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Dental implants can hijack your immune system, scientists discover
Researchers have uncovered a surprising reason dental implant infections often resist antibiotics: the implants themselves can contribute to the problem. Bacteria corrode titanium implants, releasing microscopic particles that hijack immune cells, trigger destructive inflammation, and accelerate jawbone loss.
State Fair of Louisiana Celebrates 120 Years with Championship Rodeo, Family Fun and Entertainment
Photo Courtesy of State Fair of Louisiana SHREVEPORT, La. — A Louisiana tradition 120 years in the making is gearing up for another exciting celebration as the State Fair of Louisiana returns to Sh…
State Fair of Louisiana Celebrates 120 Years with Championship Rodeo, Family Fun and Entertainment
Photo Courtesy of State Fair of Louisiana SHREVEPORT, La. — A Louisiana tradition 120 years in the making is gearing up for another exciting celebration as the State Fair of Louisiana returns to Sh…
Mobile science lab
Billy Roden, left, Seattle Children’s Mobile Science Program manager, takes answers to a question he posed to Rasa Conklin’s fifth-grade science class on Wednesday inside the mobile science classroom at Salish Coast Elementary School in Port Townsend. Dr. Noelle Machnick, rear, in lab coat, helped moderate the class.
Why Chinese pundits say France’s riots could reshape European politics
Protests stem from falling competitiveness with an eroded middle class, providing ‘fertile ground’ for polarisation, observers say.
Críticas: On bikes and politics
In college, I rode my bike everywhere I went. It was this slick yellow roadster with checkered flag rim tape. I called it el italiano. I’d take it to
Alleged mice infestation at Albuquerque middle school raises health concerns, staff & parent outrage
Staff and parents at James Monroe Middle School in Albuquerque report a recurring mice infestation, with droppings, urine, and dead rodents found throughout the campus, prompting health concerns and grievances against Albuquerque Public Schools.
Western Way Entertainment brings trick riding, mounted shooting to ABAC PCA Pro Rodeo
When the PCA Pro Rodeo returns to Abraham Baldwin Agricultural College Nov. 13-14, the competition inside the arena won’t be the only thing keeping fans on the edge of their seats.
I’ve used the Pixel 11 Pro XL and iPhone 18 Pro Max, and Apple’s ecosystem isn’t enough anymore
I've used iPhones for almost two decades, and much of what made Apple's devices an easy choice has eroded.
Symposium highlights MIT’s wide range of innovations for aging brain health
In six talks, researchers from across MIT described Aging Brain Initiative projects aimed at advancing the understanding of and interventions against neurodegenerative diseases such as Alzheimer’s, Parkinson’s, and ALS.
Study identifies protein regulator of tau linked to Alzheimer’s disease
The accumulation and tangling of tau proteins is a well-known feature of Alzheimer’s disease. Less understood is how different forms of tau are regulated and what happens to that balance as the brain ages and neurodegenerative disease develops. A study from The University of Texas at San Antonio’s Health Science Center published in July […]
Scientists uncover 3 key brain pathways linked to lasting depression relief
Researchers have uncovered three brain pathways linked to lasting improvements in people receiving deep brain stimulation for severe, treatment-resistant depression. They also discovered that patients who failed to improve after two years shared a striking pattern: insufficient stimulation of a crucial brain connection. The findings suggest that millimeters in electrode placement could make a major difference in treatment outcomes.
Sacramento health inspectors found 251 rodent droppings in this facility. Where?
Sacramento County Health Inspectors gave red placards to six eateries and cited 12 other facilities.
Health department shuts down Lexington Mexican restaurant
The health department closed the 1030 South Broadway Jalapeno’s location for “evidence of rodents.”
Lincoln City Council chair calls AG's move seeking legal fees 'political intimidation'
Lincoln City Council Chair Brodey Weber on Wednesday called Nebraska Attorney General Mike Hilgers' recent move seeking legal fees from the city “political intimidation.”
Scientists reviewed studies covering 1.17 million children and found a major research gap
Researchers identified 104 pregnancy and birth cohorts representing more than 1.17 million children across 41 countries, documenting the availability of data on early-life nutrition and neurodevelopment. Approximately 99% of participants in the income-stratified analysis came from high- or upper-middle-income countries, while differences in data collection and assessment methods complicate future international comparisons.
Tiny platform creates and directs microbubbles on demand
Set within a 3-millimeter area on a chip, the new device produces hydrogen gas bubbles on a grid of electrodes, then powers the bubbles up with acoustic energy through ultrasound.
College Still Has a Future, but It's No Longer the Default Choice (opinion)
High costs and political bias have eroded higher education’s standing.
The politics of city rats: What urban rodents tell us about housing and sanitation
Rats are on the ballot in Canadian municipal elections this fall, with several political parties promising to tackle city rat problems. While rats may seem like a niche election issue, they can point ...
The politics of city rats: What urban rodents tell us about housing and sanitation
Why have cities had so little success in reducing rat numbers? It’s usually because they’re failing to address the larger social services issues that allow rats to thrive.
Workday CEO Aneel Bhusri’s unfinished business
Workday rode a startup revolution in the 2010s to become a Fortune 500 software company. Can it turn back time to survive a new, AI-led uprising under the tutelage of one of its founders?
We're moms with 7 kids between us, and we went to Disney World alone
My friend and I are both moms and left our seven kids at home to go to Disney World. We visited three parks, rode 12 rides, and loved every minute.
NVIDIA-Backed Upscale Wants to Make Rival AI Chips Work Together
NVIDIA GPUs dominate today’s AI data centers, but they’re no longer the only processors companies want to use. Cloud providers are developing their own AI chips, while specialized accelerators are entering the market. Getting these different processors to work together efficiently is creating a new challenge for data center operators. That’s the problem Upscale hopes […]
'Freakish' discovery of 9 million-year-old capybara tooth supports idea that Atacama wasn't always a desert
A 9 million-year-old capybara tooth was found in the Atacama Desert, a surprising find given that these rodents love water.
New resolution calls rat problem in Northeast Philly a ‘public health emergency'
A new resolution urges the Health Department and other agencies to coordinate an urgent response to rodent activity in Lower Northeast Philly.
Rodenbaugh's co-owners continue 60-year legacy of downtown Allen business
Gary and Ronald Rodenbaugh continue running the downtown Allen home improvement business their father Donald opened in 1962.
Meet the former MMA fighter building his business in Prince William County
On Sept. 1, a retired mixed martial arts fighter strode into board chambers at the Prince William County government center complex in Woodbridge. This time, he was seeking a different kind of knockout.
Euro faces political, fiscal reckoning as it hovers near 17-month low
The euro struggled near a 17-month low on Tuesday, weighed down by political uncertainty and fiscal concerns across the euro zone, while the dollar extended its blistering rally as it rode US Treasury yields higher.
Why plugged-in pickle glows: Engineer burns 100-plus pickles to find answer
An engineer says glowing pickles owe their orange light to sparks igniting hydrogen near an electrode, with sodium ions supplying the color.
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
Questions persist around horse deaths at Humboldt County Fair
The events attending veterinarians said the incidents were ‘bad luck accidents,’ but also pointed to laxness of rodeo regulation versus horseracing.
Artists remember veteran concert producer Susan Lim and her decades in entertainment
Photo from Facebook/@susan.o.lim Artists and colleagues are remembering veteran concert producer Susan Lim for a career that spanned Philippine productions and overseas tours for Filipino performers. Lim died Sept. 14. Pops Fernandez, Martin Nievera and Roderick Paulate were among those who later shared public tributes, recalling both her work in entertainment and their longtime friendships with her. Lim had been active in…
Dennis Schroder 'Really Happy' to Be on Charlotte Hornets
The Charlotte Hornets acquired Dennis Schroder from the Cleveland Cavaliers.
Scientists could one day remove your bad memories. Here's how
Madeleine Finlay hears from Steve Ramirez, an associate professor of psychological and brain sciences at Boston University, whose book How to Change a Memory was shortlisted for this year’s Royal Society Trivedi science book prize. He explains how scientists have been able to locate memories in the brains of rodents, trigger them artificially and even remove them, and reveals what the practical applications of this science could one day be for humans.
In 2021, Australian scientists sprayed wheat scent across farm plots to confuse hungry mice; the treatment reduced seed loss by up to 74% in a field experiment without poisoning the rodents
Australian scientists have tested a non-toxic way to protect wheat seeds from hungry mice by making it harder for the rodents to locate them. In an experiment carried out in 2021, instead of poisoning the mice or using bait, the researchers sprayed diluted wheat germ oil across farm plots to camouflage the smell of wheat seeds.
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 […]
Louisiana adds more public money to host rodeos, college sports events
Louisiana lawmakers increased the amount of public money the state will spend on college sports championships, rodeos and other entertainment events in this fiscal year to at least $12.1 million in direct support. State budget documents show it was previously slated to spend $10.4 million in the current fiscal year.
Selling AI insurance was hard enough. Then they got into the cafe business
Corgi, valued at more than $5 billion, was forced to rein in its real estate expansion plans this month after a series of mishaps including a citation for rodents and departure of key dealmakers.
When “DEI” research is cut, what happens to community health?
“I’m just going to run to the grocery store!” How many times have we said this without thinking about it? For most of us, it's usually an easy walk or a short drive to get the cheese we forgot. In reality, though, 13% of the U.S. population (about 39 million people) live in “food deserts,” which means living more than a mile from a grocery store in urban areas and more than 10 miles in rural areas. This was the case for people in Pittsburgh’s Hill District, where a quick run to buy food wasn’t an option. In the 1930s, federal maps marked the Hill as "hazardous" for lending, a practice known as redlining that steered investment away from Black neighborhoods. Decades of disinvestment followed, and residents went about 30 years without a nearby grocery store. This made it hard to keep healthy eating habits and contributed to chronic disease. When a grocery store finally opened in the area in 2013, researchers saw the opportunity and launched the PHRESH study, which initially compared the health of participants from the Hill district to those in the Homewood district. Over time, the study expanded to other factors such as brain health and Alzheimer's risk. Residents like Roderick Blair overcame initial hesitation to share their health data, trusting it would benefit their neighborhood. Then, in August 2026, the NIH abruptly canceled the study’s grant, citing that it was “subjective” and fell outside their scientific scope—an effect of the administration’s interpretation of diversity, equity and inclusion (DEI). Research like PHRESH can help determine what changes in a neighborhood actually improve health, so cutting it has left that question unanswered. Other canceled studies have examined health issues like maternal health, preterm birth rates, or sickle cell disease. Courts have reversed some of these grant cancellations, but not all of them. If we really want America to be healthier, research into why some communities get sicker than others is absolutely critical. The law that created the federal minority health research institute passed with bipartisan support in 2000. But these days, as evidenced by grant cancellations, the political shift in attitudes toward DEI means we often lose access to the health information we need to help all communities thrive. DEI vs. health equity vs. equality and the overlap (or lack thereof) The letters “DEI” evoke very different reactions depending on who you are in the U.S. DEI programs can address gender, disability, age, and other factors, but the fiercest debate centers on race. For some people, hearing DEI brings to mind policies that may have cost them a job or a college seat because they are white. Others see DEI as a matter of justice: a way to expand representation and opportunity for groups that have been historically marginalized. Both perspectives are rooted in lived experience, and both center on the same question: whether hiring and admissions practices are fair. Hiring and admission practices, though related, are not the same as health equity. Health equity is “the attainment of the highest level of health for all people.” It’s the recognition that some groups of people consistently experience worse health outcomes than others. For instance, black mothers die from pregnancy-related complications at three times the rate of white mothers, and rural Americans are more likely to die from issues such as heart disease and cancer. Equity is also often conflated with “equality,” which leads to misunderstanding of how to actually best support communities. Equality ignores the fact that we aren’t all starting life with the same resources or circumstances, whereas equity is about helping people get what they specifically need based on their situation so they have the chance to achieve the same outcome as anyone else. For example, if every household in Pittsburgh got a $30 grocery gift card, that would be equal. But during the decades the Hill District went without a grocery store, that card wouldn’t have helped much. Equity means making sure everyone can actually access a store in the first place. DEI policies can overlap with health equity in many ways. For example, they may help expand access to quality education and stable, well-paying jobs, which in turn can provide health insurance, safer housing, and improved finances—all of which can reduce health disparities. But to make that happen, we first need data to identify disparities in communities and to develop solutions that effectively address them. What we lose when the research stops Community data is important to health equity because: You can’t fix what you don’t see: Data show which communities are most affected by health factors such as infection, heart disease, and cancer. If we don’t know what is happening and where, then we can’t develop interventions to help. Poor health costs everyone: Chronic disease is expensive—both to the individual person and to the overall economy. Understanding what groups of people are most at risk allows us to develop interventions that can save everyone money. Disparities exist for many communities: Health equity includes disparities that exist due to a whole host of factors, such as family background, race and ethnicity, rural vs. suburban residence, gender and sexual orientation, veteran status, disability, and lower income. This means many Americans can benefit from research into differences in health outcomes and how to improve them. Trust is easy to lose: Some participants in the PHRESH study were initially vocal about their concerns about participating. But that trust was earned because the researchers kept their promises and centered their work on the community. When projects are canceled mid-cycle, researchers have no choice but to leave behind communities they had promised to help. This hurts trust in the long run. It’s also a very inefficient use of resources, and it will take significant time and effort to redo the work when the government realizes this work is important again. How should we talk about health equity? This is hard because the words “equity” and “DEI” are currently very politically charged. So whether you’re a public health professional, teacher, or friend, how we talk about this topic matters. The right framing can help people who might otherwise be skeptical see why health equity research is important and deserves funding. Here are some suggestions to help your conversations: Choose your words strategically: Who are you trying to reach with your message? Are they likely to be resistant to terms like “diversity” and “equity”? If so, find alternative words to use to still get the message across. It is frustrating to be in that position, but the goal of improving health is too important not to try to make inroads. Sometimes simply reframing can help the message reach those who need to hear it. Focus on the problem: The terms “health equity” and “DEI” are abstract. Make it more specific. For example, discuss differences in maternal death or ways to improve health outcomes in rural communities. These still have equity at their core but will likely be better understood by those you’re talking with. Focus on systems: Disparities exist, but if they are communicated poorly, people can mistakenly think the issue is the individual’s fault. Disparities are largely driven by failures of the system—such as lack of access to health care and a long legacy of racism. When discussing the disparities, frame them around these systemic issues to ensure blame isn’t placed on the individuals impacted. Tell stories: Personalize these policies by using stories from those impacted that connect to the data you’re trying to convey. This helps make the policies and outcomes more concrete and meaningful. Bottom line Some communities end up sicker than others. That’s just the facts. We can argue about the best way to do that research, but canceling it simply because it may be linked to DEI doesn’t make anyone healthier. It just leaves communities like the Hill district behind. And in the end, it causes us all to move backward in our efforts to improve health in this country. Love, EM Big thanks to MacKenzie Isaac & Legairre Radden, who reviewed this piece and generously shared their expertise and lived experience to help improve it. Dr. Liz Marnik, PhD, is Executive Director of The Evidence Collective and a science communicator and immunologist working at the intersection of public trust, science, and public health. To discuss communication training on topics like health equity and storytelling, email Liz at liz@yle.health or learn more on our website. Your Local Epidemiologist (YLE) comprises a team of experts, ranging from physicians to immunologists to epidemiologists to nutritionists, working together with one goal: to “translate” ever-evolving public health science so that people are well-equipped to make evidence-based decisions. The YLE suite of newsletters reaches over 475,000 people across more than 132 countries. This newsletter is free to everyone, thanks to the generous support of fellow YLE community members. To support the effort, subscribe or upgrade below: Your Local Epidemiologist is a reader-supported publication. To receive new posts and support my work, consider becoming a free or paid subscriber. Subscribe
Dixie National Rodeo announces 2027 entertainment lineup
Agriculture Commissioner Andy Gipson announced the entertainment lineup for the 2027 Dixie National Rodeo on Tuesday during a news conference at the Mississippi Trade Mart, ahead of the Mississippi State Fair’s Oct. 8 opening.
Year-End Tax Planning: What Successful Businesses Should Do Now
Voice of Business Blog Guest post from Greater Rochester Chamber member Tiffany Brown, CPA, Bowers A profitable year is something every business owner hopes for-until they start thinking about the tax bill that comes with it. If your business is having a stronger year than expected, the good news is that you may still have…
California health officials warn of possible measles exposure in 6 counties
California health officials are on the lookout for new measles cases, after someone with the vaccine-preventable disease rode a passenger train and busses through six counties.
A 9-Million-Year-Old Tooth Just Challenged What Scientists Thought They Knew About the Atacama Desert
Scientists were surprised to discover a fossilized tooth from a capybara that lived almost 9 million years ago in what is now northern Chile’s Atacama Desert. Chile’s Atacama Desert is an unlikely place to find traces of capybaras, the world’s largest living rodents, whose lives revolve around water and wetland plants. Yet a fossilized tooth
Scientists Say Antarctica's Lost 'Supermountains' May Have Fueled an Explosion of Life on Earth
Millions of years ago, continental collisions created enormous mountains in what's now Antarctica. As they eroded, Earth's life thrived from their nutrient-rich deposits.
Backpack massages muscles when it detects they're fatigued
A backpack consisting of electrodes, cables and a soft massage head kneads muscles in the back when it picks up on them being fatigued
Scientists Just Found a Dino Artifact We’ve Never Seen Before—and It’s Answering a Major Riddle
Digital scans of the badly eroded tracks reveal how fast the most famous apex predator was walking—and why.
SCHEDULE: 2026 Brazos Valley Fair & Rodeo features youth livestock shows, live entertainment
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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]
Person with measles rode Amtrak trains and buses across CA, health officials say
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What Does the Science of Climate Change Really Look Like?
Editor’s Note: This is the second in a three-part series on how the Right should think about environmental and climate policy. Read Chris Barnard on Reclaiming Environmental Policy from the Left. More than a decade ago, the world’s governments negotiated and signed the Paris Climate Agreement, committing to hold global warming well below 2 degrees Celsius. In the following years, climate had immense cultural power. Greta Thunberg emerged. Fortune 500 companies established net-zero plans. The U.S. got the Inflation Reduction Act. Then the pendulum swung back. President Donald Trump returned to the Oval Office, speaking of green energy as a “scam” and carbon footprints as a “hoax” and on all matters of international policy emphasizing bilateral engagement and power over globalism and cooperation. The technology companies that had been at the forefront of net-zero pledges and green leadership discovered the importance of all-of-the-above power to their visions for artificial intelligence and began quietly postponing or removing their targets. On the left side of the political spectrum, rising concerns about inflation and cost pushed climate lower down in the stated priorities of voters and stump speeches of politicians. The moment is ripe for a reset on the politics of climate change and for conservatives especially to chart a course that acknowledges and addresses the real challenges in plausible ways. So what should we think about climate change as we enter a post-peak climate era? If it is neither an apocalypse nor a hoax, what will hold up as a durable view of climate change? And how does it project onto the concerns and priorities of the right-of-center’s emerging coalition? New to Commonplace_? Subscribe below to get the magazine in your inbox._ Subscribe A Solid Foundation As the politics and economics of climate careened over the past ten years, the physics carried on regardless. In 2015, the year the Paris Climate Agreement was adopted, the world emitted 41.2 gigatonnes of carbon dioxide. By 2025, emissions had risen only 2.4%, to 42.2 gigatonnes, because falling emissions from land use offset increasing emissions from fossil fuels. But slow growth in annual emissions is not rapid decline, let alone net-zero, so carbon dioxide kept accumulating in the atmosphere, going from 399 to 426 parts per million. Global temperature kept rising too, from about 1.1 degrees Celsius above the 1850–1900 average in 2015, to 1.4 degrees above it in 2025. None of this should surprise anyone. Even most prominent skeptics, like the authors of the 2025 report commissioned by the Trump administration’s Department of Energy, accept the basic physics. Carbon dioxide added to the atmosphere at industrial volumes accumulates and traps heat that would otherwise escape to space. That heat warms the upper ocean and increases temperatures at the surface. Increased ocean heat and melting of land ice cause sea levels to rise. Changes in the climate become noticeable to us as subtle shifts in temperature and precipitation, seasons arriving early or late, changes in the surrounding ecosystem, and weather extremes. The much more meaningful debate is not about whether these things are happening, but about what it all means for human societies. (While it is a proxy measure of overall risk, no one experiences global surface temperature.) This debate invokes at least three interesting questions: how much today’s warming is showing up in regional climate trends, how much more warming we should anticipate, and how extreme weather events can be understood in the context of climate change. Recent scientific advances give us new insights into each of these, but there is still much to learn. This is the context in which the next generation of conservative leaders will be the first to deal with significant climate change as a fact, not a forecast. It will be with them for their entire careers. Our evolving scientific picture of climate change will come from weather and climate records stretching further into the past, new kinds of observations in the present, better modeling tools for the future, and simply more time to observe the emergence of climate signals and their tangible effects on ecosystems and communities in the United States and around the world. The policy landscape will be shaped by not only the impacts of changes in the climate, but also by the ways in which societies respond and by the emergence of new technologies for both altering the trajectory of emissions and adapting to new climate realities. Global climate records now show the fingerprints of warming in different phenomena around much of the world. The IPCC, in its most recent assessment report, documents warming trends over all land regions, even as natural variability adds substantial variance to local trends. And the highest temperature extremes have become more intense and frequent, almost everywhere, since the 1950s. Scientists are highly confident that these changes are attributable to human influence. But confidence in detecting trends and attributing them to human influence degrades across heavy precipitation events; drought trends are heterogeneous and not attributable to human activity with great confidence. For hurricanes, tornadoes, and other severe storms there is even less confidence in trends or their relationship to climate change. In general, a fair summary of the evidence is that for well-observed phenomena, like surface temperature or heavy rainfall, with a clear relationship to warming, our multidecadal observations are consistent with human influence overcoming natural variability over long time periods and extremes increasing. For regions that are sampled more sparsely, or phenomena with a higher noise-to-signal ratio, we will need to observe them longer to understand the magnitude of the climate signal or improve dynamical understanding using models and observations together. But for Climate For those who can’t wait, we also have new techniques that attempt to understand the role climate change has in influencing particular extreme events. When the climate is changing and disaster strikes, it is natural to ask whether that disaster was somehow “caused” by climate change. For scientists and policymakers acting in good faith, answering that question helps develop a more accurate picture of the problem, how it may be getting worse, and what preparations we should be making to respond to it. It may, at some point, give some weight to how liability is assigned by courts or adaptation funding is distributed by society. But how we ask this question is extremely important. It is easy to get the analysis wrong by discounting the role that meteorology plays. As meteorologist Theodore Shepherd explained in a clear 2016 review of climate attribution methods, “if a weather or climate event is truly extreme in the present climate, then perforce it requires unusual meteorological conditions, which means that climate change is at most a contributing factor.” Share Scientists have two ways to probe climate as a contributing factor, both of which have entered media coverage of extreme weather events. One asks a probabilistic question: How much more likely is a particular event (e.g., a temperature record over a particular area) amid global warming? The answer involves using historical records and computer simulations to estimate the likelihood of such an event in both a changed and a preindustrial climate. The findings are less about the specific event, and more about events of that nature. The other question is: How has the changed climate affected the specific event in question? Here, scientists try to understand what a similar event would have looked like in the preindustrial climate. This is sometimes called the storyline approach, where the story is the specific meteorological details of the event. These methods offer ways to test the intuition of scientists about real weather extremes. In late June and early July of 2021, a persistent high-pressure ridge, or heat dome, set up over the Pacific Northwest and an extraordinary heat wave affected the area from Oregon to British Columbia. For six days, it shattered temperature records across the region and hundreds died from heat-related causes, in an area where such high, and persistently high, temperatures were well outside of experience and many live without air conditioning. Scientists have studied its connection to climate change using multiple approaches. This specific event was created by a rare combination of meteorological factors, a strong high-pressure ridge created the conditions for extreme heat, which occurred on top of higher average temperatures in the region from global warming. Probabilistic analyses showed that climate change increased the likelihood of such an event by at least 8-fold to more than 100-fold. One standout example found that such an event had effectively zero probability of occurring in the preindustrial climate. The enormous range in these assessments reflects how hard it is to estimate probabilities of events at the tail of the historical record. Estimates of the effect on the temperature of the event are more clustered. A recent review paper documents how multiple methodologies have found a positive influence, roughly 1-2 degrees Celsius of an anomaly that exceeded 15 degrees, of climate change on the temperature magnitude of the event. Multiple studies have investigated and found some positive influence of climate change in other extreme events. Attribution studies found climate likely increased the heavy rainfall that accompanied Hurricane Helene in North Carolina and surrounding regions in 2024. The extensive fires that struck Los Angeles in 2025 illustrate how the causal chain can become messy, though. Studies do detect a positive influence of climate on the event’s likelihood, but while climate change likely contributed to underlying aridity, it would not have played a role in the heavy winds or land practices that preceded disaster. These event attribution studies will become more common for extreme, or damaging, weather events. They can be produced quickly, and often are reported before peer review. As the Pacific Northwest heatwave example shows, when multiple methods converge on a positive attribution, the finding should probably carry some weight even if you have to be careful about accepting the results from a single study. I expect that as climate change proceeds and the climate thus departs further from a preindustrial counterfactual, the influence will become more detectable across a variety of extreme events and more easily identified. This will be used to cast blame, but can also be used to inform how communities and society adapt to ongoing change. We May Still Be Surprised One positive development, insofar as less climate change is better, has been that our central estimates for future climate change should probably be revised downward. Mostly, that is because the high-end warmings that scientists regularly analyzed about ten to 20 years ago, driven by high emissions throughout the twenty-first century, now appear to be somewhere between unlikely and impossible. At one time, the upper end of mainstream climate projections extended well into 4 to 6 degrees Celsius of warming by the end of this century, which, models suggest, would have wrought enormous real-world damage. Current energy and policy trends now point toward 2.5 or 3 degrees. Damages and risks are commonly modeled as increasing steeply with more warming, so this is already a better-than-previously-expected outcome for the climate (which is independent of the physical response to emissions). But we should maintain a wide range for plausible outcomes and prepare for the possibility of being surprised. Emissions trajectories are subject to deep uncertainty, the physical climate response is still developing, and whatever change occurs in the climate will then be mediated through unpredictable economic, social, and political institutions. Over the past decade, the pace of warming surprised some keen observers and appeared to accelerate, though not yet outside the range of expectation provided by climate models. The reasons for that apparent acceleration are being actively studied (as was the apparent pause in warming from 1998 to 2012), but no single driver has emerged. Some blame it on the El Niño, variability which would have no bearing on climate. Some think it is a result of factories in East Asia and global shipping fleets cutting aerosol emissions, which in the strongest version of the argument would indicate higher climate sensitivity to carbon-dioxide emissions. Others are more measured, not yet ready to draw solid conclusions as to whether climate projections require revision. We will have to see. Long-Term Thinking Climate change asks us to think over long time scales. But the pace of human-driven warming is compressing a large global change into a century. Changing weather patterns and extreme events are already causing adjustment costs and damages and will do more. Adaptation will help, but it is not free. For some communities, these costs will erode livelihoods and well-being, and may force migration. Are we prepared for large-scale managed retreats in the United States? Thankfully, American wealth, geographical diversity, and moderate climates may leave us better prepared than many around the world. But wealthy countries can still suffer serious disruption from narrowly concentrated costs, even if they appear entirely manageable in aggregate. Readers of Commonplace are familiar with the challenges of rapidly adapting to economic forces. The displacement that came from the China Shock is barely perceptible in aggregate GDP and employment data, but it affected millions of people and those people were far less mobile than economic models tended to assume. Deindustrialization rippled through the nation with enormous effects for not only our economic vitality, but also our national security. The forces surrounding climate change may not be so different; the world gets richer and must accept some diffuse costs. Those may be modest overall, but cause all manner of unpredictable effects with which policymakers must cope. In the case of the China Shock, our faith in a growing pie served us poorly. We’ll need to do better on climate. Leave a comment
Scientists create human-mouse hybrid
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This German submarine sank in 1917. It’s still leaking TNT
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This year’s rodeo event has new additions to its event list like musical performances from artists like Niko Moon Wednesday night, following the Jim Baier Chute Out.
Tri-State Rodeo celebrates 78 years with musical talent and bull-riding entertainment
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UNC Charlotte's Truman Lab awarded new $2.1 million grant from the National Institutes of Health
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UNC Charlotte's Truman Lab awarded new $2.1 million grant from the National Institutes of Health
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GenSight Biologics Provides September 2026 Business Updates
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Rodeo Tickets for Fort Worth Stock Show & Rodeo Go on Sale September 14
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Texas Association of Business Names Kelly Keel as New President & CEO
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Future Skin Seminar 2026 – Bridging Science and Innovation in Skin Research
November 16–18, 2026 | Madison Hotel, Hamburg | A 3-Day Seminar by SGS proderm
4 The Weekend: A storm of entertainment happening in Southern Arizona
You can get conned, enjoy great music with a spectacular view or experience a rodeo with all the extras. All part of the fun happening 4 The Labor Day Weekend.