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Scientists have found a new way molecules can cooperate at room temperature
What if glowing molecules could synchronize, much like fireflies flashing in unison? Researchers have discovered that molecules confined within tiny gold nanostructures can behave collectively, coordinating ...
A new process turns plastic waste into gasoline and diesel fuel
Scientists at Oak Ridge National Laboratory have developed a surprisingly simple way to turn polyethylene, the common plastic used in shopping bags and cutting boards, into gasoline and diesel-like fuels. The process uses inexpensive aluminum-based molten salts to break long plastic molecules into smaller hydrocarbons, producing about 60% gasoline under relatively mild conditions.
Scientists Created a Computer Inside a Water Drop Using Billions of DNA Molecules and It Worked
You won’t believe it, but DNA molecules can turn even a tiny drop of water into a computer.
We smell different as we age. Here's why.
An odor-producing molecule 2-nonenal is only part of the story.
Scientists infected a 'vagina on a chip' with gonorrhea — then cured it with a new antibiotic found by AI
To sift through 6 million molecules in pursuit of new gonorrhea treatments, researchers trained AI to select the best drug candidate and then tested it in a "vagina on a chip."
Can the Sugar Molecules That Coat Our Cells Predict Our Health?
Can the Sugar Molecules That Coat Our Cells Predict Our Health?: Glycans, once ignored, may revolutionize medicine
Chemists uncover how unthinkable reactions occur in unimaginable conditions
FIU chemists reveal how complex organic molecules can form in the far reaches of space.
New grant to improve discovery of potential diagnostic, therapeutic molecules
Carly Schissel, assistant professor of chemistry, is part of a multi-institution team that has been selected to receive funding from the Scialog: Automating Chemical Laboratories initiative. The initiative supports teams of early-career scientists doing fundamental science to accelerate advances in laboratory technologies using automation and artificial intelligence.
AbbVie partners with IPO-bound Iambic for AI-led drug discoveries
AbbVie is looking to a Nvidia-backed, AI-driven drug development company to accelerate its small molecule discovery.
Search for life on Mars takes major leap forward. Scientists detect longest organic molecules on planet to date | BBC Sky at Night Magazine
Scientists make discovery analysing rock pulverised for study by Curiosity rover. Largest organic compounds found on the Red Planet to date.
Scientists Push Molecules on a Surface to the Ultimate Quantum Limit
An ultra-clean crystal surface allowed individual molecules to preserve quantum coherence at the fundamental Fourier limit. A molecule placed on a surface should be easier to probe and manipulate than one hidden inside a solid or suspended in vacuum. In practice, however, surface contamination creates an unstable, noisy environment that can quickly degrade the molecule’s
A Sweet Surprise: Scientists Find Sugar Deep in Our Galaxy
It’s the first time a sugar molecule has been detected in interstellar space. The discovery provides tantalizing new clues into how life may have arisen on Earth.
Scientists Built a Molecule From Ordinary Atoms—and It Doubled Survival for a ‘Hidden’ Cancer
One giant molecule grabs the mutant proteins behind runaway tumor growth—and refuses to let go.
Here’s a look at the Nobel Prizes for science
An icy window into the cosmos, a light switch for the brain and solving the mystery of mirror image molecules all took home the top prize.
Mirror life: Scientists clash over threat of lab-engineered bacteria
Bacteria created using mirror images of natural biomolecules would pose a grave threat to life on Earth, some researchers warn, but a new study suggests they would struggle to survive in the wild
Scientists design 'tunable' biomolecules to probe how sugars behave
Sugars are not just a source of energy—they also play a crucial role in how cells communicate, how proteins interact and how materials behave in medicine and industry. But studying these processes is ...
Radio telescopes help scientists map molecules in space and uncover where and how stars form
Interstellar maps can help scientists find patterns that tell them about fundamental chemical processes in the cosmos.
Sleep, appetite, gene-editing experts contend for Nobel chemistry prize
Molecules that regulate sleep and appetite or methods for editing genes are some of the research fields commentators say could be contenders for the Nobel Prize in Chemistry announced Wednesday.This y...
25 years ago click chemistry changed science. What happened next?
Barry Sharpless and his team first introduced the concept of 'clicking' molecules together 25 years ago
Ultrafast X-rays capture chemistry unfolding atom by atom
Ultrafast X-rays revealed how a molecule converts absorbed light into motion in just trillionths of a second. Individual atoms recorded different stages of the process, opening a powerful new window into light-driven chemistry.
A Mars rover found organic carbon just sitting on a rock
The organic molecules could come from life or from ordinary chemistry — only samples returned to Earth can settle it.
Chemists set electrons free and break a decades-old chemistry barrier
Chemists have developed a catalyst that breaks a long-standing rule governing which molecules receive electrons during chemical reactions. By releasing electrons directly into solution, the technique could unlock reactions—and potentially useful new molecules—that were previously out of reach.
Eastlake science students make district history
Three Eastlake High School students made Sweetwater Union High School District history this year when they became the first students from the district to qualify for the International Science and Engineering Fair, an international competition that brings together some of the top high school researchers from around the world. Ronald Wyatt, Giles Del Priore and Ihan Sung advanced to the competition after successful runs at regional and state science fairs. Sung went a step further, placing fourth in the chemistry category at ISEF. The students were recognized on Aug. 10 during a Sweetwater Union High School District board meeting at the district office in Chula Vista.For Wyatt and Del Priore, recent Eastlake graduates, the journey began with a shared concern about dementia and the challenges faced by families caring for loved ones with memory impairment. Their engineering project, “Design and Evaluation of a Behaviorally Grounded Caregiver-Governed AI Companion for Individuals with Memory Impairment,” earned the Sweepstakes Award at the Sweetwater District STEM Fair and first place in its division at the Greater San Diego Science and Engineering Fair. The project explored whether Artificial Intelligence could provide companionship and support while helping reduce stress for people with dementia and their caregivers. “Our inspiration came from personal experience. Both of us have seen family members and loved ones affected by dementia, and we’ve witnessed how overwhelming the caregiving process can be,” Wyatt said. Del Priore said the students also wanted to address the high cost of third-party health care services while creating something that could potentially help their own families as well as people elsewhere. The students developed an AI system designed with safeguards intended to prevent misinformation reinforcement, emotional escalation and unsafe responses. In 240 controlled trials involving memory, identity, agitation and neutral scenarios, they said the system consistently prevented harmful incorrect reinforcement while using context-aware silence, de-escalation and caregiver verification. The project required the students to combine Artificial Intelligence, psychology, neuroscience and human-computer interaction. For Del Priore, one of the biggest technical challenges was getting the AI companion to communicate verbally with a patient. Hardware limitations required the students to collaborate with multiple Python libraries for speech-to-text and text-to-speech functions while keeping the cost of the companion low. “For us, the biggest challenge was translating complex behavioral and cognitive care principles into a functioning AI system,” Wyatt said.Qualifying for ISEF was a milestone that student expected. The international competition proved to be another milestone. “Competing at ISEF was an incredible experience and unlike anything we’ve ever done before,” Del Priore said. “Being surrounded by some of the most talented young researchers from around the world was both inspiring and motivating.” He said the experience stood out because of the emphasis on collaboration, innovation and scientific discovery. “The most memorable part was seeing how people from completely different backgrounds and disciplines approached solving real-world problems with creativity and passion,” he said. The students also credited teachers and mentors who supported their work. Del Priore said his sophomore-year AP Physics teacher, Dr. Price, was particularly influential. “Through all of my personal and academic struggles, Dr. Price always believed in me,” Del Priore said. “All of his faith in me really molded me into the person I am today and helped create my love for science even through tough times.” Wyatt is continuing his education at UC Santa Cruz, where he plans to study biomolecular engineering and bioinformatics, with an interest in research involving Artificial Intelligence, biology and health care. Del Priore plans to double major in chemistry and accounting. Sung, a rising Eastlake senior, qualified for ISEF after winning first place in the Engineering: Energy, Materials & Transport category at the Greater San Diego Science and Engineering Fair and first place in chemistry at the California Science and Engineering Fair. His project, “Renewable Ammonia Electrochemical Synthesis by Glow Discharge with an Iron-Based Catalyst,” involved a device he designed and engineered to produce renewable ammonia, with potential applications in fertilizer production and energy storage. Sung became interested in the project after considering the relationship between food insecurity and fertilizer costs. His system uses plasma to break apart nitrogen molecules so they can interact with hydrogen and form ammonia. At ISEF, Sung competed against more than 1,700 students from 65 countries and earned fourth place in chemistry. “I am proud to become one of te first students in the district to qualify for ISEF because this milestone can inspire others in the district to attain similar goals,” Sung said.
Scientists discover new blood group, resolving a 50 year medical mystery - Futura-Sciences
Decades of searching for a single molecule Scientists named the missing molecule from the 1972 sample the AnWj antigen. For fifty years, hematologists tried and failed to find the genetic blueprint responsible for it. A research team at NHS Blood and Transplant and the University of Bristol finally found the...
Nobel Prize 2026: Three Science Discoveries That Sound Straight Out Of Sci-Fi
This year's Nobel science winners were honoured for their research on tiny particles from space, using light to control brain cells, and studying mirror-image molecules.
Nasa rover detects potential signatures of ancient microbial life on Mars
Perseverance identifies organic carbon molecules in rocks on riverbed that carried water billions of years ago
New York Islanders vs. New Jersey Devils: Home opener thread
The Islanders host the Devils for their 2026-27 home opener Saturday night. They’re on a 7-0-1 run against the Devils so expect a certain loss. Here are the tweaked lines as Pete DeBoer searches for chemistry, whether or not he has the elements and molecules to find it: mil Heineman – Bo Horvat – Kyle […]
Scientists Resurrect 160-Million-Year-Old Molecules With Surprising Power Against Superbugs
Ancient mammalian antimicrobial peptides revealed stronger bacteria-killing activity in some cases, offering clues for designing future treatments against resistant infections. Some proteins that vanished millions of years ago may still have something to teach scientists about fighting modern infections. University of Oregon biologists have reconstructed antimicrobial molecules dating back as far as 160 million years,
Scientists found two powerful new ways to destroy forever chemicals
Scientists are testing two promising ways to destroy PFAS, the stubborn “forever chemicals” that can accumulate in water and resist normal treatment. One method uses collapsing vapor bubbles to generate extreme heat and reactive molecules, while the other uses cold plasma and rising gas bubbles to pull PFAS to the surface and break them apart.
Chemistry textbooks have been getting this wrong for nearly 100 years
A foundational chemistry concept found in textbooks for almost 100 years may have been taught incorrectly. Researchers say the inductive effect in neutral molecules appears to extend only across one chemical bond, rather than gradually weakening over three or four bonds as traditionally taught. The team argues that updating this explanation could make organic chemistry easier to understand and provide a stronger foundation for future research and innovation.
A tiny universe in a bottle reveals clues to the origins of life
Researchers have created cosmic dust from scratch by recreating space-like conditions inside glass tubes. The dust contains complex carbon-rich molecules built from elements essential to life and produces infrared signals similar to real material found in space. By studying these laboratory samples, scientists can explore how organic chemistry unfolds around stars and how comets, asteroids and meteorites may have carried those ingredients to Earth.
Your gut may be making a molecule that raises Alzheimer’s risk
Scientists have linked a gut bacterial compound called ImP to greater Alzheimer’s risk, harmful brain protein buildup, and faster cognitive decline. The finding raises the possibility that reducing ImP in the blood could one day help slow or prevent dementia.
NVIDIA Joins European Commission Initiative to Expand AI Resources for Science
Oct. 15, 2026 — Much of today’s scientific progress begins with computation. But turning accelerated computing’s potential into scientific progress — modeling climate systems, designing molecules, simulating materials and more — depends on more than breakthrough technology. Especially for smaller labs, early-career scientists or science-based startups, the hardest part of research can be everything that […]
Scientists reprogram brain immune cells to fight Alzheimer’s
A newly identified molecule called OLE helped restore the brain’s immune cells to a more protective state in Alzheimer’s models. The treatment reduced toxic plaque buildup and improved memory, raising hopes for a new therapeutic approach.
Scientists Use Ancient Rains to Map the Possible Origin Life on Mars
Billions of years ago, rain may have helped shape where the chemistry of life could begin on Mars. A new study maps how formaldehyde, an important prebiotic molecule, may have reached the surface. This map could help guide future missions searching for signs of past life on Mars.
Scientists solve a 30-year rye pollen mystery that could transform cancer research
Scientists have finally solved a nearly 30-year-old mystery surrounding two unusual molecules found in rye pollen that once showed an intriguing ability to help animals fight tumors. By determining their exact 3D structures, researchers have unlocked the blueprint needed to investigate how these natural compounds interact with the immune system and which parts may be responsible for their cancer-fighting effects.
Twisted laser light can tell mirror-image molecules apart
Scientists have created twisted laser beams that interact differently with right-handed and left-handed molecules, revealing their identity through the fragments they produce. The approach could provide a faster, simpler, and more sensitive way to analyze important molecules used in chemistry and pharmaceuticals.
Mars’s Ancient Clay Holds the Same Organic Molecules That May Have Sparked Life on Earth
The team operating a remote chemistry lab onboard NASA’s Curiosity rover won a Gizmodo Science Fair award for discovering compelling chemical evidence that Mars could have once supported life.
Radio telescopes help scientists map molecules in space and uncover where and how stars form
You may have heard the phrase "we are made of star-stuff." This statement by the astronomer Carl Sagan refers to the fact that elements heavier than hydrogen and helium were forged in the centers of the ...
Misfolded insulin may be quietly driving diabetes
Researchers found that insulin-producing cells depend on a team of helper proteins to keep insulin production on track. When one key partner was missing, damaged proteins built up and the cells made less insulin. Strengthening this system could offer a new way to protect the pancreas as diabetes progresses.
Cleveland Clinic, RIKEN and IBM Team Advance to Finals for 2026 ACM Gordon Bell Prize
Cleveland Clinic, RIKEN and IBM has been named as a finalist for the 2026 ACM Gordon Bell Prize for simulating the largest biologically meaningful molecules ever modeled with quantum computers, reaching a scale of 12,635 atoms.
Researchers gather at Cornell Tech to explore AI for molecular science
Researchers from around the world gathered at Cornell Tech for a workshop exploring how physics-aware artificial intelligence can accelerate the discovery of molecules and materials while improving the reliability of machine learning models.
Cancer’s favorite escape trick may actually make it easier to kill
Scientists have uncovered a surprising new way the immune system fights cancer, overturning a core belief that has guided immunology for decades. The research found that when cancer cells shut down a key immune-recognition molecule called MHC I—a common trick used to hide from “killer” T cells—they can actually become more vulnerable to attack by a different group of immune cells known as CD4+ “helper” T cells.
A fifth-grader in Kansas City clicked ball-and-stick atoms together in science class and asked her teacher if she'd made a real molecule — he photographed it, sent it to a chemistry professor, and at ten years old she became co-author of a published paper on a structure nobody had ever described
A ten-year-old's casual question about her chemistry model kit led to a published paper describing a molecular structure that had eluded professional scientists for decades.
Scientists cut and rebuild molecules from the inside to create new chiral nanocarbons
Nanocarbons are molecular-scale carbon structures considered to be the building blocks for next-generation materials. Until now, scientists have built them by fusing small, flat carbon molecules together ...
Two deadly flowers could inspire powerful new medicines
Scientists have figured out how two famously poisonous plants create chemicals with surprising medical potential. After tracking thousands of genes in wolfsbane and larkspur, they identified six enzymes needed to build a complex compound called atisinium. The team recreated the process inside tobacco plants, offering a sustainable way to produce and test these rare molecules in larger amounts.
New nanoparticles make hidden chemical differences light up
Scientists have developed ultra-bright nanoparticles that can detect tiny amounts of chemicals and distinguish between molecules that look almost identical. The technology could one day provide a cheaper way to catch dangerous drug impurities or trace pollutants using simple low-cost lasers.
A tiny molecular basket unlocks a powerful new kind of chemistry
Rice University chemists have found a new way to make neodymium, a rare-earth metal, interact with oxygen. Using a specially designed molecular structure described as a “basket,” the team positioned the atoms so they could form a bond once thought unlikely. The breakthrough produced highly reactive compounds that could eventually give chemists alternatives to iron-based molecules used in biological reactions and chemical manufacturing.
This is what the 2026 Nobel prize for chemistry is all about
The Nobel prize in chemistry 2026 has been awarded to two scientists, Henri B Kagan at Paris-Sud University in France and Kensō Soai at Tokyo University of Science in Japan. Their discoveries showed how chemical reactions can produce an overwhelming excess of one of two mirror image forms of a molecule. Science journalist Linda Geddes tells Madeleine Finlay how this has become an important tool in drug development, allowing a greater understanding of how medicines work in the body
Dogs may hold surprising clues to human longevity
Dogs and humans may have more in common when it comes to aging than scientists realized. Researchers with the Dog Aging Project found that patterns of small molecules in dogs’ blood were linked to longer or shorter lifespans in remarkably similar ways to those seen in people. These metabolic “fingerprints” could offer clues about the biological processes that drive aging, including metabolism, inflammation, and cellular stress.
And the science Nobels for 2026 go to …
Top prizes went for an icy window into the cosmos, a light switch for the brain and solving the mystery of mirror image molecules.
AbCellera women’s health data top ‘most aggressive upside scenario,’ putting Astellas and Bayer on notice
AbCellera has reported phase 2 results “beyond even the most aggressive upside scenario” that its CEO dared to consider, boosting the biotech’s chances of challenging Astellas and Bayer for a women’s health market. The phase 2 clinical trial compared ABCL635, an antibody targeting NK3R, to placebo in patients with hot flashes caused by menopause. Investigators enrolled 92 postmenopausal women experiencing a mean of about 10 moderate or severe hot flashes per day. By Week 4, the number of moderate or severe hot flashes had fallen by a mean of 8.8 on ABCL635 and by 3.5 on placebo. That statistically significant, placebo-adjusted reduction of 5.3 hit the trial’s primary endpoint. The level of efficacy also cleared the bar set by existing drugs. While cross-trial comparisons can be misleading, AbCellera CEO Carl Hansen, Ph.D., had seen enough to start hyping the program. “We now view ABCL635 as a potential best-in-class non-hormonal therapy with strong differentiation against approved NK3R competitors across all important dimensions, including efficacy, safety, dosing and convenience,” Hansen said on a Monday morning conference call with investors to discuss the data. “We believe ABCL635 is now a highly de-risked program.” Last week, Hansen used AbCellera’s earnings call to set expectations for readout, with the CEO defining success as a clean safety profile and efficacy comparable to the two approved small molecules. The data vaulted over that bar. Astellas linked (PDF) one of the small molecules, Veozah, to placebo-adjusted reductions in hot flash frequency of 2.1 and 2.6 at Week 4 of its two phase 3 trials. Bayer reported (PDF) placebo-adjusted reductions of 3.04 and 3.29 at Week 4 of pivotal studies for its small molecule, Lynkuet. At 5.3, the placebo-adjusted reduction in AbCellera’s trial comfortably cleared the standard set by the incumbents. Veozah and Lynkuet came to market based on evidence of their ability to reduce the frequency and severity of hot flashes. AbCellera’s phase 2 study covered both endpoints, with the Canadian biotech reporting a mean reduction in severity of 1.4 points at Week 4 on ABCL635, compared to 0.3 points for placebo. Again, the placebo-adjusted result compares favorably to data on Veozah and Lynkuet. Analysts shared Hansen’s enthusiasm for the data. The phase 2 results “firmly validate ABCL635 as a potentially best-in-class treatment,” BMO Capital Markets analysts said in a note to investors Monday. ABCL635’s apparent efficacy edge “is likely attributable to the higher dosing/target engagement the asset is able to reach vs. the oral agents due to its wider therapeutic index,” the analysts added. The analysts, who model $2.3 billion in unadjusted peak sales for ABCL635, flagged the safety profile as another positive of the phase 2 readout. While Veozah carries a boxed warning for liver damage, nobody on ABCL635 in the phase 2 trial had elevated liver enzymes or bilirubin values. If replicated in phase 3, the lack of a liver signal could allow approval without the monitoring requirements imposed on Veozah. Investors appeared equally enthused, sending AbCellera's stock up 32% to $9.21 in premarket trading Monday from a Friday closing price of $6.93. Next, AbCellera will collect the Week 12 data and talk to its advisors about further development. The results open up “a wide variety of possibilities of how we might take this forward into phase 3 studies to truly maximize the value of the asset and make sure that ABCL635 is able to demonstrate its differentiation potential,” Sarah Noonberg, M.D., Ph.D., AbCellera’s chief medical officer, told investors.
AstraZeneca - How is AI helping scientists design the next generation of biologic medicines?
Learn how AstraZeneca combines AI drug discovery, laboratory automation and biology to refine biologic molecules and inform earlier decisions.
From shampoo to cookies, consumer products get an AI makeover
French cosmetics company L'Oreal has used AI to identify molecules in its skincare products that can be repurposed for use in shampoo and can now create products four times faster than before, a senior executive told Reuters.
Microplastics Have Been Linked With Myriad Human Health Problems. Scientists May Have Finally Figured Out How They Harm the Body
Lab experiments suggest that tiny bits of plastic can react with water inside us to produce highly reactive molecules. They can lead to damaging oxidative stress and inflammation
Science Vs on the 49ers Substation: Anatomy of a Hatchet Job
In August, Pablo Torre Finds Out and Science Vs released an episode about my theory that electromagnetic fields from the electrical substation beside the 49ers facility may be contributing to the team’s run of soft-tissue injuries. As the originator of the theory, I was also a subject of the episode. I sat was interviewed by Wendy Zukerman and Rose Rimler of Sciene Vs. I sent them research, connected them with scientists, and spent hours digging through the City of Santa Clara’s and Silicon Valley Power’s records to help clarify critical details. Both Wendy and Rose came off as affable and professional, showing curiosity during the interviews, with Wendy going out of her way to question the “conspiracy theory” framing itself. Then they titled the episode We Solve the 49ers Viral Conspiracy Theory. I was familiar enough with their catalog that I never expected them to agree with my theory, but I did expect them to give it a fair hearing and to deliver their findings honestly. On both counts they came up short. They were not directly dishonest in anything they said, but rather in what they left out, in how what remained was cut, and in the picture painted by those two things in combination. They asked me to recorded the interview on my phone for better audio quality, and I held on to my copy for reference later. That turned out to be a fortuitous decision. Here is the raw audio of my first interview, unedited*. Only my side was recorded, so their questions aren’t on it, but you can generally infer them from the answers, and every claim I make below about what I said can be checked against my statements in this clip. (Note: Wendy had connection trouble at the beginning of the interview and was cutting in and out, which accounts for the false starts.) 0:00 -1:19:13 Audio playback is not supported on your browser. Please upgrade. Science Vs is a fun show. It is pitched at roughly a high-school understanding of science, for an audience that is skeptical, Snopes-oriented, and worried about misinformation. Take a claim circulating online, interview a supporter of the claim, interview consensus scientists, and then tell people which side of the line it lands on. I have listened to their episodes on raw milk, seed oils, 5G and other contested issues in the wellness space. I have problems with all of them, but each at least made an honest attempt to represent the actual range of scientific opinion by talking to credentialed scientists with differing perspectives. Dissenting researchers were heard from, answered, and often given a chance to respond. This episode did not do that. This article is not a relitigation of the science. I have written extensively about that already. This post is for the record. It is simply an accounting of what was wrong with their episode. Contents Is there a power plant next to the 49ers practice facility? — the clearest single example of getting something objectively wrong For the record — a high-level overview of all of the problems with their investigation Draw your own conclusions — why they had to make this episode at all What they left out about childhood leukemia — the exposure threshold, and playing games with statistics to minimize sick children What they left out about the mechanism — the body of literature they refused to cover, and evidence for the mechanism used against it The scientists Science Vs interviewed and did not air — four credential scientists who support myhe theory, recorded and cut, or not even called How they misrepresented me and my case — an answer severed from its question, and three telling edits How you would actually study the injuries — it doesn’t actually matter which team is the most injured, overall The theory: magnetic fields, oxidative stress, and collagen Since the episode never states my theory, here it is below. Those who are familiar with my work can skip this section. Electrical equipment produces magnetic fields, and those fields induce faint electrical currents in anything that passes through them, including people. My argument goes further than induced current. Mitochondria — the structures that generate a cell’s energy — run on continuous flows of electrons and protons, and those flows carry faint electromagnetic fields of their own. Maxwell’s principle of superposition shows that when two fields share the same space, they add together. An external field does not need to be strong to alter an internal field, it only needs to be present. The electron transport chain inside the mitochondria leaks a small fraction of its electrons by design, and those become reactive oxygen species — free radicals, which healthy cells use as signals. External magnetic fields cause the rate of leakage to change, increasing free radicals. When free radicals accumulate faster than the cell’s antioxidant systems can clear them, the result is oxidative stress. Oxidative stress is a recognized driver of chronic illness, including cardiovascular disease, neurodegeneration, diabetes and cancer, and it is in every medical school curriculum. One of its ordinary effects in connective tissue is that it switches on matrix metalloproteinases — MMPs, the enzymes that break collagen apart — while suppressing new collagen synthesis. Tendons are made of collagen. An athlete loading his soft tissue heavily six days a week is already creating oxidative stress in the tendons, so the addition of magnetic field exposure compounds the damage and inhibits repair, making him more susceptible to injury when enormous force lands on a tendon in a fraction of a second. That is the theory. We know that EMF causes oxidative stress, and we know that oxidative stress degrades collagen. The only thing missing is a study showing that direct connection. I have never claimed certainty that the substation is contributing to the elevated injury rate. I do believe it is likely, and I believe it warrants caution, and that a revenue machine like a major NFL team can easily afford to remove the exposure out of precaution. Is there a power plant next to the 49ers practice facility? Here is the clearest single instance of the problem with this episode. It requires no knowledge of electromagnetic fields at all. This story first came to me through Jon Feliciano, a former 49er, in an interview on Willard & Dibs on 95.7 The Game. Asked about why the 49ers are always injured, he said players used to joke that it was the power plant behind the practice fields. Wendy Zukerman corrects him on air. “It’s important to say that it’s not a power plant near the 49ers site.” Torre then asks her to explain the difference between a substation and a power plant. Her answer: a power plant generates electricity and transmits it to a substation, which converts the voltage into something your house can use and sends it on to your home or your business. There are two problems with that. The first is that there is a power plant on that site. The Gianera Generating Station is a natural-gas-fired peaker plant owned by Silicon Valley Power, and it has been there since 1986. I have published aerial photographs of the location from 1987 in which the gas plant is the only thing standing, before the practice facility was even there. I even mentioned the gas plant in my first interview. (Feliciano has since gone on record about this issue, and it is clear he had the substation in mind rather than the gas plant.) The second is that her definition describes a distribution substation, and the facility beside the 49ers is not that. It is the Northern Receiving Station, which takes in bulk power from outside the city’s grid and delivers it to distribution substations. Silicon Valley Power’s own map distinguishes receiving stations from substations, and Rose Rimler even reads the label out loud in the episode when she walks through that map on air. A few minutes before the map segment, Zukerman tells Torre: “like I said, we fact check everything.” Well, maybe not everything. I made a mistake On the morning of July 6th, at 10:20, I sent Rose and Wendy two studies. During the interview I had been asked which human studies show oxidative stress from electromagnetic fields, and I had not been able to name one on the spot. Rose emailed asking for the studies, I quickly searched for a couple, and I wrote that I thought these were the most relevant from that search. Unfortunately, I was busy and did not read either one closely at first. I picked them because they were topically relevant — one on substation workers, one on power plant workers. Neither were great studies, and their problems go past the ones raised in the episode. That was careless on my part. There is context that did not make the episode, though. Before that email I had been on a Zoom call with Rose talking about EMF and oxidative stress, and I pointed her to Dr. Henry Lai at the University of Washington, who has spent years aggregating the literature on this question. His tallies show that roughly 90% of studies since the late 1990s find oxidative effects from electromagnetic field exposure — hundreds of studies, systematically counted. Rose told me she was already aware of his work. So when she asked for studies, I understood her to have the aggregate view already and that she would report anything within that context. Not reading those two carefully was still a mistake, but the larger mistake was assuming the episode would be based on a thorough review of the actual body of literature, rather than on whatever I happened to send that morning. The second email At 1:49 that same afternoon — three hours and twenty-nine minutes after the first — I sent them a second email that I had been preparing for a while. It was a structured document in six numbered sections, written in response to a request they had made two weeks earlier, laying out my entire argument with citations attached to every link in the chain. The episode aired on August 13th, five weeks later, and not a single item from the second email is in it. Here is how it opens: The full email is included at the bottom of this post in Appendix B. Nearly 1,500 words in total. It contains two named mechanisms with the physics behind them. Occupational studies in humans. The literature on oxidative stress and collagen. A section addressing the strongest counter-evidence against my own theory, which I raised myself. And a closing section stating plainly what the theory cannot yet show. My entire argument, in writing, with detailed citations for every claim, provided to them five weeks before broadcast, and none of it made it into the episode. That is the single largest omission, but it is not an isolated one. The whole episode is riddled with similar problems, and the conclusion they came to is not merely a difference of opinion about the scientific evidence. Through omission and through strategic editing, Science Vs misinformed its audience — about what the evidence shows, about what I argued, and about who they spoke to. That is a notable outcome for a show whose stated purpose is correcting misinformation. For the record I am not going to tell you that Science Vs set out to discredit me, or that they had come to their conclusion before they reported the story, or that they used misleading editing to make me look like a man retreating from his own theory. I cannot know what was in anyone’s head, and I am not going to pretend otherwise, either. What I can tell you is what is on the record. They asked me for evidence and aired the weakest thing I sent. They interviewed three scientists who supported my theory and aired none of them. They discussed childhood leukemia without ever saying the exposure level at which it appears. And they took an answer I gave weeks before Ken Karipidis, the one EMF scientist who was put on air, was interviewed, and placed it directly after his critique, where it comes off as a major concession. A friend of mine who has worked as a journalist for thirty years read that last one and called it sleazy. I agree with her. Those are just the four issues that are impossible to defend as pure editorial decision, but they are not the only issues. The most glaring issues stem from what they left out: The exposure level at which the childhood leukemia association actually appears — three to four milligauss, a number the episode never states despite it being much lower than what I measured. The mechanism itself: The episode gets as far as “oxidative stress could weaken collagen,” which leaves it sounding like speculation, rather than a known pathway. The second email, and all the studies in it. Dr. Paul Héroux at McGill, whose work my proposed mechanism rests on, whose contact details I supplied, and who was never called. Dr. Beatrice Golomb at UC San Diego, who runs a research group on oxidative stress and mitochondrial function and has specific expdertice in collagen, interviewed and not aired. Dr. David Carpenter at Albany, the most prominent academic voice on the harm from magnetic field exposure, interviewed and not aired. Dr. Joel Moskowitz at Berkeley, interviewed and not even credited. The specific, testable condition I put in writing that would make me abandon the theory. My own unprompted statement of the theory’s evidentiary gap. My caveats about my own measurements. My ranking of EMF as one factor among several rather than the only one. The new equipment installed at those facilities between 2010 and 2014, and the sharp rise in system load from 2013 onward. But that is not all. What they kept, they selectively edited to serve a narrative that was not served by the raw transcripts of the interviews. A description of thousands of commercial routers in a workplace, reduced to the Wi-Fi in your house. My own acknowledgment, multiple times, that "I'm not a scientist" clipped in an episode that spends considerable energy pointing out that I am not a scientist. And a qualification I volunteered about my own measurements, cut from my answer and delivered later by their EMF expert as a correction. Together their edit produce a portrait of a wellness guy with Wi-Fi phobia and two bad studies, backing away from his theory the moment a “real” scientist looked at it. A practice facility where nothing changed because no new substation was built. Injuries written off as random because the 49ers were not quite the single most injured team in the league over the period in question. That portrait is false even though almost no individual statement made in the episode is. Draw your own conclusions At the top of the episode, Pablo Torre says his show had been flooded with requests to investigate the substation — that it was the thing they were asked to look into over and over again. Neither show went hunting for this story. It arrived from their own audience, in volume, and it could not be waved off. A thread I posted on X reached twenty-two million people. A guy with a gaussmeter and a brand-new Substack obligated a Pultizer prize winning program to spend an hour on a question about player health, that is considered fringe enough that most media operations won’t touch it. Pablo Torre Finds Out could not ignore it. So Science Vs came in and ran a “debunking” operation instead of an investigation. Everything below is what had to be left on the cutting room floor to deliver the “debunking”. They could not ignore it. So they tried debunked it instead. The demand was strong enough to force an episode, and since the episodes release the 49ers have sustained more injuries, including season ending ones, and interest has only grown. Demand from fans and playets is strong enough to force a better investigation from someone else. An omission is not a lie until you find out what was omitted. What follows is the detailed record so you can see the full picture. Draw your own conclusions. I have drawn mine. I am going to keep publishing. A note about Pablo Torre Finds Out After the episode aired I posted publicly, calling out Pablo Torre Finds Out for concerns I had about the integrity of their investigation, and about an interview directly with Pablo Torre which had been offered but never happened. I have since spoken with a producer at PTFO. The offer had rested on a misunderstanding about where things stood between us, and it fell away as the Science Vs part of the production widened past the science. He apologized for the miscommunication and I accepted. The producer also confirmed to me that they did essentially hand off the entire investigation to Science Vs for narrative purposes — so Pablo would be genuinely curious or potentially surprised by their findings — while still taking responsibility for what went out under their name. I appreciated the candor and the accountability, and I am comfortable with where we left things. So this post is not about PTFO. My disagreement is with Science Vs. What they left out about childhood leukemia Childhood leukemia appears at three milligauss. They gave no number at all. 1. They built an EMF ruler, then discussed childhood cancer without it. The sequence on air went like this: First I measured almost 9 mG, then I measured up to 50 milligauss. Torre reacts with concern — “that sounds high.” Cut to Karipidis: the public limit is 2,000 milligauss. Torre reacts again — “What happens at 2,000?” Karipidis explains that nothing happens at 2,000, that safety factors are built in. Then: at more than 50,000 milligauss you get flickers of light in the retina, and higher still, nerve stimulation. The listener now has a ruler (their ruler) to measure these numbers with. Fifty is nothing by their ruler. Then the episode turns to childhood leukemia and states, accurately, that there is a real association — but tellingly, they never give the exposure level at which that association appears. Childhood leukemia appears at three milligauss. They conveniently left that out. The pooled analyses that produced the World Health Organization’s carcinogen classification found roughly a doubling of childhood leukemia risk above three to four milligauss. That is the number that belongs in that segment, and it is more than ten times below the reading that had just been dismissed as trivial. I gave them that number myself, on tape, in the interview. Describing my own threshold, I said my comfort level for long-term chronic exposure is three to four milligauss, but preferably one. 2. Six children in thirteen million. The episode reports that these fields might explain one to four percent of childhood leukemias, then reframes it as a German estimate of perhaps six cases among thirteen million children. Torre, to his credit, is uncomfortable. What never gets explained is why that number is small. Almost no children lives above three milligauss in Europe. Fewer than two children in a hundred, in the Italian data. So even if the risk to those children doubles, the number of additional cases across an entire country stays small — not because the hazard is small, but because hardly anyone is exposed to it. Count the whole population and the few who are exposed disappear. And the reason hardly anyone is exposed is that siting rules keep housing away from transmission lines. In Europe, at least. The Dutch government has a standing precautionary policy against building new homes in any zone where the annual average magnetic field exceeds 4 milligauss — the same number the episode never mentioned. Denmark and Norway treat 4 milligauss as the level that triggers a look at mitigation. That is five hundred times below the ICNIRP figure quoted on air. The United States has no federal equivalent. That is evidence of infrastructure siting policy working. It is not evidence that there is no hazard. It is evidence that we already act as though there is one. If you listen to the raw audio you will hear that my proposed solution is EMF exposure is to build better infrastructure. What they left out about the mechanism 3. They accused me of cherry-picking, and then cherry-picked themselves. On air, Zukerman tells Torre that people who worry about electromagnetic fields dismiss the studies showing null results and collect the ones showing harm, and that this is why you have to be careful not to cherry-pick. They had two papers I had rattled off in a hurry, and a second email containing a carefully chosen set. They ran the two weakest, graded them on air, and presented the result as the state of the evidence for not only my theory, but the whole question of oxidative stress from magnetic fields. That is cherry-picking from my emails. The bigger picture is what they did with the literature as a whole. Zukerman acknowledges it exists, dismisses it, and disposes of it in a single stroke. You can go online right now, she tells Torre, and find scores of studies showing these fields increase oxidative stress. The issue, she says, is that they are not studies in people. Many of them are in people. The occupational studies in my second email are in people. That email had been in her inbox for five weeks. She waved off the literature on a factual claim that the documents in her possession contradict. (I have written separately about the evidentiary standard at work here). The effect was that they essentially baited me: ask the subject to supply the evidence, take the weakest thing he sends, and let that stand as a proxy for the whole argument. Wendy has been doing this show for ten years and clearly knows how to extract what she needs for her desired narrative. 4. They presented the collagen-improvement research as a gotcha, but I had already addressed it. The episode treats the existence of studies showing that EMF can improve collagen as a surprise that undercuts me, but I had pre-emptively addressed that five weeks earlier in the email they ignored. Those studies use measured, high-intensity pulsed dosing. The mechanism by which they work is oxidative signalling. The cell reads a controlled rise in reactive oxygen species as a warning, upregulates its antioxidant defenses, mounts a repair response, and the therapy stops before the system is overwhelmed. The key point is that it induces an oxidative response, which means those studies are actually evidence for my proposed mechanism, not against it. A field that produces a therapeutic effect cannot be biologically inert (which is the implication when they say “Nothing happens at 2,000 milligauss). Chronic ambient exposure is the same pathway with no off switch, and it is most consequential during the evening and while sleeping, when the body is in repair mode and the exposure does not stop. Section 5 of my email is titled What about the study showing improved collagen synthesis. I raised the counter-evidence myself, explained why I did not think it refuted the theory, and wrote that I was disappointed the question had not come up in the interview. That is worth holding against the cherry-picking charge in the item above: the studies they presented as inconvenient for me were studies I had gone out of my way to put in front of them. 5. Section 1 of my email stated a critical argument that was never put to the expert directly responsible for it. My email says the exposure limits exist to prevent acute effects and do not address chronic exposure at all, and that my dispute is with the entire framework. Zukerman gestures at this once. After Karipidis gives the 2,000 milligauss figure, she tells Torre that I would object because those levels do not capture “more subtle effects.” That is not my argument, and “subtle” is doing a lot of work here. My argument is that the limits are built to prevent acute effects — nerves firing, muscles twitching, etc — and were not designed to address chronic exposure at all. In fact, ICNIRP’s own documents state as much themselves. Mine is a structural objection to what the standard measures, reduced as a concern about subtlety, it becomes a matter of degree, rather than a categorical difference. They interviewed Ken Karipidis, vice chair of ICNIRP — the body that writes those limits. He was asked what the limit is, but he was never asked how it applies to chronic exposure. The scientists Science Vs interviewed and did not air 6. They interviewed four officials of the standards body. The episode credits roughly a dozen researchers. Four of them are associated with ICNIRP. Ken Karipidis is the vice chair. Rodney Croft chaired ICNIRP from 2020 to 2024 and led the development of its current guidelines. Dan Baaken is ICNIRP’s scientific secretary. Frank de Vocht sits on the Main Commission. One of them speaks in the episode. Their institution’s position is more than adequately represented — the 2,000 milligauss figure, the safety factors, the assurance that nothing happens below the line. 7. The four who were left out. Dr. Beatrice Golomb is Professor of Medicine at UC San Diego — a physics undergraduate degree, a PhD in biology, an MD. She directs a research group whose stated focus is the relationship between oxidative stress, mitochondrial function and health. That is the mechanism the episode spent its first half dismissing. Her published work includes the fluoroquinolone case series behind the FDA’s black box warning on an antibiotic class that ruptures tendons, where the accepted mechanism is oxidative stress and mitochondrial toxicity — the back half of my chain, already on a drug label. She is in the credits. She is not in the episode. She has told me she finds my theory biologically plausible, and that she has a recording of her interview. Dr. David Carpenter directed the Institute for Health and the Environment at the University at Albany for decades and is the most prominent academic voice arguing these fields cause harm. Childhood leukemia is the reason these fields carry a WHO classification at all, and Carpenter is the person you call if you want that case made by someone who has spent a career on it. He is in the credits. He is not in the episode. He has told me that when he was interviewed they could not have been less interested in what he had to say. Dr. Joel Moskowitz directs the Center for Family and Community Health at UC Berkeley’s School of Public Health. He told me directly that they interviewed him and that he thought it went well. He does not appear in the episode, and unlike Golomb and Carpenter, he does not even appear in the credits. Dr. Paul Héroux at McGill is the researcher whose work provides the foundation for the oxidative stress mechanism my theory rests on. I gave Rose his email address and phone number. He was never interviewed. They never even called him. 8. “He’s not a scientist.” The episode leans hard on the fact that I am not a credentialed scientist. Zukerman says it. Torre repeats it. “At all.” Having built a segment on that, they then left out the physicist-biologist-physician, the professor of public health, the director of a university environmental health institute, and the McGill researcher whose work the primary mechanism comes from. They spent the episode telling their audience I am not a scientist, and then kept four actual scientists who support the theory off because their argument does not survive otherwise. How they misrepresented me and my case 9. They played my words as a response to an interview I had never heard. Near the end of the hour, Zukerman says she went to me and told me the evidence was lacking. Then she plays me saying I am not wedded to it being an EMF, that I have staked my reputation on it needing more study, and that I am not certain of anything. That segment was placed immediately after Karipidis had finished taking the cherry-picked papers apart. It plays as a man folding under expert scrutiny. Commenters have used it against me since, but it is incorrect. Here is the sequence as it happened. I was interviewed. Karipidis was interviewed weeks later. I was never told what he said, or even who he was. I was never asked to respond to it. I did not know his name until the episode aired. That is not a simple editing decision. That is a quote from one interview, moved to follow a critique from a different interview it was not a response to, so that it would land as a concession. A friend of mine who has spent thirty years as a journalist read that sequence and called it sleazy. She is right. The full passage is reproduced in Appendix A, and it is worth reading. What airs is the preamble. Four paragraphs later I say “to directly answer your question” — and that answer, about what would change my mind if the team relocated, is not in the episode. Neither is the sentence two paragraphs on, where I say the EMF might turn out to be ten percent of the problem. I will say the underlying point again, though, because I meant it and I still do. I am not wedded to my theory that magnetic fields from the substation are contributing to the 49ers injuries. I could be wrong. What I am wedded to is the process of scientific inquiry, and the fact that we should be cautious around these exposures and we need more independently funded studies. 10. Three telling edits. They cut “I’m not a scientist” mid-sentence. What I said: “...and I am not certain of anything. I’m not a scientist. To me, I find the mechanisms compelling. I will go back to the fact that I got into this not because of the 49ers, but because of clients I was working with who suffer from EDS...” What aired: “...and that I am not certain of anything. I’m not.” The clip ends on the first two words of the sentence in which I say I am not a scientist, in an episode that spends considerable energy establishing that I am not a scientist. The full sequence is in Appendix A. They cut my own description of my work. Asked what I do, I said I run a wellness business, that I am focused on writing software to help people navigate environmental stressors, that environmental health is my focus, and that I also do independent journalism and research. What aired is the wellness business and the environmental health, with the software and the journalism removed from my own answer. The software engineering does come up later — narrated by them, as a hacker who grew up to write firmware — but my current work, in my own words, arrives as “wellness guy.” Thousands of commercial routers became home Wi-Fi. What I described: working at a wireless networking company surrounded by thousands of Wi-Fi routers, and a stress-induced health collapse afterward that working in that environment contributed to. What aired: Wi-Fi, the kind you have at home — reinforced by a clip of Christian McCaffrey talking about turning his router off at night. Three cuts, and every one of them makes me seem less credible. That is not a coincidence. 11. I gave them my own caveats and the test that would disprove me. In the first email I wrote that a well-designed chronic, ambient-level exposure study in tendon showing no collagen degradation, run over many months, would undercut my confidence in the theory. That is a specific, testable condition, stated in advance and in writing. There was a second interview, weeks later, which was not used in the episode, but in that I asked again for the falsification criterion to be included. What the episode presents instead is a man saying “we need more study,” which reads as a hedge, an open-ended request for the benefit of the doubt. It is the opposite of a hedge. Section 6 of my second email says, unprompted, that as far as I am aware there is not a single study showing EMF-driven oxidative stress degrading collagen in a human in vivo or in human tendon in a lab. I wrote that because it is true and because it is the first thing anyone should check. Under their standard it becomes the hinge of the entire first half, framed as something they had to surface without my cooperation. I had handed it to them five weeks earlier. And in the interview I said that my 25 to 50 milligauss readings were taken at knee level, and that these fields attenuate quickly, so by the time it reaches your head it is not that high anymore. That did not air either. The qualification arrives later, from Karipidis, as a correction. How you would actually study the injuries 12. They measured the wrong thing. The episode spends its final act on whether the 49ers are the most injured team in the NFL, finds no clean ranking, and lands on “injuries are random”. That is the wrong test. You would define the exposure — measured field levels at the facility — and the outcome narrowly: soft-tissue injuries, not a single MSK injury count that a broken finger and a ruptured Achilles both land in. Then you would compare the 49ers to themselves before and after the exposure changed, and compare that change against every other team over the same window. That controls for league-wide shifts in rules, turf and training load. It is a difference-in-differences design, and it is standard. I sent them that argument on July 28th, in writing, along with the fact that in eleven of the past twelve seasons the 49ers had finished top ten in Adjusted Games Lost. And by the episode’s own reporting, the 49ers are second in games lost to injury over the past decade, with FTN’s Aaron Schatz confirming that once you adjust for starters they come out second worst in the league — after having been one of the healthiest teams for years before that. A finding like that is where an investigation starts, not where it stops. 13. I did a lot of substation research for the episode that was never aired. I had reported that the substation next to the facility was expanded in 2014. That was wrong, and Rose Rimler and I sorted it out together. They gave me credit on air, which I appreciated, but framed it as a concession on my part to something they had found. In fact I had been investigating it myself, was uncertain before they asked, but was waiting for clarification from Silicon Valley Power. The uncertainty centered around a substation named “Esparanca” that was proposed right behind the facilities as part of the stadium construction, but now appears to never have been built. I spent days in Silicon Valley Power’s records, and did eventually reach Silicon Valley Power for confirmation and indentified the mistake myself. I also gave them highly detailed documents on what we do know about those facilities: new equipment installed between 2010 and 2014, and load growth across the system with an inflection around 2013–2014, with the Northern Receiving Station carrying the highest capacity in the system and sitting closest to the data center corridor. None of that is in the episode. I have a separate piece about it coming out soon. *I cut 2 seconds from the raw audio to remove personal information that had no connection to anything in the episode. Appendix A: the passage the clip was taken from This is the sequence from my first interview, in full. The episode uses one fragment of it. It’s tricky because my understanding is that there’s something like a 15-year half-life on collagen remodeling issues. They’re going to get a new crop of players. What I really need, though, is for the injuries to be broken down so we can see the soft tissue injuries. Right now, they’re categorized as MSK injuries, but let’s say we can actually identify them more specifically. Is that right? He was able to do that? Oh, cool. I wasn’t able to find that information. Interesting — I didn’t know that data existed. I tried so hard to get it, and I didn’t know it was available. Maybe you could connect me with that person. That would be amazing. I’m not wedded to it being an EMF, honestly. I’m not. I would say that, to a certain extent, I’ve staked my reputation on the fact that it needs more study. It’s important to look into it, and I am not certain of anything. I’m not a scientist. To me, I find the mechanisms compelling. I will go back to the fact that I got into this not because of the 49ers, but because of clients I was working with who suffer from EDS, Ehlers-Danlos Syndrome, a tendon hypermobility issue. This condition is documented to be partially caused by oxidative stress. I’ve worked with them to mitigate their EMF exposure and have seen people improve. I think it’s a bigger story. In a way, the 49ers represent an occupational cluster with specific exposure risks. If someone would conduct a study on this, I believe we could learn a lot. Perhaps we would discover that it’s like, okay, maybe it’s 10% of the problem. I don’t know the exact number, but I think either way, conducting the study would provide valuable insights. To directly answer your question, it’s challenging for me because it’s part of a bigger story. If the 49ers move and stop having injuries, I might conclude that it was related to the substation. However, if they move and still experience injuries, I would want to analyze the nature of those injuries. Are they primarily soft tissue injuries? I don’t think it’s necessarily a case closed, but the story might lose traction at that point regardless. Three things are worth noting. The aired fragment stops immediately before the sentence in which I say I am not a scientist — the cut described in item 10. It also stops four paragraphs before the words “to directly answer your question.” What the episode plays is the throat-clearing. The actual answer, about what would change my mind, never airs. And two paragraphs in, I say the EMF might turn out to be ten percent of the problem. That is the ranking the episode says I never gave. Appendix B: the full email, July 6th, 1:39 PM Hi Rose, You asked me to send you some studies a couple of weeks ago. I apologize for the delay. I have been incredibly busy. I also wanted to give you a chance to dig in yourself, and get your own perspective before I influenced you too much with mine. That said, I do want to make sure that the actual argument is abundantly clear, so here it is! One note before I begin, there are really two separate questions here: Does the substation cause the soft-tissue injuries? That was my specific claim, and what the podcast is about. Is the theory biologically sound? Can 50/60 Hz fields at these levels do anything biological below the safety limits? Question two is why people have been calling me a conspiracy theorist. The regulatory and advisory bodies (ICNIRP, etc) maintain that anything below their exposure limits is biologically inert, and that position is broadly accepted within the mainstream, but the actual science paints a different picture. To defend my theory I’ve had to defend a much larger claim: that the advisory bodies have the biology wrong. I can’t honestly answer question 1 without first addressing that. Here’s is a simplified outline of my theory, with links to studies: 1. Advisory body thresholds for biological effects The ELF magnetic-field limits (ICNIRP’s ~2,000 mG public / 10,000 mG occupational) exist to prevent acute effects from exposure. If a magnetic field is strong enough, it makes nerves fire and muscles contract. Muscles twitch. You can see faint flashes of light in your vision. People can even feel tingling or even a shock. That happens due to Faraday’s law, which states that a time-varying magnetic field induces an electric field inside the body via the creation of Eddy currents.The standards assume that those currents do nothing below the twitch threshold. They do not consider chronic effects at all. My argument is that they are biologically active and do have chronic effects. 2. There are multipe ELF-EMF mechanisms for inducing oxidative stress. This is basic biophysics. Below are the two primary mechanisms. Simplest first. Dr. Paul Héroux of McGill has the most intuitive explanation, which rests on Maxwell’s principle of superposition: because Maxwell’s equations are linear, two sets of electromagnetic waves sharing the same space simply add together. In the interview I pictured a pebble dropped into a pond, sending out clean ripples. Then a boat motors past at distance, sending larger waves, and where they meet the ripples, the two add together and the original pattern gets distorted. In our cells, the mitochondria run on continuous currents of electrons and protons that carry their own faint electromagnetic fields. An external field from a substation, by the principle of superposition, adds to those internal currents and shifts the pattern. The electron transport chain in the mitochondria leaks a fraction of its electrons by design as reactive oxygen species (ROS), which act as signalling molecules in a healthy cell. Distorting that field increases that electron leakage, creating oxidative stress. A tiny electromagnetic interference results in a large downstream effect. https://www.sciencedirect.com/science/article/pii/S2405844025006474 The more complex pathway is Dimitris Panagopoulos’s Ion Forced-Oscillation / Voltage-Gated Ion Channel (IFO-VGIC) mechanism. Weak, polarized, low-frequency fields force the ions (calcium, potassium, sodium) next to an ion channel’s voltage sensor to oscillate; because that force scales with the inverse cube of the distance involved, fields far below the stimulation threshold can still force the channel open, disrupting the cell’s ion balance and driving ROS overproduction (Nitric oxide and superoxide interact and produce peroxynitrite, a highly unstable cytotoxin that breaks down into free radicals). https://www.researchgate.net/publication/366088934 https://www.spandidos-publications.com/ijo/59/5/92 https://www.mdpi.com/1422-0067/22/18/10041 https://www.frontiersin.org/journals/public-health/articles/10.3389/fpubh.2025.1585441/full https://pmc.ncbi.nlm.nih.gov/articles/PMC3772193/ 3. Evidence of oxidative stress, in vivo, in humans from ELF-EMF There are many studies, and the strongest are occupational, which applies to the 49ers situation. 115 power-plant workers vs. 145 office controls. Serum malondialdehyde (MDA, the standard lipid-peroxidation marker), superoxide dismutase, and catalase were all significantly higher in the exposed group, and the markers rose with increasing field exposure. https://journals.sagepub.com/doi/abs/10.3233/WOR-203244 A follow-up where they reversed the oxidative stress in power plant workers. A double-blind randomized controlled trial: 91 power-plant workers given vitamin E, vitamin C, both, or placebo for 90 days. The antioxidant groups showed reduced lipid peroxidation and raised antioxidant capacity versus controls. https://pubmed.ncbi.nlm.nih.gov/32191586/ A spot-welder study: 46 welders occupationally exposed at 50 Hz, showed significantly altered red-blood-cell antioxidant enzyme activity and concluded ELF-MF “might act as an oxidative stressor… even at the recommended levels of exposure.” https://pubmed.ncbi.nlm.nih.gov/18504600/ A substation-specific study found oxidative stress and DNA damage https://pubmed.ncbi.nlm.nih.gov/24460415/ 4. Oxidative stress degrades collagen This half isn’t controversial at all. Oxidative stress activates the matrix metalloproteinases (MMPs) that break collagen down and suppresses its synthesis. Here are three example studies: Siwik et al. 2001: Oxidative stress raises MMPs and lowers collagen synthesis in cardiac fibroblasts. https://pubmed.ncbi.nlm.nih.gov/11121376/ Fisher et al. 2009: Collagen fragmentation drives oxidative stress and elevates MMP-1 in aged human skin. https://pmc.ncbi.nlm.nih.gov/articles/PMC2631323/ Varani et al. 2006: Decreased collagen production in oxidatively aged skin. https://pubmed.ncbi.nlm.nih.gov/16723701/ 5. What about the study showing improved collagen synthesis I’m glad you asked this question, and I’m bummed we didn’t get to it in the interview because it is a great question, and very important to understand. Superficially it may appear to be a refutation of my theory, but I would argue that it actually supports the underlying argument. That study used a short, high-intensity pulsed dose: therapeutic-PEMF, the same type of field used clinically to stimulate bone and tissue healing. The reason this works is because it triggers the very same biological pathways that can lead to oxidative stress. The exposure still stimulates ROS production, but done at a controlled dosage, for a limited duration it has a different effect. The cell reads the ROS as a warning signal and it upregulates its antioxidant defenses, and mounts a repair/proliferation response. The therapy is then stopped before the cell gets overwhelmed. That is essentially a hormetic response: a small dose of a stressor producing a beneficial adaptation. Two things follow: At the very least, this means the field is biologically active, which by itself undercuts the regulatory claim that these fields are inert below their thresholds. There is a wealth of literature on PEMF (pulsed EMF) bone regeneration and calcium channel signalling (which is the second mechanims in section one). Here is one. https://www.nature.com/articles/srep13856 At best, it leads us straight to my actual concern, which is that under chronic, chaotic and unregulated exposure, the cell’s antioxidant capacity gets overwhelmed, resulting in oxidative stress. There are plentiful examples of things that are beneficial at controlled doses, but harmful at uncontrolled doses. Excecise is one obvious, uncontroversial example. Botox is perhaps a more interesting example. 6. What about a study that shows EMF causing collagen degradation in humans? As far as I am aware there is not a single study showing EMF-driven oxidative stress degrading collagen in a human, in vivo, or in human tendon in a lab. There are studies involving isolated fibroblasts though, which secrete collagen. The most relevant one showed that human fetal scleral fibroblasts exposed to 50 Hz ELF-EMF showed a significant decrease in collagen synthesis and that MMP-2 expression was upregulated, which is the exact mechanism I described in section 2. https://pmc.ncbi.nlm.nih.gov/articles/PMC3626379/ That’s it! Thanks again for the interview. Best, Peter Anthony Cowan Environmental Health · Wellness Tech · Researcher & Journalist Publisher & Editor, Living Energy Bio: petercowan.comSocial: X · Instagram · TikTokApp: sunlightis.lifePhone: [redacted]
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Scientists have directly observed how two negatively charged DNA molecules can pair up despite normally repelling each other. Positively charged metal ions appear to bridge the gap, helping matching DNA helices align groove for groove like a molecular zipper. The discovery confirms a theory proposed two decades ago and could help researchers understand DNA interactions involved in cancer and other cellular processes.
Scientists Use AI to Find Stable Forms of Molecules for Drug Discovery
Using deep learning, NYU researchers predict tautomeric states—an important foundation for reliable drug design
Scientists win chemistry Nobel for discoveries about mirrored molecules that led to many drugs
Portraits of Henri Kagan and Kenso Soai are shown on the screen as they are awarded the 2026 Nobel Prize in Chemistry, at the Royal Swedish Academy of Sciences in Stockholm, Sweden, on Oct. 7, 2026. Photo: (Fredrik Sandberg/TT News Agency via AP)By ADITHI RAMAKRISHNAN, KOSTYA MANENKOV and STEFANIE DAZIO STOCKHOLM (AP) — Scientists Henri B. Kagan and Kenso Soai...
Scientists Watched Two DNA Double Helices ‘Zip’ Together for the First Time
Metal ions may help DNA molecules overcome their mutual electrical repulsion.
Can NAD+ supplements help us age more healthily? Here’s what the science shows
The supplement industry has a new favourite molecule: NAD+. Scientists are interested too, but evidence of its anti-ageing benefits in humans remains limited.
FDA scientists flag concerns with peptides, the trendy molecules RFK Jr. supports
Documents reviewing the research on peptides note lack of good evidence of efficacy or safety. Yet an FDA panel will consider easing access to them later this month.
Scientists achieve the first total synthesis of a complex alkaloids isolated from plant
Monoterpenoid indole alkaloids (MIAs) are plant-derived molecules with unique pharmaceutical potential, but their highly complex and intricate structures make them difficult to produce in the laboratory. Now, researchers from Japan have developed a new strategy that enables the total synthesis of bisleuconothine A and bousigonine B, two biologically relevant oligomeric MIAs. Their findings lay the foundation for further studies of this family of molecules. Monoterpenoid indole alkaloids (MIAs) are plant-derived molecules with unique pharmaceutical potential, but their highly complex and intricate structures make them difficult to produce in the laboratory. Now, researchers from Japan have developed a new strategy that enables the total synthesis of bisleuconothine A and bousigonine B, two biologically relevant oligomeric MIAs. Their findings lay the foundation for further studies of this family of molecules.
Nobel prize in chemistry awarded for work on mirror-image molecules
Henri B Kagan and Kensō Soai awarded prize for discovery of nonlinear effects and autocatalysis in asymmetric organic synthesis
Phone breathalyser can detect when your body switches to burning fat
A handheld breathalyser picks up on a molecule called acetone, revealing that your body is using fat for energy
New science on algae die-offs is too late for the Reflecting Pool
Iron and hydrogen peroxide trigger cell death via ferroptosis, which cascades killer molecules through the population, causing mass die-offs of algae.
NASA rover finds record-breaking trove of complex organic molecules on Mars
Data from NASA’s Perseverance rover confirms the presence of macromolecular carbon on Mars – another potential piece of the puzzle in the search for life.
Breakthroughs in RNA science
Most people first heard about mRNA during the 2020 pandemic, but this molecule that carries instructions from DNA to make proteins has been studied since the 1960s. Decades of basic
Report: Media Molecule New Game Set to Be Revealed in 2027, First Info Leaks
Four months ago, we reported that LittleBigPlanet developer Media Molecule was busy toiling away on a new IP with "open-world content." For those wondering what happened to the studio, they…
Scientists mix a simple molecule into perovskite solar layer, and efficiency climbs past 25.6%
Tests showed the combined layer was less prone to clumping and covered the surface more completely.
A nanoparticle revealed the tiny impact of a single gas atom
The force exerted by a gas usually results from many atoms or molecules at once. But scientists isolated the force of a lone particle.
Scientists Captured Trillionth-of-a-Second Snapshots of a Chemical Reaction Essential to Life
Learn how scientists are able to capture “snapshots” of extremely rapid processes, called proton-coupled electron transfer (PCET) reactions.
Life Is Asymmetric. The Scientists Who Figured Out Why Won the 2026 Nobel Prize in Chemistry
Henri Kagan and Kensō Soai designed chemical reactions producing only one of the two mirror-image forms of a molecule—an important finding for the synthesis of pharmaceuticals and other biological substances.
FDA scientists flag concerns with peptides, the trendy molecules RFK Jr. supports
Documents reviewing the research on peptides note lack of good evidence of efficacy or safety. Yet an FDA panel will consider easing access to them later this month.
Scientists Thought Venus Was Too Acidic for Complex Chemistry. It May Actually Be Weirdly Hospitable
MIT researchers recreated a Venus-like stew of 98% sulfuric acid to test complex signaling molecules, like peptides, in the lab. Looks like they passed.
Scientists Wipe Out 99% of Cancer Cells in Lab Using Vibrating Molecules
No chemo or radiation.
AZ's R&D chief Barr touts internal 'science success story' after IL-33 antibody's stellar showing in COPD
With a detailed data drop that AstraZeneca’s R&D chief described as an internal “science success story,” the British Big Pharma has secured an FDA priority review for what it believes could become a flagship biologic in chronic obstructive pulmonary disease (COPD). In detailed results from the late-stage Oberon and Titania trials—first teased in March and detailed in full at the European Respiratory Society Congress in Barcelona this week—the drugmaker laid out the extent of its IL-33 inhibitor’s potential to reduce moderate and severe exacerbations in a wide range of COPD patients still struggling with those “lung attacks,” as AstraZeneca’s Sharon Barr, Ph.D., called them, despite using standard-care inhaled therapy. In the headline results, a 300 mg dose of tozorakimab given once every four weeks curbed those moderate and severe exacerbations in the studies’ primary population of former smokers by 29% in the Oberon study and 34% in Titania. In the overall population of both current and former smokers, these reductions were 30% and 29%, respectively, versus placebo and inhaled standard of care. The benefits also extended to clinically meaningful exacerbation reductions in all prespecified patient subgroups and specifically turned up promising signals in patients across a range of blood eosinophil counts, with Barr telling Fierce that “it’s the details that make this even more exciting than the high-level results that we’ve already shared.” In fact, during AZ’s tozorakimab poster presentation at the ERS 2026 Congress this past weekend, attendees were so enamored by the data that event organizers had to encourage people to clear the room and look at the other presentations on offer, Barr said in an interview. “I think it really speaks to the fact that there is a lot of buzz around these data because the entire respiratory community has been so desperate for new therapies for these patients,” she explained. The respiratory disease continues to represent a “staggering unmet medical need,” Barr said, highlighting the COPD exacerbations that the Oberon and Titania studies homed in on, which she added carry a greater mortality risk than a heart attack. “When a patient has a severe exacerbation, only about half of them are still alive within three and a half years,” she pointed out. As for tozorakimab specifically, Barr christened the molecule “an AstraZeneca science success story,” harkening several years back to the point at which researchers began to explore IL-33 as a driver of respiratory disease, and COPD in particular. At the same time, “there was still so much that wasn’t understood,” she admitted, highlighting the insight that IL-33 signals through both ST2 and EGFR through the RAGE pathway, a discovery Barr attributed to AstraZeneca's own scientists. Understanding the need to tackle both pathways in COPD—and aware of competitor candidates in the hopper, including one that bound ST2—the company ultimately had to make some “courageous decisions,” Barr said. These included taking a prior COPD molecule offline and going back to the drawing board to reinvent its potential IL-33 label “to make sure that we had a molecule that could block signaling through both arms of the pathway, through both the reduced form and the oxidized form, knowing that we wouldn’t be first, but striving to be best.” “When we put [tozorakimab] into the clinic, we firmly believed that we had a differentiated molecule, and we saw the other molecules blocking just ST2 or partially blocking IL-33, unable to deliver two positive pivotal studies in COPD,” Barr explained. “We kept marching forward because we believed our molecule was differentiated, and now I think we have the clinical validation that supports that.” Ultimately, AstraZeneca finds itself on much better footing these days when it comes to potential biologic rivals to tozorakimab in COPD. Sanofi and Regeneron’s Dupixent, for instance, is approved to treat COPD exacerbations in patients with high eosinophil counts, but not low ones. Meanwhile, the future has become cloudier for other next-gen IL-33 candidates from Sanofi and Regeneron, as well as Roche, which have suffered trial flops in recent years. One other potential ingredient for AstraZeneca’s success in its duo of studies was that the company was “ambitious in the trial design, willing to look at an all-comers population,” Barr said, “and willing to enroll the most severe patients.” Prior studies for would-be biologics rivals in COPD “avoided enrolling” those patients, she pointed out. She also highlighted the Big Pharma’s painstaking design of exacerbations in its trial, which “gave us a very rigorous readout,” and pointed to “the extra effort and investment” the company put in to understand the effect of mucus plugs in patients. Barr described mucus production as a “key feature in disease diversity,” noting that mucus plugs—obstructing clumps of mucus that block patients’ airways—are associated with worse outcomes in COPD. In its data announcement, AstraZeneca noted that an integrated analysis of Oberon and Titania found tozorakimab “demonstrated a reduction in patients’ mucus plug score,” with the pharma claiming its biologic is the first to deliver such results in a broad COPD population. “So being able to reduce those mucus plugs, we expect, is an important part of driving benefit for patients who are living with COPD,” Barr said. Again touching on the breadth of the study populations, Barr added that tozorakimab “worked across all eosinophil levels in both current and former smokers across all levels of lung function,” which she suggested “really simplifies decision-making for clinicians, and it allows them to offer therapy to the broadest possible patient population.” In the highest patient eosinophil count group, tozorakimab helped chart a 43% reduction in exacerbation risk, which Barr stressed were “unprecedented data.” In the mid-level group, AZ’s drug delivered a 23% reduction and, in the lowest group, a 34% reduction in eosinophils, which Barr said suggests efficacy “in all patient subgroups.” As for AZ’s recent guidance upgrade on the medicine’s sales opportunity, the lift from a $3 billion to $5 billion range to $5 billion plus was informed by multiple factors, Barr said, including the fact that “in 2024, there were multiple competitors, and there aren’t anymore.” Additionally, “we know that this is a massive unmet medical need, and this is a really incredible set of data that we think will be very convincing to the clinical community,” Barr said. Looking ahead to a potential evolution of the COPD treatment landscape, Barr noted that most patients start treatment in the community with an option like a triple therapy, and for them, having an option like AstraZeneca’s inhaler Breztri will remain a “really important part” of that journey. But of the patients uncontrolled on triple therapy, which Barr described as “about half of them today,” just a “small fraction” are currently eligible for biologic therapy, which she emphasized AstraZeneca is working to change. Understanding that COPD is not a “one-size-fits-all” disease, AstraZeneca is also looking at its antibody drug Tezspire for patients with T2-driven disease, and the company continues to think about new mechanisms for tackling COPD through both systemic and inhaled drugs, Barr said.
Cleveland Clinic, RIKEN and IBM Team Advance to Finals for 2026 ACM Gordon Bell Prize
Joint research team modeled a 12,635-atom protein, the largest-known to be simulated using quantum computers. Breakthrough was achieved through quantum and classical methods working together, expanding quantum-centric supercomputing’s potential in life sciences research.
Scientists uncover a hidden map of the brain with 539 distinct regions
Scientists have uncovered a hidden layer of organization in the brain by creating the first detailed 3D map of its lipids, the fatty molecules essential for brain structure and communication. By analyzing millions of measurements from mouse brains, researchers identified 539 distinct chemical zones, revealing patterns and boundaries that traditional brain maps have missed. Surprisingly, even white matter, once thought to be relatively uniform, contains a complex patchwork of chemically distinct regions.
Sugar discovered floating in deep space for the first time
Similarly sweet molecules may have jumpstarted life on Earth over 4 billion years ago.
Microplastics Have Been Linked With Myriad Human Health Problems. Scientists May Have Finally Figured Out How They Harm the Body
Lab experiments suggest that tiny bits of plastic can react with water inside us to produce highly reactive molecules. They can lead to damaging oxidative stress and inflammation
Scientists are uncovering how common viruses may quietly increase cancer risk
Everyday viral infections may be quietly reshaping the body’s network of molecules that support cells and tissues in ways that can raise cancer risk over time
Scientists win chemistry Nobel for discoveries about mirrored molecules that led to many drugs
Scientists Henri B. Kagan and Kenso Soai won the Nobel Prize in chemistry for untangling mysterious mirror images in molecules, a discovery that has been used to develop countless drugs.
Scientists uncover a hidden power in our bodies that could fight depression - Futura-Sciences
When Muscles Talk to the Brain: The Role of Apelin During exercise, muscles secrete a protein capable of crossing the blood-brain barrier and influencing neural activity. This molecule, called apelin, has been identified in mouse studies as a missing link in the connection between physical activity and mood. The findings...
Why Robots Still Can't Do Science
Why Robots Still Can't Do Science: AI can read the literature in an afternoon and design molecules a chemist never would. So why can't a robot hold a pipette?
Scientists finally see how nature moves energy so efficiently
Researchers have captured key steps in a chemical reaction that helps nature transfer energy with remarkable efficiency. Ultrafast X-rays revealed how changes involving electrons and protons are closely linked to the rearrangement of surrounding water molecules. Because similar reactions drive photosynthesis and other energy-conversion processes, the technique could help scientists develop better catalysts, fuel cells, and flow batteries.
Structural alignments to design functional RNAs
Nature Computational Science - A new method designs RNA sequences by learning from alignments of structurally similar molecules, producing aptamers and ribozymes that are experimentally validated.
How a Brain Messenger Protein Drives Progression of Alzheimer’s Disease
In mice, a brain protein called Arc helps spread toxic molecules from sick brain cells to healthy ones. If therapies could be designed to target the spread, they could be a powerful tool to stop disease progression.
“Zombie” Cells Reveal a Surprising New Driver of Chronic Inflammation
Dysfunctional mitochondria may drive age-related inflammation by helping switch on inflammatory genes, and blocking SLC25A1 reduced that activity. As people age, senescent cells accumulate in the body. These so-called “zombie” cells have stopped dividing but remain metabolically active, releasing inflammatory molecules that can contribute to persistent inflammation associated with frailty, cardiovascular disease, cancer, neurodegeneration, and
Making Our Own Luck
We are cross-posting a piece that former NIH official Kris Willis wrote for Macroscience. Kris is now the President and Founder of the Woodley Park Institute, for which I’m a board member. Picking winners or hedging bets? Federal science agencies have long wrestled with the question of how to ensure their billions of dollars of grants and contracts result in maximum benefits for Americans. On the surface, it might seem that a goal-oriented, interventionist style of management would be the best policy: prioritize our most pressing problems and distribute funding accordingly.This top-down strategy creates a unique hazard, though: bad choices can send resources in the wrong direction, resulting in slow progress that impedes the delivery of tangible benefits to citizens. Moreover, if decision makers pursue an applied advance when the underlying scientific principles remain poorly understood, they risk costly failures and a loss of support for the research enterprise at large. Examples include Nixon’s 1971 War on Cancer, undertaken on the premise that a cure could be achieved in less than a decade, the drive to build an operational commercial fusion plant by the mid-1990s, and the National Plan to Address Alzheimer’s Disease, which failed to produce the effective treatments and prevention strategies promised by 2025. The contrasting laissez-faire approach is to hedge your bets. If the path to an advance is impossible to predict, then the wisest choice might be to distribute funding to as widely as possible. The main risk of this strategy is that spreading funding thinly may limit the resources available to the most promising research, resulting in the same negative outcomes as the interventionist approach: limited support for the most promising topics, slow progress, and delayed returns. In reality, at science agencies like the National Science Foundation and National Institutes of Health, program managers navigate between these two extremes, setting some funds aside to target high-priority areas and using the rest to cover the widest possible range of meritorious proposals. This middle path seems like the most rational way to proceed, but it still requires making choices. How much should be set aside for high priority topics? What should those topics be? How should we define merit? Expert opinion can provide a helpful guide, but leading experts can have remarkably different opinions about what matters and what should be prioritized. Moreover, experts and administrators alike can be risk averse, giving an edge to high-profile, well-established concepts. What’s really needed is a data-driven framework to help guide decision-making, one that doesn’t simply repackage prestige or incumbency. Recognizing breakthroughs years in advance Many breakthroughs fail to attract funding or recognition at the earliest stages of development. Katalin Karikó, for example, spent years struggling to win grants for work on mRNA that would eventually win her and Drew Weissman a Nobel Prize. Similar stories can be told about Jim Allison’s groundbreaking studies leading to the development of cancer immunotherapy, Stan Pruisner’s demonstration that prions can self-replicate without DNA, or Robin Warren and Barry Marshall’s proof that Helicobacter pylori, not stress, causes ulcers. Yet at some point, the scientific community recognizes and responds to transformative breakthroughs like these. How does that change happen? And what if science funders could identify the areas that are on the cusp of a breakthrough? Those questions led my collaborators and me to study how scientists responded to past breakthroughs. Based on patterns in that data, we developed a means of predicting future breakthroughs, using biomedicine as a proof of concept. It’s worth taking a moment to describe how our approach works. Briefly, our prediction process begins by grouping the 18 million or so peer-reviewed papers in PubMed, the authoritative database of biomedical research, into roughly 50,000 unique topics. A small subset of these topics are so widely acclaimed as breakthroughs that they have been recognized with a major prize like a Nobel or a Lasker Award. We theorized that studying the development of these outliers over time, especially before they gained acclaim, was the key to identifying future instances of them. After defining topics, we chose 21 representative breakthroughs and asked what they looked like before they won prestigious prizes. To answer that question, we re-ran our topic-mapping algorithm repeatedly, winding back the clock one year each time, stringing together the years to follow the progress of each field as it grew and advanced. We found that in each case, the years leading up to a discovery followed a pattern: a burst of papers on a new, rapidly evolving topic, many of which quickly became influential. These characteristics—the percent of papers that are new, the percentage of papers that are brought in from other topics, and the influence of each individual paper—can all be measured separately for any given topic. Together, they act as a predictive signal that is detectable an average of five years before a transformative discovery is made, and up to thirty years before the discovery receives a major prize. Scanning the current research landscape for topics that display this signal allows us to predict what work will likely produce a future breakthrough. Each year we analyzed includes four or five signals, a number that appears to have remained constant across a twenty year time frame. In their classic work on the sociology of science, Bruno Latour and Steve Woolgar established that the desire to participate in a major discovery is an important motivator for scientists as they consider whether they should take up (or abandon) a research problem. Although further work is needed, the simplest explanation for our results is that this behavior is widespread enough to detect at scale. A foundational advance, or something like it, draws the attention of scientists and causes them to change the direction of their research. They vote with their feet, staking their own reputation and careers by publishing on and citing the new idea. That upswell of interest is the foundation of our breakthrough signal. What kind of research does our model identify as a breakthrough? After building a model based on the patterns in our 21 preselected breakthroughs, we tested it by identifying all early signals of discovery from 1994 through 1997. Of the 18 signals we found in that time period, 17 can be traced forward in time to a breakthrough. Examples include super-resolution fluorescence microscopy (see the image above), the directed evolution of proteins and enzymes (Chemistry Nobel, 2018), and sequencing the human genome (National Medal of Science, 2008). The discovery of the role of leptin signaling in obesity is a particularly interesting case study. Around 1950, scientists noticed the existence of a type of lab mouse that suffered from a unique inherited form of obesity. When given the freedom to choose their own diet, these mice ate more than normal and preferred food that was high in fat. Researchers had few clues as to why the animals overate; early experiments pointed to the existence of a soluble ob factor found circulating in the bloodstream that regulated appetite, but its identity was unknown. In 1994, Jeffrey Friedman and colleagues identified and sequenced the ob gene, noting that the protein it encoded appeared to fit the profile of a circulating factor. A year later, a trio of high-profile publications demonstrated that ob was a hormone that regulated body weight and fat deposition by regulating appetite. One of these was co-authored by Friedman, who christened it leptin from the ancient Greek word for thin. Using our model, the data from 1996 make it clear this advance would become a breakthrough. Scientists had flocked to study the biology of the new hormone, generating the flurry of new papers and citations required to produce a signal. One of these demonstrated that serum leptin concentrations reflected the amount of adipose tissue in the human body, providing clinical validation of the earlier mouse studies. Before the identification of leptin, scientists were unable to point to a specific molecule that controlled appetite and adiposity, so that it was impossible to rule out non-physiological causes of obesity; its characterization fundamentally changed our concept of weight gain. In 2010, Friedman and fellow pioneer Douglas Coleman were awarded a Lasker for the discovery. Our work also identifies breakthroughs in clinical practice and behavioral and social sciences, even though these areas are less likely to draw the attention of major prize committees. One example that falls into this category is the introduction of endovascular aneurysm repair, a minimally invasive surgical procedure for the treatment of abdominal aortic aneurysm, a leading cause of death among Americans over the age of 65. Relative to the previous standard of care, it reduces in-hospital mortality by almost four-fold. In 2017, Timothy Chuter received the American College of Surgeons’ prestigious Jacobsen Innovation award for his multiple refinements to the technique. Another under-recognized breakthrough identified by our model is the development of standardized survey instruments to assess the quality of life for HIV+ patients. The antiretroviral cocktails introduced in the mid-1990s reduced AIDS mortality, but treatment came with serious side effects. The new evaluations showed that patients whose disease progressed had worse physical functioning than Americans with other chronic diseases, while those who were asymptomatic maintained a health-related quality of life on par with the overall US population. This evidence made it possible for patients and activists to argue that even in the absence of a total cure, and in spite of the side effects, alleviation of symptoms was a worthwhile priority for clinicians. My colleagues and I have failed to identify any significant recognition for the physicians and health policy experts who pioneered this advance, although in 2016, researchers called for the World Health Organization to set targets for good health-related quality of life as part of its framework to end the AIDS pandemic. From forecasting to funding How should science funders use our predictions? Any serious discussion of what we should do with this new capability needs to begin with an understanding of its limitations. We can’t (and shouldn’t) invest all of our resources in the small number of topics predicted to produce breakthroughs. Innovative new fields are born from existing ones; they rarely arise de novo. If funders don’t maintain a diverse portfolio, the breakthroughs of tomorrow will have no antecedents. Think of this as eating the seed corn, or killing the goose that lays the golden egg. There are also multiple goals of funding beyond basic scientific discovery, including translating discoveries into clinical practice, developing new technologies, supporting economic development, and training new scientists. The investments needed to accomplish these goals are likely different from those required to support emerging breakthroughs. Finally, we must be aware that we may not capture every instance of a breakthrough. The concept is fuzzy, and not every significant discovery is recognized with a major award. Further, breakthroughs are rare, meaning that our dataset is, by necessity, small. This makes formal estimates of accuracy challenging. Although our overall success rate appears to be high, any one signal may turn out to be a false positive. We found one apparent example: the development of the third generation COX-2 inhibitors, Vioxx and Celebrex, which were much celebrated in the early 2000s as effective but non-addictive pain relievers, meets all the algorithmic criteria of a breakthrough. Five years after it received FDA approval, researchers demonstrated that Vioxx was associated with serious cardiovascular complications, and the manufacturer voluntarily pulled the drug from the market. Celebrex remains available, although like other NSAIDs, it carries an FDA warning for increased cardiovascular risk. Decision makers who were overly focused on the breakthrough potential of this research might have wasted substantial resources nurturing an area that ultimately proved to be a failure—but so would those who relied on expert opinion at the time. That said, the potential benefits of funding the next mRNA vaccine or cancer immunotherapy years earlier than we might have are large. When we can’t assume the outcome of an action, it’s worth conducting an experiment. Can targeted support for areas that are poised to produce a breakthrough increase the return on scientific investment without cannibalizing future advances? With the necessary administrative infrastructure in place, conducting this experiment would be straightforward. First, identify all the breakthrough signals between 2018 and 2023, select half at random, and commit to a decade of investment. For biomedicine, a six year window should yield about 30 topics with the potential to produce a breakthrough. Providing strong support to half of these might be accomplished for $300 million a year. That’s roughly half of the recent annual budget of the NIH Common Fund or around 20% of the fiscal year 2025 budget for ARPA-H. After five years, then again at ten, compare to see which group — the one that was actively managed, or the control — produced more breakthroughs, and on what timescale. Although we used biomedicine as an example, the same experiment could just as well be run for physics, materials science, or any other discipline. Any attempt to undertake such an experiment should keep three points top of mind. First, we can predict the topic of future breakthroughs, but the people and vision for how to move the work forward are still important. In practice, this means success requires active program managers with the expertise to develop the science and the authority to do so, including by recruiting investigators. Second, we would be wise to learn from the failures of past attempts to fund transformative research. High among these are funding modestly repackaged work, confusing the genuinely novel with the merely unfamiliar, and relying too much on incumbent investigators. All of these risks can be mitigated by thoroughly and intelligently integrating high quality data into portfolio management. Finally, we need to have patience. Even with strong funding support, producing a breakthrough takes time. If supporting breakthroughs is the best way to nurture the birth of new fields, we also need to accurately describe and properly manage the other two stages, so that we invest wisely throughout the productive lifetime of ideas and divest once they reach the point of diminishing returns. We would benefit from more study of all of these phases, especially the transition from one to another. More research could answer questions like: When does a breakthrough become an established field? How do the availability of funding, the size and characteristics of the available workforce, and the accumulation of evidence that disagrees with prevailing models affect a field’s decline? Exactly how do old ideas give birth to new ones, and can we speed up the process? The more we understand about the dynamics of scientific progress, the better we can maximize the odds that our curiosity leads to results. I’d call that finding a way to make our own luck.
Henri Kagan and Kenso Soai awarded the Nobel Prize in chemistry for unraveling mystery of asymmetric chemistry
The 2026 Nobel Prize in chemistry has been awarded to Henri B. Kagan and Kenso Soai for groundbreaking work in the field of asymmetric chemistry – unraveling the mystery of how molecules exist in non-identical mirror images of each other.