows repeated cloning causes grave genetic mutations
1,206 cloned laboratory mice were generated by the scientists from a single female donor mouse from 2005 to 2025 in research conducted in Japan.
Your Thymus and Your Healthspan
Our thymus gland plays a central role in the development or our immune system, specifically for supporting T cell development (how these cells got their name, maturation and differentiation in the thymus) and discriminating between self and foreign, non-self antigen proteins with production of dendritic cells. As we age, our thymus gland shrinks—the process known as involution—with progressive change from spongy to fatty tissue, with loss of functionality. But this process, with respect to timeline and extent, markedly varies from one person to the next. And to make things even more complicated, our thymus gland anatomy and precise location in the chest also is highly variable. So the famous Frank Netter diagrams from the 1960s (such as at left below) don’t capture the remarkable heterogeneity that a random set of 12 chest CT scans (below at right). What I consider as 2 landmark papers in Nature this week (here and here) used AI to quantify health of the thymus in 2 large cohorts, and then correlate the metric to a broad array of health outcomes. In this edition of Ground Truths, I’m going to cover three questions: (1) How was thymus health determined by AI?; (2) How is thymus health linked to key clinical outcomes? and (3) Are there ways we can promote a healthy (aka rejuvenate) thymus gland in our later years? Subscribe 1. How was thymus health determined by AI? This was accomplished by extensive work developing and validating an AI pipeline for 2 stages, the first for localization and segmentation of the thymus bed, and the second to quantify a digital marker, termed the thymic health score. There’s a lot to this algorithmic development, so I won’t go into all the details, but just provide a rudimentary outline of what was done. The 1st stage used supervised learning with 2 radiologists reviewing 2,461 chest CT scans. That work trained a 3D U-Net model to automatically identify the thymic bed’s 3D cropped region using center of mass coordinates, which reached 99.8% accuracy. The 2nd stage used a foundation model that was pre-trained with SwAV (which stands for Swapping Assignment between multiple Views), a self-supervised model, that generated a high-dimensional thymus representation of 4,096 features. That compares to the radiology reductionist and subjective scoring of 0 to 3 where 0 means the thymus is fully degenerated and fatty, and 3 is considered dense, intact glandular soft tissue. Notably, the self-supervised learning (SSL) performance was superior to supervised (AUC ~0.75 vs 0.55, respectively) reflecting the shallowness of the 0-3 classifier vs SSL’s holistic, self-taught AI. The thymic health score ranged from 0 to 100, with the highest number indexed to fully preserved thymic health. The algorithmic work extended to explainability with both Shapely value distribution, meaning the model was holistic not relying on any “magic” pixel, and occlusion sensitivity, demonstrating the model’s performance was not affected by ribs, sternum, lung tissue, but rather focused on the thymic bed directly. Below are a few saliency maps from the occlusion sensitivity that indicate the thymic bed focus, not affected by neighboring structures, using the jet color scale. Now the AI was ready for processing ~25,000 CT scans, each over 30 MB files, from the 2 large participant cohorts to provide a thymic health score, it did so in less than 14 hours, which is less than 2 seconds per scan! Share 2. How is thymus health linked to key clinical outcomes? The two cohorts were the National Lung Screening Trial, NLST (N=25,031) and the Framingham Heart Study, FHS (N=2,581) each with baseline demographics and long term follow up of >12 years for health outcomes. From the NSLT, you can see below that increased age and body-mass index were correlated to reduced thymic health. And, overall, men had reduced thymic health scores compared with women. There are a lot of graphs in the paper for outcomes, for both the NLST and FHS cohorts. To simplify the major outcomes, below is a composite Figure with striking reduction of all-cause mortality and for the different causes of death. The results were consistent between the 2 cohorts. For example, the cardiovascular mortality hazard ratio average was 0.57 in NLST and 0.38 in FHS (weighted to be 0.53 for the aggregate). The reduction of mortality also extended to digestive diseases and pulmonary disease (data not shown below). Lung cancer incidence was reduced by 36% for high vs low thymic health (Figure below, with a panel -incidence and b panel-mortality, adjusted for age, sex, BMI, smoking status). Notably, there was a smoker’s paradox: lower incidence and improved survival for lung cancer in smokers who had a high thymus health score. Smoking was associated with lower thymic scores whereas alcohol was not. Higher thymic health was linked to higher HDL cholesterol, lower triglycerides, lower fasting blood glucose, and lower systolic and diastolic blood pressure. Inflammation biomarkers, such as C-reactive protein and interleukin-6, were elevated in the people with lower thymic health scores. In their second paper, the same team looked at the relationship between thymic score and outcomes for 3,476 patients receiving cancer immunotherapy. The non-small cell lung cancer progression-free survival was reduced in patients with low thymic health score. A parallel relationship for survival was seen for other types of cancer including melanoma, breast, and kidney with a 44% lower risk among high thymic scores (Figure). A similar pattern was seen with different immune checkpoint inhibitors. The thymus health score outperformed programmed death ligand-1 (PD-L1)and tumor mutation burden (TMB) assay of the tumor and was an independent prognostic marker of progression-free survival. In this dataset, a direct connect with thymus score and adaptive immune function was noted with a correlation before cancer treatment for both T-cell diversity and thymus T-cell production (a metric known as T cell receptor excision circles). Thymus Removal Study There is a highly relevant citation about thymus function before moving onto ways to rejuvenate it. In 2023, a very important study of thymus removal during cardiothoracic surgery was published, with 1146 patients undergoing thymus removal vs 1146 matched controls (mean age 55 years). The adverse outcomes for thymus removal were striking, with a 2.9 higher risk of all-cause mortality and doubling of cancer incidence, 1.5 fold increase in cancer mortality, and 1.5-fold increase in autoimmune diseases. The immune function showed marked compromise after thymus removal, as reflected by CD4+ and CD8+ T cells (Figure below) Share Ground Truths 3. Are there ways we can promote a healthy (aka rejuvenate) thymus gland in our later years? In recent months we’ve learned a lot about the process of thymus involution and the pathways by which this may be modulated. Thymus involution is primarily due to loss to thymus epithelial cells (TECs) and there are 2 subtypes with different functions: the cortical, responsible for positive selection of T cells, and the medullary, for negative selection. When adipose tissue infiltrates the thymus, thymic adipocytes are pro-inflammatory, knocking out T-cell output. Likewise, systemic inflammation, or “inflammaging,” from smoking, obesity, and chronic stress promote thymic adipocytes. Now, from preclinical studies, we know about key pathways that account for these processes. Historically, back in 2014, FOXN1 was recognized as a single master transcription factor essential for TEC function, with studies in mice with forced FOXN1 upregulation leading to thymus regeneration. That laid the foundation for potential regrowth of quiescent thymus cells. It took awhile to find pathways to accomplish this goal and to even refute its role as the master regulator. The Liver-Thymus Axis Feng Zhang and his team recently showed that injection of an mRNA vaccine to the liver encoding DLL1, IL-7 and FLT3-L in combination, factors known to support thymopoiesis (Figure), successfully enhanced immune function in aged mice. However, the effect was transient. The FGF21 Story Two reports in 2025 addressed the thymus gland’s production of FGF21, a growth factor (fibroblast growth factor 21) and its control of thymus involution. This growth factor is also produced by the liver, but it doesn’t have impact on the thymus in aged rodent models. In contrast, The liver’s hepatocyte growth factor (HGF) has been shown to reverse senescent TEC structural changes. Growth hormone stimulates production of insulin growth factor-1 (IGF-1) in the liver and the thymus. Two small studies in human participants (TRIIM, for Thymus Regeneration, Immunorestoration, and Insulin Mitigation) of 6 and 50 people, respectively, treated with combined human growth hormone, metformin and DHEA, suggested the potential of slowing epigenetic aging and improving thymus mass and function. But the combination of drugs, small sample, and lack of controls make conclusions murky. Increased thymus FGF21 led to increased CD8 T cells in old mice and extended healthspan and improved physical performance. Building on the previous FOXN1 data, ablation of β-klotho, the obligatory co-receptor for FOXN1, accelerated thymic aging. The benefit to FGF21 was confirmed in a companion paper using an FGF21 knock-in mouse model showing thymus enlargement and increased TECs throughout the lifespan. (schematic Figure below). The accompanying editorial for these 2 papers speculated: “The proposed link between age-associated thymus involution and organismal aging is intriguing, and suggests we might seek to achieve systemic rejuvenation by counteracting thymic involution.” Other Factors Lessons from the Axolotl (Mexican Salamander) In an elegant set of experiments of the axolotl (Figure), known for its complete thymus regeneration after total surgical removal, mediators were identified. Surprisingly FOXN1 was dispensable. But midkine, a growth factor, appeared to be the driver, the initiator of thymus cell growth, survival, and repair. Other components that contributed were Postn+ (periostin-expressing mesenchymal niches) and Ccl19, a chemokine protein from the bloodstream. RANK and RANKL RANK (receptor activator of nuclear factor κB its ligand (RANKL) have been considered key regulators of medullary TECs. In a study of both aged mice and human thymus cell cultures, their key role was confirmed, with multiple benefits of resorting TEC function, recruitment of progenitor cells, and T cell development. Subscribe Summing Up This body of work strongly supports the health of the thymus gland as a critical regulator of human healthspan, not just a correlate or link. The new landmark studies are reinforced by the regenerative biology experimental models that have shown, via an array of mediators, that healthspan of aged mice is at least in part dependent on thymus gland function and its critical role for maintaining adaptive immunity. It sure seems that we’d be better off having an immune reservoir of naive T cells instead of a profile in older adults of exhausted, low quality, memory T cells, with a senescent phenotype. It is striking that we ignored the importance of the thymus gland for many decades. A wake-up call was the results of the thymectomy matched control study reviewed here, with the opposite of high thymic health score improved health outcomes. The convergence of AI and healthspan here is notable. The exceptional and laborious work for developing and validating (no less explaining) the AI to quantify thymus health set the foundation for probing the connect the major health outcomes in two cohorts with extensive follow-up. We’ve never had a way to meaningfully quantify the thymus gland before, so this represents important leverage of supervised, self-supervised, and transformer models. The study wouldn’t have been possible without AI. And it begs the question as to whether there are ways we can maintain our thymus at a high health score. But it’s not so simple to rejuvenate our thymus. There are multiple risks including the induction of autoimmunity, increasing the risk of cancer, and inducing a pro-inflammatory state. For example, factors that increase TEC proliferation could compromise the medulllary negative selection process and leak out auto-reactive (self-attacking) T cells. Thymic cells could be induced to proliferate, but we know, for example, that growth hormone and IGF-1 are associated with an increase risk of cancer. If thymus rejuvenation doesn’t clear out the accumulated senescent cells in older adults, then inflammation within the gland could block the production of TECs. Keeping these risks in mind, we now have identified many ways to keep our thymus healthy as we age that undoubtedly will be tested in clinical trials going forward. Ultimately, the benefit-to-risk tradeoffs will be defined. In the meantime, we have desperately needed an immunome. As I’ve stressed in multiple prior Ground Truths, we have no test in the clinic to assess a patient’s immune status! It was very encouraging for me to get an email from Hugo Aerts, the senior author of the landmark papers in the days after they were published: “I also wanted to say that your Substack on “Why We Need an Immunome” was inspiring for this work. We found it a very compelling perspective and greatly enjoyed reading it.” Just having an assessment of a person’s immune status via a chest CT scan, with millions of these performed per year, might help in guiding the right immunotherapy for cancer (e.g. more intensive, combinations for those with low thymic health scores) and help define people who are increased risk for age-related diseases of cancer, cardiovascular, and neurodegenerative. The main theme of Super Agers is that we now have many layers of data (genetics, proteins, biomarkers, organ clocks that can be integrated via multimodal AI) for us to define a person’s specific risk decades before one of these age-related diseases leads to symptoms, enabling prevention. From the new studies this week, we can add thymus health score as yet another way to understand a person’s risk, a window into their adaptive immune system and healthspan. And perhaps someday we will be able to safely rejuvenate the thymus, or maintain its health through one’s life, and use the thymus health score to monitor. NB: I wrote this post (No A.I.) A Quick Poll Loading... ********************************************************************* Thanks to Ground Truths subscribers (now > 200,000) from every US state and 212 countries. Your subscription to these free essays and podcasts makes my work in putting them together worthwhile. Please join! If you found this interesting PLEASE share it! Share Ground Truths Paid subscriptions are voluntary and all proceeds from them go to support Scripps Research. They do allow for posting comments and questions, which I do my best to respond to. Please don’t hesitate to post comments and give me feedback. Let me know topics that you would like to see covered. Leave a comment Many thanks to those who have contributed—they have greatly helped fund our summer internship programs for the past two years. It enabled us to accept and support 47 summer interns in 2025! We aim to accept even more of the several thousand who will apply for summer 2026.
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