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Is 50 the new 60?
Subscribe TL;DR: Younger generations are showing signs of worse health compared to earlier-born cohorts at the same age This backward “drift” is showing up both in mortality risk and chronic disease Worsening trends in obesity and diabetes are the most consistent signals Taking the long view, we’ve made astonishing gains in health and life expectancy in the last century. Global average life expectancy has more than doubled from 32 years in 1900 to 73 years in 2024. (But don’t forget, there were still old people when life expectancy was 32). As people lived longer, they also generally lived healthier along the way. It turns out that avoiding things that can kill you early, like malnutrition and lots of childhood infections, also keeps you healthier later in life. In a classic 2004 paper, Finch and Crimmins proposed that cohorts of children who benefited from fewer early life infections had less lifetime exposure to inflammation and cardiovascular disease later in life, accelerating mortality improvements at older ages. Poor nutrition in the womb has also been linked to a higher risk of later chronic disease. The upshot is that improvements in childhood health can pay dividends many decades later. The combination of better living conditions (nutrition, sanitation) and medical advances (antibiotics, vaccines, blood pressure meds, etc) meant that people’s healthy lifespan generally expanded, even as they lived longer. Aging researchers call this best-case scenario “compression of morbidity”—meaning we delay the onset of disease and disability even faster than the years of life we are adding. During my 20+ year research career, we could generally bank on the idea that younger generations would not only live longer but also keep getting healthier along the way. “60 is the new 50” as they say… Enter “Generational Health Drift” Sadly, this expectation of steady progress may be changing. You’ve probably heard that US life expectancy gains have slowed to a crawl in the past couple of decades. Mortality improvements are also slowing (though less dramatically) in many other high-income countries (you can read more about that in a review paper I wrote here). Mortality is a very blunt health measure, but it is often a good barometer for the broader population health trends happening underneath. And we are now seeing that younger generations may be in worse health at similar ages compared to earlier born cohorts. My collaborator Prof. George Ploubidis at University College London coined this worsening health in more recently born cohorts “generational health drift.” “Generational health drift” is bad news on multiple fronts. Most obviously, we don’t want our health progress to go backward. But the timing is also bad, since our populations are aging. In demographic terms, “population aging” means that the proportion of the population at older ages (i.e >65 years) is increasing. Fun demography fact: Current population aging is not due to the recent declines in the birth rates making the news, but declines in fertility decades ago, after the “baby boom.” As baby boomers reach older ages, the smaller cohorts behind them mean the percentage of older adults will increase. For example, the share of the population age 65 and older in the US increased from 12.4% in 2004 to 18.0% in 2024. This story of population aging was written long ago. Many worry that population aging will put pressure on health care and pension systems. But if people reach older ages in better health than in years past, those fiscal pressures would be less dire than projected. Healthy older people can also continue to contribute to society in many valuable ways, including paid work, caregiving, community service….even high political office 🤷. On the flip side, if younger generations reach retirement age in worse health and with more disabling conditions, this could magnify the societal challenge of population aging. Evidence for worsening generational health A recent paper that I LOVED in the Proceedings of the National Academy of Sciences by Dr. Leah Abrams and colleagues examined which birth cohorts (aka generations) were behind worsening US mortality. Behold the Lexis diagram (cue swooning demographers). Calendar time is on the x-axis, age on the y-axis. Birth cohorts can be followed over time as they age on the diagonal lines moving up and to the right. This figure plots the year-on-year % change in all-cause mortality at a given age. Green shading indicates mortality improvements over time, white is stagnation, and gray shading indicates worsening mortality. Following the diagonal line for those born in 1950, you can see a noticeable shift from green to gray that follows this cohort for most of their lives. This gray shading shows generally worsening mortality for the 1950 to 1959 birth cohorts compared to their predecessors across all ages. Concerningly for my GenX and elder millennial peeps, there was also a deterioration in mortality for birth cohorts born in the 1970s and 1980s, visible as dark gray areas at ages 30 to 45 during the 2010s. While some of these mortality changes reflect specific shocks such as the opioid epidemic, most deaths still occur from major causes of death such as cardiovascular disease and cancer. For cancer, the gray in the top left corner of the figure below reflects the legacies of smoking for older cohorts, followed by a period of green with improvements in cancer mortality as smoking rates declined. But the white/gray shading in the bottom right corner highlights a stagnation and reversal of the cancer trends, with cohorts born around 1970 to 1985 experiencing worsening cancer mortality. This deterioration was most noticeable for colon cancer mortality, possibly linked to obesity or dietary factors. Not just dying more, but less healthy along the way. A recent paper by Dr. Laura Gimeno of University College London (of which I am a co-author), found evidence that more recently born cohorts in Great Britain have stagnating or worsening health. A stylized picture of what“generational health drift” might look like: The review paper found: Rates of childhood overweight and obesity were highest among Gen Z. Rates of diabetes in the 40s almost doubled from 3.1% among the Baby Boomers to 5.9% in Generation X. Gen Z reported higher rates of poor mental health in adolescence compared to earlier-born groups. These UK results are consistent with studies showing worsening health across generations in the US as well. A 2021 US study found that more recently born cohorts had worse biological markers (like blood pressure and blood sugar) than earlier generations at the same age. A separate 2022 study of Americans aged 50 and over found that more recently born generations had a higher number of chronic diseases, with younger age of disease onset. A 2024 Lancet paper found that in the US, women born in 1945 had 33% obesity prevalence at age 50, rising to 48.2% for women born in 1970 turning 50. So what’s going on, and can we turn it around? We don’t have a definitive answer for what’s causing the deteriorating health of younger cohorts, but circumstantial evidence points to worsening trends in obesity and diabetes in both the US and UK. Remember that cohort trends reflect lagged effects of early environments, and younger generations have faced both earlier onset and more severe obesity across their lifetimes. Despite these very concerning trends, the future is not set in stone. We’ve reversed poor generational health trends before: drops in smoking are a major reason cancer and heart disease deaths fell so dramatically in recent decades. GLP-1 drugs may finally turn the tide against rising rates of obesity and diabetes, though it is still early days. But things could also get worse…for example from a return to higher levels of childhood infectious diseases that can have a lasting impact on health. See for example: [ ](https://jenndowd.substack.com/p/dont-you-forget-about-measles-the) [ Don’t You Forget About Me(asles): The Virus That Erases Immune Memory ](https://jenndowd.substack.com/p/dont-you-forget-about-measles-the) Jenn Dowd, PhD · March 24, 2025 [ Read full story ](https://jenndowd.substack.com/p/dont-you-forget-about-measles-the) Even as an optimist, emerging data on the “generational health drift” has my full attention. For most of my research career, we took it for granted that each generation would be healthier than the last. But if present trends continue, **50 could be the new 60….**and Gen Z celebrities will soon look older than Paul Rudd :). Stay well, Jenn Share the Health! If you found this post useful, please share it with a friend. Share
The Big Holes in Wearable Heart Rate Variability And Readiness Scores
On September 9th, Apple announced it was revamping its Apple Watch Health Sensing System, rolling out a Readiness score (0 to 10), and increasing the frequency of heart rate variability (HRV) outputs 24-fold. This can be viewed as upping its competition with various other consumer wearable sensors. These “readiness scores” as a composite of multiple metrics, with heart rate variability (HRV) being front and center for most. The majority of Americans are now using wearable sensors, which equates to well over 100 million adults. HRV and Readiness scores are increasingly being marketed as a measurement of autonomic nervous system health, a digital marker for future disease, a clock for biological age, and a holistic metric to promote healthspan and even longevity. (Apple also introduced a new longevity tab and “Health Age”.) None of this has been proven. In this edition of Ground Truths I am going to review what we know about heart rate variability and readiness scores. Heart Rate Variability HRV is the variation in normal heart cycle timing. The variability of the heart rate, the barely perceptible millisecond changes in time between consecutive heart beats (see R-R intervals in the Figure below, left panel), is due to interplay between the sympathetic and parasympathetic (vagal nerve) inputs. Distinct from heart rate, individuals with the same heart rate can have very different HRVs. It is a rough reflection of the autonomic nervous system (ANS) activity, inadequate to say whether a person’s ANS function is abnormal. For more than three decades, heart rate variability (HRV) has been measured and several studies have found an association of low HRV and clinical outcomes, particularly a link with higher all-cause and cardiovascular mortality. There have also been less well established links of low HRV to risk of early cognitive impairment, dementia, mental illness, Type 2 diabetes and substance abuse. An important reminder is that HRV is a surrogate marker without any established cause-and-effect relationship. If you increase your HRV, that doesn’t mean it will improve health outcomes. In fact, there is no hard evidence for that. All that work linking to health outcomes was done with electrocardiogram (ECG) derived HRV. Now, in the era of consumer wearables, this is getting assessed differently, by optical pulse (yes, the lights you see) plethysmography (PPG) or what is called pulse rate variability (PRV). They are not the same, as shown below (right panel) and only concordant when the delay between the ECG and pulse is kept constant, which basically means at rest. I should mention there’s also what I will call MPV, a mattress mechanical movement sensor, a derived heart rate variability, that companies like Eight Sleep use, even further away from directly measuring HRV. HRV has not one uniform measurement but many different types of quantification, such as RMSSD, the magnitude of difference between successive R-R intervals of normal sinus beats (N-N) or SDNN, the standard deviation of NN intervals, both in milliseconds. SDNN is one of the so-called frequency domain HRVs (others are LF, HF, LF/HF). Different wearable sensors use different metics; Apple has relied on SDNN and nearly all of the others use RMSSD, which is generally considered the more accurate metric. There’s also the different length of time measured, such as for a matter of minutes, all day, or an overnight’s sleep. Short measurements are especially problematic since they don’t capture enough of respiratory modulation and other factors that influence HRV. Share Ground Truths How well does HRV correlate with PRV? There are very limited studies, especially independently done. One that is commonly cited was conducted by Air Force researchers in only 13 healthy adults assessing Oura ring 3 and 4, Whoop 4.0, and Garmin Fenix 6 and showed a correlation coefficient of 0.88 to 0.97 and a mean absolute percentage error from 6 to 10%. The correlation is not a perfect 1.0, but there’s at least a fairly high level of correlation. HRV is supposed to increase during the night due to takeover of the parasympathetic nervous system, and higher during deep sleep. A recent example of my 1 week, all day “HRV,” and one during sleep is shown below. As you can see, the N of 1 data are inconsistent for the same days from different sensors (Oura, AppleWatch, Fitbit Air, and Eight Sleep) by patterns, absolute numbers, and comparison with prior days and weeks. The largest study in over 8 million Fitbit users (the old version, not Google Fitbit Air, introduced in May 2026) gives you a sense of the effect of age, sex, and the 2 different main HRV (here PRV) metrics, with RMSSD on the left and SDRR (=SDNN) on the right below. That study, from data collected in 2018, is a major outlier, since all the more recent ones are tiny with respect to sample size. Many of the companies have not had independent evaluation of their HRV, such as Eight Sleep, but have published a low standard error on their website. There are some other published studies on the correlation between HRV and PRV, but they are all small and only in healthy adults. A scoping review emphasized the lack of study in underrepresented individuals, including the aged, people of color (which affects the PPG signal), and individuals who are underweight or obese. Add the typical adult age 60 plus with one or more chronic diseases. For example, one study in over 900 adults found poor correlation of HRV and PRV, non-uniformly underestimated across many chronic diseases (cardiovascular, endocrine, neurological, respiratory, and others), concluding PRV is “an invalid surrogate for HRV.” A recent systematic review of 43 studies comparing HRV and PRV found reasonable pooled absolute standardized error (HRV as gold standard) but only 10 of the studies provided quantitative synthesis in ideal conditions. Their main conclusion was similarly cautious: “PPG-derived HRV [PRV] should not be regarded as universally interchangeable with ECG-derived HRV across all devices, populations, and recording contexts.” Factors Affecting HRV and PRV That gets me to the long list of factors that affect HRV (and PRV) besides the device, the type of measurement (RMSSD, SDNN or others), the person’s signal, the sensor site, the duration of data capture, if weighting by sleep stage is used, how artifact is processed and corrected. And this list is not complete!: Oura puts out data from their community of users (who input data) on what affects their overnight HRV. The factors currently provided are: no alcohol (increase 8%), melatonin (increase 2%, float tank (increase 2%), wine (decrease 4%), and party (decrease 14%) in overnight HRV. Must be some big parties! Subscribe What is a PRV measurement good for? It has been falsely characterized as an index of “autonomic balance” and a specific indicator of stress. A 2018 review of the studies available for HRV and its relationship to stress, not using any of the current wearables, found that stress can lower HRV. But so can many other factors. The non-specificity of the signal, indexed to the table above, is striking. Evidence from a UK Biobank study of over 46,000 participants with actual HRV looked at genetically predicted HRV, a genetic risk score, that failed to show the expected HRV-mortality link, indicating that _HRV is likely not causa_l, but rather a reflection of person’s physiologic state. A review of consumer wearable HRV data from 5 longitudinal studies showed that nighttime PRV was not associated with perceived stress, and surprisingly higher HRV, in the largest cohort (N=717 participants), was correlated with higher stress. An Oura ring cohort of 525 first-year college students found a link between overnight PRV and perceived stress, but that was also seen with resting heart rate, sleep, and respiratory rate. Several very small studies have examined the relationship of HRV and athletic injuries or guiding training with mixed, and predominantly negative results. HRV biofeedback training with paced breathing had no significant effect on reducing stress or raising HRV, as demonstrated with sham controlled trials. When HRV for multiple days showed a decline in conjunction with body temperature, the Oura ring published data for prediction of Covid. The WHOOP company sponsored an observational study, published in 2026, of 30,000 users for 72 weeks, without a control group, that reported reduced alcohol intake (5.8 % points) by self-report. That doesn’t tell us much, and particularly about the merits of HRV for behavioral change. If you use the same device and conditions as longitudinal trends for multiple (at least 2-3) weeks that may be the one way to get something useful from the measurements. Data for overnight sleep with minimal motion and using RMSSD is the best proxy for real HRV. The reason to look at trends rather than any given night is that it more likely represents something, even though you won’t know with certainty what the “it” is. Keep in mind there are no data, no peer-reviewed evidence, to show that HRV fluctuation in-person has any correlation with health outcomes. Share Readiness Scores These are proprietary scores that integrate different metrics for each of the wearables: no algorithms have been disclosed. They are unvalidated against health outcomes. In a review of 14 composite health scores of readiness and recovery, HRV contributed 86% to the scores, followed by reading heart rate (79%), physical activity and sleep duration (both at 71%). That review noted the substantial variability in measurement protools and lack of standardization. Sleep staging is notoriously inconsistent and inaccurate by these sensors, which adds further to the HRV uncertainties for what the scores, which use sleep stage data, mean. Only resting heart rate has been shown consistently across devices to be extremely accurate. I’ve made a Table to summarize what we know about which metrics are included, the scores, any peer-reviewed studies that compared the readiness score with health outcomes, and the corresponding (if any, NA-not available) citation. You will note that some companies do not use the term “readiness," such as WHOOP for recovery, and Garmin, which has 2 different scores, one of which is Body Battery. Eight Sleep uses the term “Fitness Score.” They all include HRV; Apple includes a new metric they call “Recovery HRV” which among other components uses 7-days of sleep, but it is unclear what this means or how it is differentiated from other scores (there are clearly no data for outcomes). We have no knowledge of how the different components are weighted or whether any of these scores are better than resting heart rate, HRV alone, physical activity, or any other single metric. Since none of these are standardized, they are not interchangeable, so if you get a 90 for Oura that has no relationship to a 90 on a Google Fitbit Air. Notably, the company can update its algorithm for readiness score at any point without notification to device users. Without any useful evidence of actionability for these scores or established relationship with health outcomes, it is hard to make a case for their value. At the Apple recent announcement they showed their Readiness score (0-10) on the watch (Figure below) but there are no published data on this score, not even on their website. It’s available only on their new Watch Series 12 or Ultra 4 [of course, ;-)]. That exemplifies the problems with these scores, lack of data and evidence for being meaningful to promote health. Perhaps the best study (which isn’t saying much) is the WHOOP Recovery for golfer performance, because it did correlate with an objective outcome, even though there was no control group and the authors were all from the company. Among the 389 pro golfers, an absolute 10-per cent point increase in Recovery score was associated with about 0.5 fewer strokes per round. But that’s hardly a health outcome! WHOOP is also conducting a study in over 2,700 runners to see if their recovery score will be linked to less injuries and improved performance, but that is not yet published and has no control group or randomization. Putting This in Context For two decades I’ve been enthusiastic about the potential for digital health and particularly wearable biosensors. Over the years, we’ve seen some great progress for their ability to promote physical activity and accurately detect atrial fibrillation (the first FDA cleared deep learning AI for consumers). That work was the subject of rigorous research. But there are holes in the data and evidence for other metrics. One notable one is the “VO2 max” story that I wrote about earlier this year. At that time many subscribers asked me to cover heart rate variability, which I finally got to here. When I dived into the research and publication for HRV and readiness scores, I expected to find at least some that were of high quality and demonstrated their utility by linkage to health outcomes. To my surprise, I found none. The wearable sensor measurements for HRV (PRV) are, for the most part, accurate, but that validation work has only been done in small studies of healthy adults and does not take into account the long list of factors, from the device, software side, and the user side, that affect HRV measurements. Moreover, this metric chiefly relies on optical sensing and, as we have learned for heart rate PPG sensing, may be less accurate in people of color. Keep in mind that all of the health outcome association evidence comes from ECG-derived HRV; none are from wearable sensor data. I will repeat the key point: there's no peer-reviewed evidence to show that in-person HRV fluctuation—or efforts to raise your HRV— has any correlation with health outcomes. For those of you who look at your HRV on awakening, or even 2+ week trends of it being low, I hope this context helps to relieve any anxiety. Yes, low HRV (not PRV) has been shown to increase risk of some diseases as summarized above. But efforts to raise your HRV—a surrogate metric— has not been established for improving any health outcomes. HRV does not have any evidence of causality (the genetic evidence actually goes against this possibility). In this summary, I have not included data for other wearable sensors such as Polar, Samsung, Withings, Suunto, Amazfit, Coros, Ultrahuman, or additional mattress sensors. These are beyond my first-hand experience, and as far as I know from my in-depth review none have any peer-reviewed published data that differ from the 6 sensors I’ve reviewed here. From the points I’ve gone over above, we’re not ready for readiness scores. Besides being proprietary, they are predominantly based on metrics that have their own issues. It’s compounding the problem, like building a house without a solid foundation that has never undergone a rigorous inspection, and then selling it. Like I mentioned for PRV, you can look at trends over weeks rather than any single day, to get a handle, but even that may not be helpful. There’s simply no evidence that these scores meaningfully relate to health outcomes. I’d emphasize they might, but that requires doing prospective or randomized studies to prove it. None exist. There’s great promise for HRV/PRV utility_. For example**,**_ Prof Maiken Nedergaard, who discovered the brain glymphatics that are essential in eliminating metabolic waste products from the brain during sleep, has posited that HRV could be a non-invasive marker for neuromodulator oscillations, brain-body regulatory circuits, and brain clearance. That would be extremely useful, but like everything else on HRV and readiness scores it requires solid research and validation. The lay media isn’t helping much to get the story straight. Earlier this year The Economist published a piece entitled “The most useful indicator of your overall health” which ordained HRV as an “accumulated stress score.” That’s akin to the false assertion about VO2max: “V02 max is the singular most powerful marker for longevity.” As I’ve summarized here, that is not established. The fact is that so many things can lower HRV, including physical exercise (especially an intense workout), reduced sleep quality, stress, the list above, no less the device, signal, and software. Whatever fluctuations observed have not been correlated with any health outcome. Sadly, “datamaxxers” are widely using HRV and readiness scores that have never been validated to mean anything. We already know that for some people using the sensors for sleep metrics, it can induce “orthosomnia,” an obsession to get high sleep quality, with associated high levels of anxiety. In an experiment done by a company to promote sleep quality for its employees, “For those employees who did use the trackers, many reported feeling perfectly rested until their tracker told them they had had a terrible night. Others were told that they had slept like a baby when they had actually been lying awake worrying about the quality of their sleep. “ The same problem can result from preoccupation with HRV or readiness scores, with anxiety that would lead to further reduction in both. It you are using a wearable like >100 million American adults, it’s OK to look at these data, but contextualized with the major caveats reviewed here. If you are one to require evidence that HRV or readiness scores are linked to health outcomes, you may not even want to look. The companies make it hard to turn them off! Let me end with the companies that make and sell wearables. Apple’s doubling down on HRV (24-fold more reporting and heart rate very 5 seconds) and introduction of a Readiness score tells us that consumers have bought into these metrics and they are joining the club. However, all of this is occurring with a backdrop of tens millions of users, claims about the data that are not backed up by adequate evidence, marketing way out in front of whatever limited data exists, and not being transparent about their readiness score algorithms. The companies can well afford to do the research that is needed to connect these metrics with health outcomes show, once and for all, that increasing HRV or using readiness scores promotes our health. If they believed and invested in the products they are selling, we’d not be in this position of not knowing. That’s essentially where we are with HRV and readiness scores. Perhaps someday this will change and we’ll have good reason to embrace them. NB: I wrote this post. No AI. I have no conflicts of interest with any of its content. Loading... Ground Truths has 215,000 subscribers from every US state and 214 countries. There are over 300,000 followers of Ground Truths so more than 90,000 folks who can easily convert to be free subscribers. Your subscription to these free essays and podcasts makes my work in putting them together worthwhile. If you’re not a subscriber, please join! If you found this interesting PLEASE share it! Share Ground Truths The proceeds from all voluntary paid subscriptions go to support our summer internship program. It enabled us to accept and support a record number of 62 summer interns that joined us in 2026! These are high school, college and medical students selected from thousands of applicants. We couldn’t do this expanded program without the funds coming in through Ground Truths. Thank you!
Science Vs on the 49ers Substation: Anatomy of a Hatchet Job
In August, Pablo Torre Finds Out and Science Vs released an episode about my theory that electromagnetic fields from the electrical substation beside the 49ers facility may be contributing to the team’s run of soft-tissue injuries. As the originator of the theory, I was also a subject of the episode. I sat was interviewed by Wendy Zukerman and Rose Rimler of Sciene Vs. I sent them research, connected them with scientists, and spent hours digging through the City of Santa Clara’s and Silicon Valley Power’s records to help clarify critical details. Both Wendy and Rose came off as affable and professional, showing curiosity during the interviews, with Wendy going out of her way to question the “conspiracy theory” framing itself. Then they titled the episode We Solve the 49ers Viral Conspiracy Theory. I was familiar enough with their catalog that I never expected them to agree with my theory, but I did expect them to give it a fair hearing and to deliver their findings honestly. On both counts they came up short. They were not directly dishonest in anything they said, but rather in what they left out, in how what remained was cut, and in the picture painted by those two things in combination. They asked me to recorded the interview on my phone for better audio quality, and I held on to my copy for reference later. That turned out to be a fortuitous decision. Here is the raw audio of my first interview, unedited*. Only my side was recorded, so their questions aren’t on it, but you can generally infer them from the answers, and every claim I make below about what I said can be checked against my statements in this clip. (Note: Wendy had connection trouble at the beginning of the interview and was cutting in and out, which accounts for the false starts.) 0:00 -1:19:13 Audio playback is not supported on your browser. Please upgrade. Science Vs is a fun show. It is pitched at roughly a high-school understanding of science, for an audience that is skeptical, Snopes-oriented, and worried about misinformation. Take a claim circulating online, interview a supporter of the claim, interview consensus scientists, and then tell people which side of the line it lands on. I have listened to their episodes on raw milk, seed oils, 5G and other contested issues in the wellness space. I have problems with all of them, but each at least made an honest attempt to represent the actual range of scientific opinion by talking to credentialed scientists with differing perspectives. Dissenting researchers were heard from, answered, and often given a chance to respond. This episode did not do that. This article is not a relitigation of the science. I have written extensively about that already. This post is for the record. It is simply an accounting of what was wrong with their episode. Contents Is there a power plant next to the 49ers practice facility? — the clearest single example of getting something objectively wrong For the record — a high-level overview of all of the problems with their investigation Draw your own conclusions — why they had to make this episode at all What they left out about childhood leukemia — the exposure threshold, and playing games with statistics to minimize sick children What they left out about the mechanism — the body of literature they refused to cover, and evidence for the mechanism used against it The scientists Science Vs interviewed and did not air — four credential scientists who support myhe theory, recorded and cut, or not even called How they misrepresented me and my case — an answer severed from its question, and three telling edits How you would actually study the injuries — it doesn’t actually matter which team is the most injured, overall The theory: magnetic fields, oxidative stress, and collagen Since the episode never states my theory, here it is below. Those who are familiar with my work can skip this section. Electrical equipment produces magnetic fields, and those fields induce faint electrical currents in anything that passes through them, including people. My argument goes further than induced current. Mitochondria — the structures that generate a cell’s energy — run on continuous flows of electrons and protons, and those flows carry faint electromagnetic fields of their own. Maxwell’s principle of superposition shows that when two fields share the same space, they add together. An external field does not need to be strong to alter an internal field, it only needs to be present. The electron transport chain inside the mitochondria leaks a small fraction of its electrons by design, and those become reactive oxygen species — free radicals, which healthy cells use as signals. External magnetic fields cause the rate of leakage to change, increasing free radicals. When free radicals accumulate faster than the cell’s antioxidant systems can clear them, the result is oxidative stress. Oxidative stress is a recognized driver of chronic illness, including cardiovascular disease, neurodegeneration, diabetes and cancer, and it is in every medical school curriculum. One of its ordinary effects in connective tissue is that it switches on matrix metalloproteinases — MMPs, the enzymes that break collagen apart — while suppressing new collagen synthesis. Tendons are made of collagen. An athlete loading his soft tissue heavily six days a week is already creating oxidative stress in the tendons, so the addition of magnetic field exposure compounds the damage and inhibits repair, making him more susceptible to injury when enormous force lands on a tendon in a fraction of a second. That is the theory. We know that EMF causes oxidative stress, and we know that oxidative stress degrades collagen. The only thing missing is a study showing that direct connection. I have never claimed certainty that the substation is contributing to the elevated injury rate. I do believe it is likely, and I believe it warrants caution, and that a revenue machine like a major NFL team can easily afford to remove the exposure out of precaution. Is there a power plant next to the 49ers practice facility? Here is the clearest single instance of the problem with this episode. It requires no knowledge of electromagnetic fields at all. This story first came to me through Jon Feliciano, a former 49er, in an interview on Willard & Dibs on 95.7 The Game. Asked about why the 49ers are always injured, he said players used to joke that it was the power plant behind the practice fields. Wendy Zukerman corrects him on air. “It’s important to say that it’s not a power plant near the 49ers site.” Torre then asks her to explain the difference between a substation and a power plant. Her answer: a power plant generates electricity and transmits it to a substation, which converts the voltage into something your house can use and sends it on to your home or your business. There are two problems with that. The first is that there is a power plant on that site. The Gianera Generating Station is a natural-gas-fired peaker plant owned by Silicon Valley Power, and it has been there since 1986. I have published aerial photographs of the location from 1987 in which the gas plant is the only thing standing, before the practice facility was even there. I even mentioned the gas plant in my first interview. (Feliciano has since gone on record about this issue, and it is clear he had the substation in mind rather than the gas plant.) The second is that her definition describes a distribution substation, and the facility beside the 49ers is not that. It is the Northern Receiving Station, which takes in bulk power from outside the city’s grid and delivers it to distribution substations. Silicon Valley Power’s own map distinguishes receiving stations from substations, and Rose Rimler even reads the label out loud in the episode when she walks through that map on air. A few minutes before the map segment, Zukerman tells Torre: “like I said, we fact check everything.” Well, maybe not everything. I made a mistake On the morning of July 6th, at 10:20, I sent Rose and Wendy two studies. During the interview I had been asked which human studies show oxidative stress from electromagnetic fields, and I had not been able to name one on the spot. Rose emailed asking for the studies, I quickly searched for a couple, and I wrote that I thought these were the most relevant from that search. Unfortunately, I was busy and did not read either one closely at first. I picked them because they were topically relevant — one on substation workers, one on power plant workers. Neither were great studies, and their problems go past the ones raised in the episode. That was careless on my part. There is context that did not make the episode, though. Before that email I had been on a Zoom call with Rose talking about EMF and oxidative stress, and I pointed her to Dr. Henry Lai at the University of Washington, who has spent years aggregating the literature on this question. His tallies show that roughly 90% of studies since the late 1990s find oxidative effects from electromagnetic field exposure — hundreds of studies, systematically counted. Rose told me she was already aware of his work. So when she asked for studies, I understood her to have the aggregate view already and that she would report anything within that context. Not reading those two carefully was still a mistake, but the larger mistake was assuming the episode would be based on a thorough review of the actual body of literature, rather than on whatever I happened to send that morning. The second email At 1:49 that same afternoon — three hours and twenty-nine minutes after the first — I sent them a second email that I had been preparing for a while. It was a structured document in six numbered sections, written in response to a request they had made two weeks earlier, laying out my entire argument with citations attached to every link in the chain. The episode aired on August 13th, five weeks later, and not a single item from the second email is in it. Here is how it opens: The full email is included at the bottom of this post in Appendix B. Nearly 1,500 words in total. It contains two named mechanisms with the physics behind them. Occupational studies in humans. The literature on oxidative stress and collagen. A section addressing the strongest counter-evidence against my own theory, which I raised myself. And a closing section stating plainly what the theory cannot yet show. My entire argument, in writing, with detailed citations for every claim, provided to them five weeks before broadcast, and none of it made it into the episode. That is the single largest omission, but it is not an isolated one. The whole episode is riddled with similar problems, and the conclusion they came to is not merely a difference of opinion about the scientific evidence. Through omission and through strategic editing, Science Vs misinformed its audience — about what the evidence shows, about what I argued, and about who they spoke to. That is a notable outcome for a show whose stated purpose is correcting misinformation. For the record I am not going to tell you that Science Vs set out to discredit me, or that they had come to their conclusion before they reported the story, or that they used misleading editing to make me look like a man retreating from his own theory. I cannot know what was in anyone’s head, and I am not going to pretend otherwise, either. What I can tell you is what is on the record. They asked me for evidence and aired the weakest thing I sent. They interviewed three scientists who supported my theory and aired none of them. They discussed childhood leukemia without ever saying the exposure level at which it appears. And they took an answer I gave weeks before Ken Karipidis, the one EMF scientist who was put on air, was interviewed, and placed it directly after his critique, where it comes off as a major concession. A friend of mine who has worked as a journalist for thirty years read that last one and called it sleazy. I agree with her. Those are just the four issues that are impossible to defend as pure editorial decision, but they are not the only issues. The most glaring issues stem from what they left out: The exposure level at which the childhood leukemia association actually appears — three to four milligauss, a number the episode never states despite it being much lower than what I measured. The mechanism itself: The episode gets as far as “oxidative stress could weaken collagen,” which leaves it sounding like speculation, rather than a known pathway. The second email, and all the studies in it. Dr. Paul Héroux at McGill, whose work my proposed mechanism rests on, whose contact details I supplied, and who was never called. Dr. Beatrice Golomb at UC San Diego, who runs a research group on oxidative stress and mitochondrial function and has specific expdertice in collagen, interviewed and not aired. Dr. David Carpenter at Albany, the most prominent academic voice on the harm from magnetic field exposure, interviewed and not aired. Dr. Joel Moskowitz at Berkeley, interviewed and not even credited. The specific, testable condition I put in writing that would make me abandon the theory. My own unprompted statement of the theory’s evidentiary gap. My caveats about my own measurements. My ranking of EMF as one factor among several rather than the only one. The new equipment installed at those facilities between 2010 and 2014, and the sharp rise in system load from 2013 onward. But that is not all. What they kept, they selectively edited to serve a narrative that was not served by the raw transcripts of the interviews. A description of thousands of commercial routers in a workplace, reduced to the Wi-Fi in your house. My own acknowledgment, multiple times, that "I'm not a scientist" clipped in an episode that spends considerable energy pointing out that I am not a scientist. And a qualification I volunteered about my own measurements, cut from my answer and delivered later by their EMF expert as a correction. Together their edit produce a portrait of a wellness guy with Wi-Fi phobia and two bad studies, backing away from his theory the moment a “real” scientist looked at it. A practice facility where nothing changed because no new substation was built. Injuries written off as random because the 49ers were not quite the single most injured team in the league over the period in question. That portrait is false even though almost no individual statement made in the episode is. Draw your own conclusions At the top of the episode, Pablo Torre says his show had been flooded with requests to investigate the substation — that it was the thing they were asked to look into over and over again. Neither show went hunting for this story. It arrived from their own audience, in volume, and it could not be waved off. A thread I posted on X reached twenty-two million people. A guy with a gaussmeter and a brand-new Substack obligated a Pultizer prize winning program to spend an hour on a question about player health, that is considered fringe enough that most media operations won’t touch it. Pablo Torre Finds Out could not ignore it. So Science Vs came in and ran a “debunking” operation instead of an investigation. Everything below is what had to be left on the cutting room floor to deliver the “debunking”. They could not ignore it. So they tried debunked it instead. The demand was strong enough to force an episode, and since the episodes release the 49ers have sustained more injuries, including season ending ones, and interest has only grown. Demand from fans and playets is strong enough to force a better investigation from someone else. An omission is not a lie until you find out what was omitted. What follows is the detailed record so you can see the full picture. Draw your own conclusions. I have drawn mine. I am going to keep publishing. A note about Pablo Torre Finds Out After the episode aired I posted publicly, calling out Pablo Torre Finds Out for concerns I had about the integrity of their investigation, and about an interview directly with Pablo Torre which had been offered but never happened. I have since spoken with a producer at PTFO. The offer had rested on a misunderstanding about where things stood between us, and it fell away as the Science Vs part of the production widened past the science. He apologized for the miscommunication and I accepted. The producer also confirmed to me that they did essentially hand off the entire investigation to Science Vs for narrative purposes — so Pablo would be genuinely curious or potentially surprised by their findings — while still taking responsibility for what went out under their name. I appreciated the candor and the accountability, and I am comfortable with where we left things. So this post is not about PTFO. My disagreement is with Science Vs. What they left out about childhood leukemia Childhood leukemia appears at three milligauss. They gave no number at all. 1. They built an EMF ruler, then discussed childhood cancer without it. The sequence on air went like this: First I measured almost 9 mG, then I measured up to 50 milligauss. Torre reacts with concern — “that sounds high.” Cut to Karipidis: the public limit is 2,000 milligauss. Torre reacts again — “What happens at 2,000?” Karipidis explains that nothing happens at 2,000, that safety factors are built in. Then: at more than 50,000 milligauss you get flickers of light in the retina, and higher still, nerve stimulation. The listener now has a ruler (their ruler) to measure these numbers with. Fifty is nothing by their ruler. Then the episode turns to childhood leukemia and states, accurately, that there is a real association — but tellingly, they never give the exposure level at which that association appears. Childhood leukemia appears at three milligauss. They conveniently left that out. The pooled analyses that produced the World Health Organization’s carcinogen classification found roughly a doubling of childhood leukemia risk above three to four milligauss. That is the number that belongs in that segment, and it is more than ten times below the reading that had just been dismissed as trivial. I gave them that number myself, on tape, in the interview. Describing my own threshold, I said my comfort level for long-term chronic exposure is three to four milligauss, but preferably one. 2. Six children in thirteen million. The episode reports that these fields might explain one to four percent of childhood leukemias, then reframes it as a German estimate of perhaps six cases among thirteen million children. Torre, to his credit, is uncomfortable. What never gets explained is why that number is small. Almost no children lives above three milligauss in Europe. Fewer than two children in a hundred, in the Italian data. So even if the risk to those children doubles, the number of additional cases across an entire country stays small — not because the hazard is small, but because hardly anyone is exposed to it. Count the whole population and the few who are exposed disappear. And the reason hardly anyone is exposed is that siting rules keep housing away from transmission lines. In Europe, at least. The Dutch government has a standing precautionary policy against building new homes in any zone where the annual average magnetic field exceeds 4 milligauss — the same number the episode never mentioned. Denmark and Norway treat 4 milligauss as the level that triggers a look at mitigation. That is five hundred times below the ICNIRP figure quoted on air. The United States has no federal equivalent. That is evidence of infrastructure siting policy working. It is not evidence that there is no hazard. It is evidence that we already act as though there is one. If you listen to the raw audio you will hear that my proposed solution is EMF exposure is to build better infrastructure. What they left out about the mechanism 3. They accused me of cherry-picking, and then cherry-picked themselves. On air, Zukerman tells Torre that people who worry about electromagnetic fields dismiss the studies showing null results and collect the ones showing harm, and that this is why you have to be careful not to cherry-pick. They had two papers I had rattled off in a hurry, and a second email containing a carefully chosen set. They ran the two weakest, graded them on air, and presented the result as the state of the evidence for not only my theory, but the whole question of oxidative stress from magnetic fields. That is cherry-picking from my emails. The bigger picture is what they did with the literature as a whole. Zukerman acknowledges it exists, dismisses it, and disposes of it in a single stroke. You can go online right now, she tells Torre, and find scores of studies showing these fields increase oxidative stress. The issue, she says, is that they are not studies in people. Many of them are in people. The occupational studies in my second email are in people. That email had been in her inbox for five weeks. She waved off the literature on a factual claim that the documents in her possession contradict. (I have written separately about the evidentiary standard at work here). The effect was that they essentially baited me: ask the subject to supply the evidence, take the weakest thing he sends, and let that stand as a proxy for the whole argument. Wendy has been doing this show for ten years and clearly knows how to extract what she needs for her desired narrative. 4. They presented the collagen-improvement research as a gotcha, but I had already addressed it. The episode treats the existence of studies showing that EMF can improve collagen as a surprise that undercuts me, but I had pre-emptively addressed that five weeks earlier in the email they ignored. Those studies use measured, high-intensity pulsed dosing. The mechanism by which they work is oxidative signalling. The cell reads a controlled rise in reactive oxygen species as a warning, upregulates its antioxidant defenses, mounts a repair response, and the therapy stops before the system is overwhelmed. The key point is that it induces an oxidative response, which means those studies are actually evidence for my proposed mechanism, not against it. A field that produces a therapeutic effect cannot be biologically inert (which is the implication when they say “Nothing happens at 2,000 milligauss). Chronic ambient exposure is the same pathway with no off switch, and it is most consequential during the evening and while sleeping, when the body is in repair mode and the exposure does not stop. Section 5 of my email is titled What about the study showing improved collagen synthesis. I raised the counter-evidence myself, explained why I did not think it refuted the theory, and wrote that I was disappointed the question had not come up in the interview. That is worth holding against the cherry-picking charge in the item above: the studies they presented as inconvenient for me were studies I had gone out of my way to put in front of them. 5. Section 1 of my email stated a critical argument that was never put to the expert directly responsible for it. My email says the exposure limits exist to prevent acute effects and do not address chronic exposure at all, and that my dispute is with the entire framework. Zukerman gestures at this once. After Karipidis gives the 2,000 milligauss figure, she tells Torre that I would object because those levels do not capture “more subtle effects.” That is not my argument, and “subtle” is doing a lot of work here. My argument is that the limits are built to prevent acute effects — nerves firing, muscles twitching, etc — and were not designed to address chronic exposure at all. In fact, ICNIRP’s own documents state as much themselves. Mine is a structural objection to what the standard measures, reduced as a concern about subtlety, it becomes a matter of degree, rather than a categorical difference. They interviewed Ken Karipidis, vice chair of ICNIRP — the body that writes those limits. He was asked what the limit is, but he was never asked how it applies to chronic exposure. The scientists Science Vs interviewed and did not air 6. They interviewed four officials of the standards body. The episode credits roughly a dozen researchers. Four of them are associated with ICNIRP. Ken Karipidis is the vice chair. Rodney Croft chaired ICNIRP from 2020 to 2024 and led the development of its current guidelines. Dan Baaken is ICNIRP’s scientific secretary. Frank de Vocht sits on the Main Commission. One of them speaks in the episode. Their institution’s position is more than adequately represented — the 2,000 milligauss figure, the safety factors, the assurance that nothing happens below the line. 7. The four who were left out. Dr. Beatrice Golomb is Professor of Medicine at UC San Diego — a physics undergraduate degree, a PhD in biology, an MD. She directs a research group whose stated focus is the relationship between oxidative stress, mitochondrial function and health. That is the mechanism the episode spent its first half dismissing. Her published work includes the fluoroquinolone case series behind the FDA’s black box warning on an antibiotic class that ruptures tendons, where the accepted mechanism is oxidative stress and mitochondrial toxicity — the back half of my chain, already on a drug label. She is in the credits. She is not in the episode. She has told me she finds my theory biologically plausible, and that she has a recording of her interview. Dr. David Carpenter directed the Institute for Health and the Environment at the University at Albany for decades and is the most prominent academic voice arguing these fields cause harm. Childhood leukemia is the reason these fields carry a WHO classification at all, and Carpenter is the person you call if you want that case made by someone who has spent a career on it. He is in the credits. He is not in the episode. He has told me that when he was interviewed they could not have been less interested in what he had to say. Dr. Joel Moskowitz directs the Center for Family and Community Health at UC Berkeley’s School of Public Health. He told me directly that they interviewed him and that he thought it went well. He does not appear in the episode, and unlike Golomb and Carpenter, he does not even appear in the credits. Dr. Paul Héroux at McGill is the researcher whose work provides the foundation for the oxidative stress mechanism my theory rests on. I gave Rose his email address and phone number. He was never interviewed. They never even called him. 8. “He’s not a scientist.” The episode leans hard on the fact that I am not a credentialed scientist. Zukerman says it. Torre repeats it. “At all.” Having built a segment on that, they then left out the physicist-biologist-physician, the professor of public health, the director of a university environmental health institute, and the McGill researcher whose work the primary mechanism comes from. They spent the episode telling their audience I am not a scientist, and then kept four actual scientists who support the theory off because their argument does not survive otherwise. How they misrepresented me and my case 9. They played my words as a response to an interview I had never heard. Near the end of the hour, Zukerman says she went to me and told me the evidence was lacking. Then she plays me saying I am not wedded to it being an EMF, that I have staked my reputation on it needing more study, and that I am not certain of anything. That segment was placed immediately after Karipidis had finished taking the cherry-picked papers apart. It plays as a man folding under expert scrutiny. Commenters have used it against me since, but it is incorrect. Here is the sequence as it happened. I was interviewed. Karipidis was interviewed weeks later. I was never told what he said, or even who he was. I was never asked to respond to it. I did not know his name until the episode aired. That is not a simple editing decision. That is a quote from one interview, moved to follow a critique from a different interview it was not a response to, so that it would land as a concession. A friend of mine who has spent thirty years as a journalist read that sequence and called it sleazy. She is right. The full passage is reproduced in Appendix A, and it is worth reading. What airs is the preamble. Four paragraphs later I say “to directly answer your question” — and that answer, about what would change my mind if the team relocated, is not in the episode. Neither is the sentence two paragraphs on, where I say the EMF might turn out to be ten percent of the problem. I will say the underlying point again, though, because I meant it and I still do. I am not wedded to my theory that magnetic fields from the substation are contributing to the 49ers injuries. I could be wrong. What I am wedded to is the process of scientific inquiry, and the fact that we should be cautious around these exposures and we need more independently funded studies. 10. Three telling edits. They cut “I’m not a scientist” mid-sentence. What I said: “...and I am not certain of anything. I’m not a scientist. To me, I find the mechanisms compelling. I will go back to the fact that I got into this not because of the 49ers, but because of clients I was working with who suffer from EDS...” What aired: “...and that I am not certain of anything. I’m not.” The clip ends on the first two words of the sentence in which I say I am not a scientist, in an episode that spends considerable energy establishing that I am not a scientist. The full sequence is in Appendix A. They cut my own description of my work. Asked what I do, I said I run a wellness business, that I am focused on writing software to help people navigate environmental stressors, that environmental health is my focus, and that I also do independent journalism and research. What aired is the wellness business and the environmental health, with the software and the journalism removed from my own answer. The software engineering does come up later — narrated by them, as a hacker who grew up to write firmware — but my current work, in my own words, arrives as “wellness guy.” Thousands of commercial routers became home Wi-Fi. What I described: working at a wireless networking company surrounded by thousands of Wi-Fi routers, and a stress-induced health collapse afterward that working in that environment contributed to. What aired: Wi-Fi, the kind you have at home — reinforced by a clip of Christian McCaffrey talking about turning his router off at night. Three cuts, and every one of them makes me seem less credible. That is not a coincidence. 11. I gave them my own caveats and the test that would disprove me. In the first email I wrote that a well-designed chronic, ambient-level exposure study in tendon showing no collagen degradation, run over many months, would undercut my confidence in the theory. That is a specific, testable condition, stated in advance and in writing. There was a second interview, weeks later, which was not used in the episode, but in that I asked again for the falsification criterion to be included. What the episode presents instead is a man saying “we need more study,” which reads as a hedge, an open-ended request for the benefit of the doubt. It is the opposite of a hedge. Section 6 of my second email says, unprompted, that as far as I am aware there is not a single study showing EMF-driven oxidative stress degrading collagen in a human in vivo or in human tendon in a lab. I wrote that because it is true and because it is the first thing anyone should check. Under their standard it becomes the hinge of the entire first half, framed as something they had to surface without my cooperation. I had handed it to them five weeks earlier. And in the interview I said that my 25 to 50 milligauss readings were taken at knee level, and that these fields attenuate quickly, so by the time it reaches your head it is not that high anymore. That did not air either. The qualification arrives later, from Karipidis, as a correction. How you would actually study the injuries 12. They measured the wrong thing. The episode spends its final act on whether the 49ers are the most injured team in the NFL, finds no clean ranking, and lands on “injuries are random”. That is the wrong test. You would define the exposure — measured field levels at the facility — and the outcome narrowly: soft-tissue injuries, not a single MSK injury count that a broken finger and a ruptured Achilles both land in. Then you would compare the 49ers to themselves before and after the exposure changed, and compare that change against every other team over the same window. That controls for league-wide shifts in rules, turf and training load. It is a difference-in-differences design, and it is standard. I sent them that argument on July 28th, in writing, along with the fact that in eleven of the past twelve seasons the 49ers had finished top ten in Adjusted Games Lost. And by the episode’s own reporting, the 49ers are second in games lost to injury over the past decade, with FTN’s Aaron Schatz confirming that once you adjust for starters they come out second worst in the league — after having been one of the healthiest teams for years before that. A finding like that is where an investigation starts, not where it stops. 13. I did a lot of substation research for the episode that was never aired. I had reported that the substation next to the facility was expanded in 2014. That was wrong, and Rose Rimler and I sorted it out together. They gave me credit on air, which I appreciated, but framed it as a concession on my part to something they had found. In fact I had been investigating it myself, was uncertain before they asked, but was waiting for clarification from Silicon Valley Power. The uncertainty centered around a substation named “Esparanca” that was proposed right behind the facilities as part of the stadium construction, but now appears to never have been built. I spent days in Silicon Valley Power’s records, and did eventually reach Silicon Valley Power for confirmation and indentified the mistake myself. I also gave them highly detailed documents on what we do know about those facilities: new equipment installed between 2010 and 2014, and load growth across the system with an inflection around 2013–2014, with the Northern Receiving Station carrying the highest capacity in the system and sitting closest to the data center corridor. None of that is in the episode. I have a separate piece about it coming out soon. *I cut 2 seconds from the raw audio to remove personal information that had no connection to anything in the episode. Appendix A: the passage the clip was taken from This is the sequence from my first interview, in full. The episode uses one fragment of it. It’s tricky because my understanding is that there’s something like a 15-year half-life on collagen remodeling issues. They’re going to get a new crop of players. What I really need, though, is for the injuries to be broken down so we can see the soft tissue injuries. Right now, they’re categorized as MSK injuries, but let’s say we can actually identify them more specifically. Is that right? He was able to do that? Oh, cool. I wasn’t able to find that information. Interesting — I didn’t know that data existed. I tried so hard to get it, and I didn’t know it was available. Maybe you could connect me with that person. That would be amazing. I’m not wedded to it being an EMF, honestly. I’m not. I would say that, to a certain extent, I’ve staked my reputation on the fact that it needs more study. It’s important to look into it, and I am not certain of anything. I’m not a scientist. To me, I find the mechanisms compelling. I will go back to the fact that I got into this not because of the 49ers, but because of clients I was working with who suffer from EDS, Ehlers-Danlos Syndrome, a tendon hypermobility issue. This condition is documented to be partially caused by oxidative stress. I’ve worked with them to mitigate their EMF exposure and have seen people improve. I think it’s a bigger story. In a way, the 49ers represent an occupational cluster with specific exposure risks. If someone would conduct a study on this, I believe we could learn a lot. Perhaps we would discover that it’s like, okay, maybe it’s 10% of the problem. I don’t know the exact number, but I think either way, conducting the study would provide valuable insights. To directly answer your question, it’s challenging for me because it’s part of a bigger story. If the 49ers move and stop having injuries, I might conclude that it was related to the substation. However, if they move and still experience injuries, I would want to analyze the nature of those injuries. Are they primarily soft tissue injuries? I don’t think it’s necessarily a case closed, but the story might lose traction at that point regardless. Three things are worth noting. The aired fragment stops immediately before the sentence in which I say I am not a scientist — the cut described in item 10. It also stops four paragraphs before the words “to directly answer your question.” What the episode plays is the throat-clearing. The actual answer, about what would change my mind, never airs. And two paragraphs in, I say the EMF might turn out to be ten percent of the problem. That is the ranking the episode says I never gave. Appendix B: the full email, July 6th, 1:39 PM Hi Rose, You asked me to send you some studies a couple of weeks ago. I apologize for the delay. I have been incredibly busy. I also wanted to give you a chance to dig in yourself, and get your own perspective before I influenced you too much with mine. That said, I do want to make sure that the actual argument is abundantly clear, so here it is! One note before I begin, there are really two separate questions here: Does the substation cause the soft-tissue injuries? That was my specific claim, and what the podcast is about. Is the theory biologically sound? Can 50/60 Hz fields at these levels do anything biological below the safety limits? Question two is why people have been calling me a conspiracy theorist. The regulatory and advisory bodies (ICNIRP, etc) maintain that anything below their exposure limits is biologically inert, and that position is broadly accepted within the mainstream, but the actual science paints a different picture. To defend my theory I’ve had to defend a much larger claim: that the advisory bodies have the biology wrong. I can’t honestly answer question 1 without first addressing that. Here’s is a simplified outline of my theory, with links to studies: 1. Advisory body thresholds for biological effects The ELF magnetic-field limits (ICNIRP’s ~2,000 mG public / 10,000 mG occupational) exist to prevent acute effects from exposure. If a magnetic field is strong enough, it makes nerves fire and muscles contract. Muscles twitch. You can see faint flashes of light in your vision. People can even feel tingling or even a shock. That happens due to Faraday’s law, which states that a time-varying magnetic field induces an electric field inside the body via the creation of Eddy currents.The standards assume that those currents do nothing below the twitch threshold. They do not consider chronic effects at all. My argument is that they are biologically active and do have chronic effects. 2. There are multipe ELF-EMF mechanisms for inducing oxidative stress. This is basic biophysics. Below are the two primary mechanisms. Simplest first. Dr. Paul Héroux of McGill has the most intuitive explanation, which rests on Maxwell’s principle of superposition: because Maxwell’s equations are linear, two sets of electromagnetic waves sharing the same space simply add together. In the interview I pictured a pebble dropped into a pond, sending out clean ripples. Then a boat motors past at distance, sending larger waves, and where they meet the ripples, the two add together and the original pattern gets distorted. In our cells, the mitochondria run on continuous currents of electrons and protons that carry their own faint electromagnetic fields. An external field from a substation, by the principle of superposition, adds to those internal currents and shifts the pattern. The electron transport chain in the mitochondria leaks a fraction of its electrons by design as reactive oxygen species (ROS), which act as signalling molecules in a healthy cell. Distorting that field increases that electron leakage, creating oxidative stress. A tiny electromagnetic interference results in a large downstream effect. https://www.sciencedirect.com/science/article/pii/S2405844025006474 The more complex pathway is Dimitris Panagopoulos’s Ion Forced-Oscillation / Voltage-Gated Ion Channel (IFO-VGIC) mechanism. Weak, polarized, low-frequency fields force the ions (calcium, potassium, sodium) next to an ion channel’s voltage sensor to oscillate; because that force scales with the inverse cube of the distance involved, fields far below the stimulation threshold can still force the channel open, disrupting the cell’s ion balance and driving ROS overproduction (Nitric oxide and superoxide interact and produce peroxynitrite, a highly unstable cytotoxin that breaks down into free radicals). https://www.researchgate.net/publication/366088934 https://www.spandidos-publications.com/ijo/59/5/92 https://www.mdpi.com/1422-0067/22/18/10041 https://www.frontiersin.org/journals/public-health/articles/10.3389/fpubh.2025.1585441/full https://pmc.ncbi.nlm.nih.gov/articles/PMC3772193/ 3. Evidence of oxidative stress, in vivo, in humans from ELF-EMF There are many studies, and the strongest are occupational, which applies to the 49ers situation. 115 power-plant workers vs. 145 office controls. Serum malondialdehyde (MDA, the standard lipid-peroxidation marker), superoxide dismutase, and catalase were all significantly higher in the exposed group, and the markers rose with increasing field exposure. https://journals.sagepub.com/doi/abs/10.3233/WOR-203244 A follow-up where they reversed the oxidative stress in power plant workers. A double-blind randomized controlled trial: 91 power-plant workers given vitamin E, vitamin C, both, or placebo for 90 days. The antioxidant groups showed reduced lipid peroxidation and raised antioxidant capacity versus controls. https://pubmed.ncbi.nlm.nih.gov/32191586/ A spot-welder study: 46 welders occupationally exposed at 50 Hz, showed significantly altered red-blood-cell antioxidant enzyme activity and concluded ELF-MF “might act as an oxidative stressor… even at the recommended levels of exposure.” https://pubmed.ncbi.nlm.nih.gov/18504600/ A substation-specific study found oxidative stress and DNA damage https://pubmed.ncbi.nlm.nih.gov/24460415/ 4. Oxidative stress degrades collagen This half isn’t controversial at all. Oxidative stress activates the matrix metalloproteinases (MMPs) that break collagen down and suppresses its synthesis. Here are three example studies: Siwik et al. 2001: Oxidative stress raises MMPs and lowers collagen synthesis in cardiac fibroblasts. https://pubmed.ncbi.nlm.nih.gov/11121376/ Fisher et al. 2009: Collagen fragmentation drives oxidative stress and elevates MMP-1 in aged human skin. https://pmc.ncbi.nlm.nih.gov/articles/PMC2631323/ Varani et al. 2006: Decreased collagen production in oxidatively aged skin. https://pubmed.ncbi.nlm.nih.gov/16723701/ 5. What about the study showing improved collagen synthesis I’m glad you asked this question, and I’m bummed we didn’t get to it in the interview because it is a great question, and very important to understand. Superficially it may appear to be a refutation of my theory, but I would argue that it actually supports the underlying argument. That study used a short, high-intensity pulsed dose: therapeutic-PEMF, the same type of field used clinically to stimulate bone and tissue healing. The reason this works is because it triggers the very same biological pathways that can lead to oxidative stress. The exposure still stimulates ROS production, but done at a controlled dosage, for a limited duration it has a different effect. The cell reads the ROS as a warning signal and it upregulates its antioxidant defenses, and mounts a repair/proliferation response. The therapy is then stopped before the cell gets overwhelmed. That is essentially a hormetic response: a small dose of a stressor producing a beneficial adaptation. Two things follow: At the very least, this means the field is biologically active, which by itself undercuts the regulatory claim that these fields are inert below their thresholds. There is a wealth of literature on PEMF (pulsed EMF) bone regeneration and calcium channel signalling (which is the second mechanims in section one). Here is one. https://www.nature.com/articles/srep13856 At best, it leads us straight to my actual concern, which is that under chronic, chaotic and unregulated exposure, the cell’s antioxidant capacity gets overwhelmed, resulting in oxidative stress. There are plentiful examples of things that are beneficial at controlled doses, but harmful at uncontrolled doses. Excecise is one obvious, uncontroversial example. Botox is perhaps a more interesting example. 6. What about a study that shows EMF causing collagen degradation in humans? As far as I am aware there is not a single study showing EMF-driven oxidative stress degrading collagen in a human, in vivo, or in human tendon in a lab. There are studies involving isolated fibroblasts though, which secrete collagen. The most relevant one showed that human fetal scleral fibroblasts exposed to 50 Hz ELF-EMF showed a significant decrease in collagen synthesis and that MMP-2 expression was upregulated, which is the exact mechanism I described in section 2. https://pmc.ncbi.nlm.nih.gov/articles/PMC3626379/ That’s it! Thanks again for the interview. Best, Peter Anthony Cowan Environmental Health · Wellness Tech · Researcher & Journalist Publisher & Editor, Living Energy Bio: petercowan.comSocial: X · Instagram · TikTokApp: sunlightis.lifePhone: [redacted]
Wilmington health tech founder launches new venture
Several years after launching his health tech startup Artemis Immersive, founder Adam Isley is setting his sights on new horizons. Co-founded in 2023 by husband-and-wife Adam Isley and Kaylan Barbrey, along with Matthew Raffa and Bill Blakesley, Artemis Immersive began as a spatial medtech company that created digital renderings of medical scans for viewing in augmented reality (AR). Isley said the firm, which won an NC Tech award in the Biotech + HealthTech Innovation category last year, has raised $1.2 million in total in seed funding since launching. Isley has since created a new venture, Research and Me, building on the Artemis platform. Like Artemis Immersive’s core software, VoxScan, Research and Me combines health data with artificial intelligence in a 3D interactive environment to help patients better understand health outcomes and provide integrative wellness support. While the Artemis product is no longer Isley’s primary focus, he said the company’s technology and ambitions have evolved into different ventures, like Research and Me. "It's a different venture building on the Artemis platform, and there'll probably be more,” Isley said. He added, "I was very disappointed in the quality of the information available to general patients about their healthcare... I wanted to give patients more and a better plate of choices." Research and Me is still in its beta phase, Isley said, with usability testing ongoing in partnership with the firm’s partner, Medicap Pharmacy and Wellness Center, owned by Barbrey. "As someone who's kind of dedicated their life to working in healthcare, I've tried to bring this spirit and passion to it,” he said, “and a lot of the resources that we'll be providing are free — like a base level of free care for any patients, or medical education if they've got specific conditions." Isley describes Research and Me as a “patient-first” platform designed to securely store and pseudonymize health data and use AI and medical literature to generate insights. The insights are presented in an interactive 3D environment for patients and providers to explore conditions, treatments and wellness plans together. "It's almost like a democratization of understanding medical information," Isley said. "We take a whole bunch of clinical data, we take a whole bunch of peer‑reviewed, published studies on PubMed, and we try to turn them into chunks of information that normal humans can understand." Like VoxScan, the Research and Me platform lets users interact with 3D anatomical models for visualization. The platform provides a space for tracking, notes and insights. The platform also supports video conferencing, Isley said, allowing providers or coaches to examine models and data together. "We wanted to create a safe environment where you can start to learn and experiment with new features about your health, using agents to do that,” Isley said. While Research and Me is in beta-phase testing with Medicap Pharmacy, Isley said he envisions the platform serving a wellness-oriented community, working with sports performance clinics and hormone optimization. Isley, who is working towards a wellness-coach board certification, also plans to offer functional wellness consults through the platform. Long‑term, Isley says he wants the platform to embody an “integrative health practitioner” approach, “connecting experts of different fields and specializations in a way that they can make a greater impact in people's lives.” “For people in the state of North Carolina, it's already a win,” Isley said of the Medicap rollout, noting that partner clinics get “immediate resources for learning about their health and wellness conditions… out of the box.” Isley plans to launch Research and Me’s provider portal in 2028 and begin pursuing integrations with larger systems, he said.
ChatGPT for Healthcare unveils Epic integration as part of data consolidation strategy
In addition to providing Epic users with access to the popular LLM, OpenAI said all clinicians that use its platform will be able to access public databases, including ClinicalTrials.gov and PubMed, with the proper plug-ins in place.
August Monthly Review: ChatGPT In Epic
Death, taxes, another frontier lab healthcare launch inspiring truly insane LinkedIn takes. As much as I want to stay away, I repeatedly am the crewman unplugging his ears whenever we pass these sirens. So it’s not the first and probably not the last time we dial up the typewriter rather than tie ourselves to the mast. The full blow-by-blow timeline: Health API Guy is a reader-supported publication. To receive new posts and support my work, consider becoming a free or paid subscriber. Subscribe The End of the Standalone PHR (Jan 8): ChatGPT Health arrives for consumers, at the time powered by b.well. I was bullish on the approach in that the best way for the PHR to finally solve distribution was to meet consumers were they already are (i.e. When Horizontal Meets Healthcare (Jan 9): OpenAI for Healthcare puts out the shingle for enterprises, with SharePoint ingestion standing in for the EHR integration the product actually needed. Another One: Anthropic’s Healthcare Debut (Jan 16): Claude's version, on HealthEx rails instead of b.well, with Agent Skills for FHIR development as the one true vertical-specific investment. ChatGPT for Clinicians: The Trap Sprung (Apr 24): OpenAI filled in the missing GTM middle with a free product for verified clinicians, effectively peeling the enterprise wrapper off ChatGPT for Healthcare and taking the PLG fight directly to OpenEvidence. OpenAI’s Second Attempt at Health (Jul 31): a relaunch of their patient specific app, now branded Health in ChatGPT, where the privacy partition came out, the connectors thinned, and b.well disappeared in favor of first-party FHIR work against a smaller network Beyond a Shingle So what was announced now? Today, we’re introducing a new electronic health record integration that brings authorized patient context from Epic into ChatGPT for Healthcare, along with the Healthcare Public Data plugin for direct, structured access to official healthcare datasets like PubMed, DailyMed, and CMS Coverage. Together, these capabilities bring ChatGPT closer to the systems and sources healthcare teams trust, while supporting the controls and compliance healthcare work requires. The core portfolio is unchanged from prior announcements we delineated and discussed (aside from the relaunch of patient-facing). Since trade publications still seem to be confusing them by using the wrong names: Enterprise sales motion: ChatGPT for Healthcare Protecting their core product / PLG: ChatGPT for Clinicians Consumer/patient-facing product: Health in ChatGPT So really, this is a feature release (specifically for ChatGPT for Healthcare when it comes to EHR integration). What’s cool about it, though, is that we are moving beyond just putting out a shingle. Everything in the January enterprise launch was horizontalizable: Horizontal tech companies thus generally start verticalization with their “putting out a shingle phase”. Telling the world you’re open for business as a horizontal tech company reliably attracts early inbound interest from buyers who are already trying to force-fit horizontal tools into domain-specific workflows and are eager for any signal that the vendor intends to support their use case more directly. Nothing was really vertical specific, which is exactly what you'd expect from the ultimate hypergrowth horizontal company dipping their toes into specific industries. But eventually you have to stop changing the sign on the door and start changing the product. Can you guess where the horizontal product was going to run out of road? This is the core dilemma writ large: verticalization requires differentiation, while scale economics of consumer and horizontal push toward unification. I’ve buried the lede so deep here it will be painful to some readers, but what should be shocking to no one is that my perspective is that EHR integration is the only path that meaningfully resolves this tension for ChatGPT for Healthcare. Integration with Microsoft Sharepoint is fine, but it is categorically insufficient for any product that hopes to influence clinical decision-making. SMART Money Well here we are, eight months later! Real vertical investment has begun, which surprised a few people. One friend in the industry messaged me: “Absolutely no way Epic gave ChatGPT API access.” Looking forensically at the announcements, the integration is notably read-only across appointment notes, laboratory results, medications, and specialist documentation. So while I’m not a betting man, I'd wager the house this is a SMART on FHIR launch: That sounds a lot like USCDI! The recommended path for the workflow they outline would be SMART on FHIR Their Health AI lead’s post is evocative of both standalone and EHR launch SMART, which another termed “ChartGPT” and “EHR Plugin” The implementation burden for SMART on FHIR is the lowest of the available integrative paths This is the team who literally did patient-facing SMART on FHIR with Epic last month Most importantly, if you’re a horizontal company, you generally still haven’t taken the full plunge and thus (overly) value reusability. SMART on FHIR is the logical compromise: healthcare-specific enough to matter, but standardized enough to reuse. Nobody Asked Judy Another friend asked “I thought they had to go to each health system, or did they go direct to Epic and now health systems opt in?” Given the trust paradigms in healthcare, this functionally cannot be Epic hoovering up all the data for OpenAI and shoving ChatGPT in their customers’ faces (or they would revolt). However, I do believe the aforementioned terrible coverage by TechCrunch and other outlets is probably responsible for that question, given the 325 million reference. When using FHIR as a business associate to an Epic customer, there is no EHR gatekeeping to speak of, as that isn’t how fhir.epic.com works: You register an app You pick your APIs You test against the sandbox APIs You list as “Ready for Production” Hospitals pick your app You test and go live with them Bluntly, nobody had to say yes or no in Verona (nor were they given the chance). Vendor Services (their next developer tier up that I doubt OpenAI is using quite yet in this initial release) certainly has contractual paperwork that some resent, but even there, the twin pressures of mounting antitrust and information blocking make outright gatekeeping increasingly fraught. My friend’s sentiment is, to me, representative of a broader industry neurosis, perhaps a sort of scar tissue of prior eras: people assume the gate is still there and never actually try the door. There are certainly other ways Epic (and any EHR) can put its thumb on the scale, but they are not so dumb as to stand in front of a federally mandated API and play bouncer at this exact moment in time. So I think they can and probably should go deeper, as this release is at best parity and at worst behind vertical-specific competition. OpenEvidence did a basic SMART launch with Sutter Health in February, allowing for more convenient evidence search by providers. They then add patient-context (the equivalent SMART on FHIR flow to what we see here) when Cedars-Sinai went enterprise-wide in May. UpToDate has four distinct applications across deeper workflows like patient engagement listed in Epic Showroom and announced a partnership with Epic to power Art at UGM Abridge and other ambient scribes have invested deeply into the deepest bidirectional clinical copilot workflow with integrations well beyond SMART on FHIR. In that light, the “Who is OpenAI primarily targeting here?” is clear. This release brings them into striking distance of OpenEvidence, but not the others quite yet. They are the only one of the three you can reach without building something truly Epic-specific. When will they go further? Competition is a great motivator to overcome the horizontal demons and start building things that can’t be reused: not across industries, not across EHRs, maybe not past the customer you built them for. That’s the price of actually verticalizing. The question is if and when OpenAI will be willing to pay it. Month in Review Here is the monthly review. As a reminder, this is a regular round-up of the month’s posts and other content to surface things you may have missed across regulation, litigation, interoperability, and beyond. AI assistance is used in these bullet summaries so I can focus on articles. Articles Published: None this month Video Content: The Information Exchange: Standards-based Thruple Edition (Aug 14): Back to school for us too, with Brad reporting in from the CMS Health Tech Ecosystem’s one year anniversary in DC. We get into the January CMS-0057 deadline, the fall rulemaking reading list, and why enrollment still keeps most apps off FHIR. The Information Exchange: Epic Dúnadan Edition (Aug 25): A UGM roundup with Ryan Brickner joining for the first time to check our takes against what the building actually thinks. Rangers, Ergo sitting on top of EHI, and a down-market lineup that needs some cuts. Regulatory: Stacked Deck, Bad Hand (Aug 05): ONC’s website refresh took the entire HIT Policy Committee record with it, so I rebuilt the archive and went looking for the regulatory capture story everyone assumes is buried in there. Stacking the deck and winning the hand turn out to be very different things. The Sixth Generation of Patient Access (Aug 19): A quick catalog of the five generations of patient access we’ve layered on since HIPAA, and the two candidates now competing to be the sixth. One is planned. The other is the market routing around the plan entirely. Court cases: Three Cases Walk Into a Docket (Aug 06): Two surprise settlements cleared the board in a single week, and then Judge Maddox dropped ninety-four pages on Vyne v. Henry Schein. The sleeper is a DMCA holding that makes direct-to-database a considerably riskier business model. Epic v. Health Gorilla: Into the MDL (Aug 10): Nine class actions are headed to Miami, and the Panel signaled it wants to bring the case that spawned them along too. That would leave Epic arguing the requests were obviously fraudulent in one courtroom and unknowable in the other. Amazon v. Perplexity: Agents Are Legalized! (Aug 11): The Ninth Circuit vacated the injunction against Comet, holding that the user is the one accessing the servers rather than the company that built the agent. A real win for agentic access, and a much narrower one than the headline suggests. Veeva v. Epic: Come At Me, Bro (Aug 26): Epic’s response brief wants the dismissal affirmed and, unusually, wants the opinion published as precedent. Buried in it is Epic’s own description of what its non-competes actually prohibit, which current and former employees should read closely. EHRs: The Contract Epic Would Never Sign Today (Aug 04): A 1999 SEC exhibit catches Epic licensing nearly its entire product line, Tapestry included, to the company that became TriZetto. The marketing services menu attached to it is the part that will make you blink. Forecast from Verona (Aug 07): The Epic Almanac makes one argument six different ways: the AI is only as good as the networks behind it. Emmie headlines, Art’s context stack is the most ambitious part, and Penny finally gets an autonomous coding date on the calendar. Works With Epic MyChart (Aug 17): Epic’s first new Showroom category since the death of Workshop certifies hardware instead of software, badge on the box and all. Made for iPhone, but for blood pressure cuffs, and rough news for anyone selling the RPM stack sitting in between. UGM Hot Takes 2026 (Aug 20): Everyone else covered the AI announcements, so I went after Savvy deleting the payment gateway, Rangers as Boost with the timer removed, and a down-market lineup with too many entries. Plus the Health Grid tidbits I cannot help myself on. MyChart Central Grows Up (Aug 24): Device data and Emmie turn Epic’s identity hub into a full consumer platform, which is both a logical answer to ChatGPT and a bit of a mistake. It also happens to be the best scraping target Epic has ever shipped. Industry Analysis: The Wrong Yardstick (Aug 12): Vertical software keeps getting judged against Superhuman and Notion, which is the wrong bar entirely. Your user is comparing your product to a whiteboard and forty phone calls before lunch. Primitives vs. Abstractions (Aug 27): Developers want building blocks, systems of record prefer to hand out business logic, and both sides have a real case. There’s no test from the outside that separates the engineering reason from the competitive one, which is why this keeps ending up in court. Cross-industry Comparisons: The Two Kinds of Platform Power (Aug 18): Attention power and record power are different problems that keep getting handed the same regulatory toolkit. Congress’s latest swing at Big Tech shows both what’s possible and where it falls apart. The Dogs of (Platform) War (Aug 21): A CourtListener alert turned up a property management fight with healthcare’s exact shape and none of the Cures Act. Shell prospects, ghost accounts, a notetaker bot that came back to haunt someone, and a lawyer arguing both sides of the same theory in two states. Fractals All the Way Down (Aug 31): Yardi dominates property management right up until you zoom into one segment, where AppFolio owns it outright and Yardi doesn’t appear at all. Where you draw the line around a B2B software market is about to decide an awful lot of cases. Other News: If Judy Had the Courage (Aug 13): A short eulogy for the era when software was allowed to look insane: WinAMP, bold colors, and everything the grey chatbot era has taken from us. External Media: Portland Monthly Health Tech Meetup: Erin O’Brien channeled my own feelings - maybe it’s just because it’s August and beautiful, but the monthly edition of the PDX Health community meetup was a ripper. Make sure to reach out if interested to join for the next one. STAT’s Coverage of Epic This Month: Brittany Trang of STAT did a fantastic job of breaking the FTC investigation that’s been lurking, as well as UGM related coverage, so I had to give her her wish of a meme. Fall Conferences: I’m pumped to be kicking off my fall conference season in NYC at Nabla Accelerate next month, which Chrissy provided the link to apply for. Here’s the rest of my schedule in case you want to meet up: Commonwell (Redwood Shores, CA): Oct 13-14 Open@Epic (Madison, WI): Oct 21-22 eHealthExchange (Austin, TX): Oct 27 Sequoia Project (Austin, TX): Oct 28-29 HLTH (Vegas): Nov 15-18 RSNA (Chicago): Nov 29-Dec 3 Posts I Liked: HTI-6 Should Unbundle API Certification: Josh Mandel makes the case that HTI-6 should split (g)(10) into separate authorization and data certifications, so a PACS or a genomics platform can certify only the role it actually performs. Imaging is the urgent example, but the structure solves a much bigger problem. On implementing ePrior Auth with Epic: Scott Rossignol’s field notes from a live ePrior Auth build on Epic, including the two app registrations nobody warns you about and the CPT mapping problem waiting at the end. CMS-0057 implementations are going to be such a beast. Healthcare point solutions are starting to look a lot like streaming services: Spencer Dorn runs the cable-to-streaming arc against health IT and lands squarely on the bundling half of the cycle. Bundling can be good! It can also be bad! Life is nuanced. Health API Guy is a reader-supported publication. To receive new posts and support my work, consider becoming a free or paid subscriber. Subscribe
Florida-Based Science and Technology Company Crescel Announces Landmark Peer-Reviewed Medical Publication
Crescel LLC, a Florida-based innovative science and technology company, today announced publication of its landmark PubMed-indexed, peer-reviewed clinical study showing that its biobotanical technology produced statistically significant improvements over the leading prescription standard of care for rosacea in a randomized, double-blind, controlled clinical trial. Published in the Journal of Cosmetic Dermatology, the study represents a major scientific milestone for the company's pioneering prop
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.
We can create the future of science right now
Paul Litvak is the founder and Executive Director of the Robyn Dawes Institute and a Visiting Scholar at UC Berkeley. He has a PhD in Behavioral Decision Research from Carnegie Mellon where he studied emotions and the sunk cost bias. Over 15 years in industry, he solved a wide range of challenging technical problems. At Meta he created models optimizing the ad review process. At Google he ran experiments to measure social influence. At Airbnb, he was a product manager leading machine learning teams optimizing search ranking and price suggestions. He also co-founded and led product at Rhythmic Health, a venture-backed biosensing startup, creating an accurate low cost system using a color changing strip and a smart phone to measure salivary lactate. The bottleneck At this point, it is uncontroversial to say that science needs to stop using the PDF article as the unit of knowledge and currency. The unbearable slowness of scientific publishing, the profit motive and margins: I’m not saying anything new. The PDF also sucks because it’s hard to extract structured information, which makes it hard to do evidence synthesis. As a result, we do much less evidence synthesis than is needed. And evidence synthesis ultimately undergirds most policy and medical decision-making. I can see second-by-second real-time odds for any sporting or newsworthy event, but a school board can’t see the best evidence on whether their 8th graders should be taught algebra. As a society, we don’t treat this as an important problem. Again, not controversial. Not only is the problem well understood, but the solution has already been laid out. What we need is AI-assisted living evidence synthesis - (1) an open knowledge graph of atomic claims, (2) claims linked to evidence, (3) assessment and synthesis of each piece of evidence, and (4) continuous updating with new data. What few realize (yet) is that the technical capacity to build this vision for a significant portion of science already exists. Not only that, scientists and startup teams are already building many of these components. I know this because I’ve been surveying the space and talking to many of the builders. There are some missing pieces: for example, evaluations of how well some of the components work. But at this point, most of what’s missing is a fully end-to-end working integration of all of these parts. In the rest of this essay, I’m going to lay out all the parts of a working living evidence layer for science and who is working on them, and propose concrete next steps for building this system. What’s now possible The diagram above outlines the components of a living evidence synthesis platform, including some of the teams working on each component1. Scientific PDFs are processed into claims with associated evidence. The evidence is subjected to a forensic audit, methodological evaluation and robustness and reproducibility checks. Finally it’s given a weight in a continuously updating synthesis. What follows is a description and status of each component and a few of the teams working on them. Document understanding The first thing you need to be able to do is turn an article into structured data. Mostly that means parsing PDFs. There are often multicolumn layouts that confuse non-specialized PDF to text processing libraries. For scientific papers, there is the added complexity of parsing formulas and tables and figures. This is a really hot area - there are startups offering APIs, and it seems like a new open source package gets posted to Github every few weeks. What follows isn’t exhaustive. A package called GROBID was the state of the art for a while, they didn’t update their package for nearly two years until very recently. In the meantime reducto.ai released an AI powered PDF extraction API, PaddleOCR became popular, IBM released a model called Docling, and both Mistral and Gemini created models and libraries. I also know of at least one other well-funded psychology research group working on a paper parser. By contrast, there are few open evals in this space, with no extensive evals for complex table comprehension in particular. Nonetheless, I’m confident this will be a solved problem soon, given the combination of LLM advances and developer interest. Hypothesis level extraction There has been increasing interest in comprehending the extracted text of papers and linking information to evidence for each hypothesis. A lot of work has already been done. Trialstreamer (Marshall et al. 2020) and RobotReviewer LIVE (Marshall et al. 2023) demonstrated automated extraction of trial population, intervention, and outcome at scale on clinical RCTs. PaperQA2 (Skarlinski et al. 2024) and Ai2 ScholarQA (2024) extended this to retrieval-augmented question answering with citation grounding. Elicit, Consensus, and SciSpace operationalized claim-level extraction for end users. OpenEval (Booeshaghi et al. 2026) is the most recent and most ambitious: 1.96 million atomic claims extracted from 16,087 eLife manuscripts using Claude Sonnet 4.5, grouped into ~299,000 results, with LLM evaluations showing 81% agreement with human peer review on a 2,487-paper subset. None of these solutions link claims to test-statistics, as you would need to evaluate randomized controlled trials. This is why I built the evidence.guide API - to extract hypotheses and associated test statistics from behavioral science papers. The best public eval of this kind of extraction I’m aware of comes from the recent SCORE project - they had humans code thousands of psychology papers to extract their claims by hand. It would be extremely helpful to the world if all scientific PDFs were available as structured open data. I’ve been working to make this happen, both directly at Berkeley and through coordination with large entities I can’t yet speak of; as hard as it is to do, I think it’s possible2. Forensic audit A lot of work has been done on forensic audit, but some gaps remain. Of course, for biology papers that rely on images for evidence, there are a variety of tools (notably Proofig and ImageTwin) to spot anomalies. These are still well short of what sleuths like Elizabeth Bik can do on her own, but these tools are constant companions among fraud analysts. There’s someone working on auditing Excel files for anomalies, and a number of teams are automating numerical checks like GRIM and SPRITE, including Scrutiny project, the INSPECT-SR team as well as statcheck. The regcheck team is building a way to use AI to compare preregistrations to analyses in papers, to ensure there aren’t significant deviations. Nonetheless, there are many other kinds of anomalies to screen for, both public and less publicly known. And there are no formal evals for anomaly detection that I’m aware of. Still, there’s a lot to draw from in this space and I’m pretty certain we will be able to scan papers for most kinds of obvious anomalies in the near future. Methodological review This area has been white hot, though I fear for many of the startups in this space, because this capability may become commoditized. There are at least six different AI peer review companies, including Refine.ink, Reviewer3, ReviewerZero.ai, Q.E.D. Science, Paper Wizard, and Isitcredible. Coarse (a pun on refine) was also recently created as an open source alternative. These systems provide qualitative feedback on the content of papers, spotting methodological weaknesses and mathematical errors. They seem to work pretty well, and many academics report bitterly that they exceed the average quality of typical peer reviewers. But there are few evals here either. What evals exist so far involve using LLM-as-judge (circularity problems abound) or comparing against human reviews of questionable quality. What you’d ideally want is an eval that measures capturing known errors in papers3. Reproducibility and robustness Another active area has been using AI agents to automate computational reproducibility4 and robustness5 checks in papers that report numerical results. For more recent papers where data and code are available, AI agents can see whether they can re-run the analyses and produce the numbers reported in the published paper. In addition to a handful of individual academics who have been experimenting using Claude Code for this, the Institute for Replication is a leading group working on building an end to end system. The evals related to this problem are the most mature, with CORE-Bench (Siegel, Kapoor, Narayanan 2024) and PaperBench (OpenAI 2025) available to benchmark agents on this task. There is also work on getting AI agents to test alternative ways of analyzing the data to ensure the results are robust to small analytic design choices. Synthesis This is the most underdeveloped area where significant investment is required. Although some automated evidence synthesis systems exist — for example, otto-sr is building an AI agent to write systematic reviews — none of these incorporate the full range of paper level signals to weight evidence appropriately. Nor is there anything like an eval or a gold standard for a good systematic review. Arguably Cochrane reviews are the closest we have to gold standard human systematic reviews, though I’ve heard academics in the know complain about their uneven quality. A key question for a synthesis platform is how to weight anomalies and methodological issues in assessing the quality of a piece of evidence. This is an unsolved problem and one I’m very keen to work on. Continuous updating There are many pieces of basic infrastructure available for monitoring for new research and initiating updates. OpenAlex is the current open citation graph. Retraction Watch integrated into Crossref in October 2023. Scite tracks how citations support, contrast, or mention prior claims. The Living Evidence Network demonstrated continuous-update workflows in clinical guidelines. Engineering this is a relatively straightforward task. When you look over this technical architecture and all the progress being made, it’s hard not to be optimistic that a living guide to scientific evidence will be built. The stakeholders are ready The social infrastructure for this is starting to coalesce — it’s not just a pie in the sky academic exercise to imagine this coming into existence. Institutions like the Center for Open Science, the Institute for Replication, the INSPECT-SR, the Living Evidence Network and more are all working on scaling work to improve research quality. Funders are also aligned. The Sloan Foundation has funded living evidence work through COS. Coefficient Giving supports the Institute for Replication and COS. The Astera Institute and the Institute for Progress have shown interest in this space. NIH has established an Office for Replication and Reproducibility. Although there are (very unfortunately) serious headwinds in science funding generally, there is an active group of funders interested in metascience. A brief word about what I’ve been doing at RDI. First, as a Visiting Scholar at Berkeley I’ve been actively figuring out how a non-profit and a public university can conduct and make public the results of large-scale academic article data mining. With some of the money I raised from donors, I commissioned a legal analysis of recent case law and publisher text data mining (TDM) agreements in order to understand whether a massive open data mining of academic articles is possible (with caveats, it is). I’ve also been working to bring together stakeholders in this space, and identify gaps. I’ve also been doing some software development in this space, with more to come. A pilot proposal The assumption undergirding all of this is that an AI, given all this information, would make the right judgment about a scientific claim with lots of conflicting evidence, weighing all the factors appropriately. That’s the hypothesis we need to test. Randomized control trial research is the best place to focus on first. RCTs are used to make many of the important decisions in society - from medical trials to public policy changes. And they use a relatively uniform set of inferential statistics with lots of known and available diagnostics. Behavioral science experiments, within the broader realm of RCTs, should be first used as a testbed whose results can be generalized. Because behavioral science is at the vanguard of open science practices, replications abound (there are thousands of them) to serve as ground truth training data. Key Hypothesis Therefore the pilot would test, in behavioral RCTs that have been replicated, whether the quality of evidence for a claim can be used to accurately predict whether that claim will replicate. Secondary Hypotheses Compared to claims that replicated, non-replicated claims demonstrate a greater share of forensic anomalies in their source literatures. Hypothesis level claim and statistic extraction is accurate enough to scale living evidence without onerous human review costs. Replication prediction is more accurate than prediction markets6 or journal prestige. If all the different quality signals we gather do accurately predict which studies will replicate, then we can use that model to score evidence to power the living evidence layer. Why this is informative regardless of outcome If the pilot succeeds, the architecture extends to medical RCTs (where Living Evidence already operates and integration is mostly about claim representation), then to slices of basic biology with stable replication structure. If it fails, the field learns which quality signals are load-bearing and which ones metascience has oversold. Either result is a contribution to knowing what the literature supports. Implications for funders Because this burgeoning ecosystem of builders already exists, a well-informed philanthropic or government funder could play a crucial catalyzing role in bringing this future about. They could play at least three roles: creating open structured datasets, publishing open benchmarks and incentivizing the solving of key technical challenges. First, open archives of papers that the government maintains, like PubMed, could be turned into structured data amenable to large scale metascience and claim aggregation. I know the US government already has an interest in doing this, though some key open questions remain unanswered. How do you determine the best models and systems for accurately extracting information from papers? How can you establish a robust way to allow researchers to flag errors and correct them? And finally, how do you create a legal regime in working with publishers to maximize the scope of available papers? For the latter, a university or a private philanthropy may be better positioned to make structured data publicly available under journal subscription terms or fair use. Philanthropists or government funders could also coordinate to create or commission benchmarks that evaluate whether important problems have been solved. For example, an open benchmark for claim extraction from a range of different scientific article types would be extremely helpful. Ensuring the underlying data are accurate is vital for creating these evaluations. I’ve discussed opportunistically using various human-created datasets for this purpose, but a consistent problem is that errors in human data make it difficult for them to serve as a gold standard. Finally, with structured data and benchmarks available, the government or private philanthropy could use them to incentivize groups to develop machine learning systems that meet these benchmarks. Prizes are one potentially valuable tool for this. For example, you could establish a prize for a system that accurately updates a living meta-analysis for a small set of claims. Prizes are particularly useful as signals of problem importance, and can help create vibrant ecosystems of public and private research—see, for example the role the government played in kickstarting the current work on nuclear fusion. Conclusion The drawbacks of the current scientific publishing system are known. Scientists agree, metascientists agree, philanthropists agree: the published PDF plus citation graph isn’t the right substrate for maintaining a representation of the evidence base in science. The pieces needed to build the alternative either already exist or are rapidly taking shape. The community is forming around exactly this problem, with concrete partnerships and shared infrastructure. A pilot should start on behavioral science RCTs because that’s the slice of empirical science most amenable to legibility, where replication ground truth is richest, and where the failure modes are best documented. What’s been missing is the galvanizing mission to assemble these pieces into something that works. That’s what I’m proposing to build. *** 1 I have a broader field map that I’ll release publicly soon. This is me, building in public! 2 If this is something that you are excited about, please reach out and talk to me. 3 More on this very soon too! 4 This tests whether, given the code and the data, you can get the same statistics as reported in the published paper. 5 This tests whether the results are the same as a paper’s given alternative analytical decisions in conducting the analysis (like outlier omission). Closely related is the idea of a “multiverse” where you come up with many different ways of answering the same underlying research question with the same data, and test whether the results hold in all those alternative methods. There’s been work on the latter as well. 6 Some of the replications, e.g. those from the SCORE project, had paired the experiments with forecasts from prediction markets. So we get to look at this for free.
NASA Spaceline Current Awareness List #1,202 29 May 2026 (Space Life Science Research Results)
The abstract in PubMed or at the publisher's site is linked when available and will open in a new window
I’m an IVF Doctor. Business Is Booming Because Ob-Gyns Aren’t Doing Their Jobs.
Just last Monday, a woman sat across from me in my office and asked a question I have come to dread. Why had no one told her? She is 33, a therapist, married three years, and she has been to her gynecologist every year since high school. She was also on the brink of perimenopause. She had assumed that when she was ready, her body would be too. No one in two decades of annual visits had ever explained that the most consequential decisions about her capacity to bear children were being made by her ovaries on a calendar she could not see, while her doctor took her blood pressure and refilled her birth control. She is the patient I see several times a month. She is the most preventable tragedy in American medicine. I am board certified in both obstetrics and gynecology, and reproductive endocrinology. There’s a fertility crisis happening right now in America—and a furious debate about who is to blame. The alleged culprits include housing, smartphones, and capitalism. One group is getting off lightly: ob-gyns. Read [ How Perimenopause Became America’s New Health Scare ](https://www.thefp.com/p/how-perimenopause-became-americas) In July, the Centers for Disease Control and Prevention (CDC) reported that the U.S. fertility rate had fallen to fewer than 1.6 children per woman—the lowest figure in our history—despite a 2025 survey of American Gen-Z women that found that nearly three-quarters intended to become mothers. American women are not opting out of building a family. They are running out of time.
Glyphosate: A story of science, risk, and nuance
In the summer of 2014, a California groundskeeper named Dewayne Johnson started noticing patches of raw, weeping skin spreading across his body. He had spent years applying Roundup, Monsanto’s glyphosate-based herbicide, for a school district, sometimes drenched in it when equipment malfunctioned. By 2014, he had a diagnosis: non-Hodgkin’s lymphoma. In 2018, a jury awarded him $289 million in damages, later reduced on appeal. Tens of thousands of lawsuits followed. The story hasn’t quieted down. It’s all over the internet, swinging between “this will kill you, buy organic” and “relax, you’re fear-mongering.” Some of that recent chatter stems from an Executive Order protecting glyphosate and its production, which set off intense infighting within the MAHA movement. Some of it reflects a deeper truth: Americans genuinely care about harmful chemicals in their environment (see poll below). And the conversation isn’t going anywhere, with a Supreme Court case involving Monsanto set for this April. Glyphosate (the active ingredient in Roundup) is one of the most widely used herbicides in the world. But does glyphosate cause cancer? And how much exposure is actually risky? With so much mistrust in institutions and corporations (and some genuine conflicts of interest), making sense of the actual scientific evidence is genuinely hard. Here is a translation of what the scientific evidence actually says. Does glyphosate cause harm? Glyphosate is an herbicide that kills most plants it contacts rather than targeting specific species. It works by blocking an enzyme pathway (EPSPS) that plants and many microorganisms need to produce essential amino acids. Without those amino acids, the plant can’t grow and dies. Glyphosate was first developed by Monsanto in the 1970s and became ubiquitous after the company introduced “Roundup Ready” crops in the 1990s. In 2024, Bayer removed glyphosate from residential Roundup-branded products due to litigation pressure. But today it is still the most widely used herbicide in the world. Farmers also discovered they could spray it directly on crops like oats, lentils, beans, and peas just before harvest to dry them out faster and make harvesting easier. Because of its widespread use, it’s obviously really important to understand if it’s harmful to humans. The key principle: The dose makes the poison The most important concept in toxicology is that “the dose makes the poison.” Sixteenth-century physician Paracelsus articulated what remains the foundational principle of toxicology: sola dosis facit venenum. Water will kill you if you drink enough of it. Aspirin saves lives at 81 milligrams and causes internal bleeding at higher chronic doses. So, at what dose is glyphosate poisonous? The LD50 in rats (the dose that kills half the test animals) is around 5,600 mg/kg body weight. Table salt is roughly 3,000 mg/kg. By that classic measure, glyphosate is less acutely toxic than salt. But some people are exposed to a lot of glyphosate through their work. And among the general public, there are many questions about low-dose, cumulative exposure from multiple sources over long periods. Does glyphosate cause health problems? Cancer Correlation maps are striking, with one analysis finding that 60% of counties that spray the most glyphosate have non-Hodgkin’s lymphoma rates above the national average. But correlation alone doesn’t establish cause, which is why animal and human studies matter. In animals: Rat studies are typically what most fear is rooted in, but most people don’t know the study details on the dosage given to rats. A pooled analysis of the 13 most rigorous rat studies found evidence that very high doses, around 55,000 times greater than typical food residue exposure, can cause certain cancers. In humans: One of the strongest studies followed 55,000 herbicide users over 20 years and found no overall increased cancer risk. There was one signal: among those with the highest use, rates of acute myeloid leukemia (AML) appeared elevated. A broader meta-analysis of 18 human studies also found no overall cancer risk, though a separate meta-analysis focused specifically on non-Hodgkin lymphoma found that people with high cumulative glyphosate exposure faced a 41% higher relative risk compared to those with low or no exposure. These human studies are observational studies (randomized controlled trials would be unethical), and meta-analyses are only as reliable as the studies they pool. But the story seems consistent: at very high exposure levels, there may be some cancer risk. But that’s about as far as the science currently takes us. Emerging research: gut and reproductive health Gut: Because glyphosate targets a pathway that exists in some gut bacteria, scientists have questioned whether it could affect the microbiome. In mice, a 2023 University of Iowa study found that glyphosate altered gut bacterial composition and raised markers of intestinal inflammation. A 2024 systematic review found similar patterns: disrupted gut bacteria and problems with the mucus layer that protects the intestinal wall in mice. Whether this translates to humans is an open question. The human gut is highly variable and resistant, and we don't yet have strong studies confirming the same effects in people. Reproductive health: Animal studies have found that glyphosate-based herbicides can interfere with reproductive hormones, including disrupting egg cell development in mice and reducing the number of eggs available in sheep’s ovaries. However, the doses used in these experiments were high, so it’s not yet clear whether the same effects would occur in humans. On the human side, a 2021 pilot study led by Mount Sinai researchers tested urine samples from pregnant women across the U.S. and found glyphosate in 95% of them. The study also found a possible connection between higher glyphosate exposure during pregnancy and a subtle physical difference measured in female newborns. That said, some connections weren’t statistically reliable and this was a small study. The researchers themselves said more and larger studies are needed before drawing firm conclusions. What do regulators say about glyphosate safety? In 2015, the International Agency for Research on Cancer (IARC), part of the World Health Organization, classified glyphosate as "probably carcinogenic to humans" (Group 2A). The classification is worth taking seriously. But, there’s an important distinction: IARC classifies hazard, meaning the potential to cause harm under some conditions. It does not assess risk, which accounts for actual exposure levels and the real-world probability of harm. The U.S. EPA, the European Food Safety Authority, Health Canada, and regulatory agencies in Australia and Japan have all concluded that glyphosate is “unlikely to be carcinogenic to humans” at realistic exposure levels. They’re asking a different question: given how much of this people actually encounter, what is the probability of harm? Your actual exposure is what determines your actual risk. What does glyphosate mean for your daily life? At the grocery store: Food residues are small. The EPA’s acceptable daily intake is 1.75 mg/kg of body weight per day. To hit that threshold from oatmeal alone, a 150-pound adult would need to eat roughly 50 pounds of oats every day. But this calculation addresses only one pathway (food), and we don’t yet have robust tools to measure people’s actual total exposure. If reducing exposure matters to you, organic certification prohibits synthetic herbicides, and organic oat products generally test at lower or undetectable levels. Either way, a diet rich in whole grains, conventional or organic, is far better for your health than one that omits them out of fear of residues. On the farm: Occupational exposure is orders of magnitude higher than consumer exposure. Farmers and farm workers who mix, load, and apply glyphosate-based herbicides, especially without protective equipment, face meaningfully different risk profiles. Proper PPE isn’t optional. Integrated weed management strategies that rotate chemical modes of action are also worth taking seriously, both for health and for long-term effectiveness. If you live near a farm: Spray drift is real. Concentrations near field edges can spike during and after application, particularly on windy days. This is an area where I think public health could really step up and empower rural communities with buffer zones, rather than placing the onus on individuals. But for now, knowing your local agricultural calendar and keeping windows closed during application are the first steps. Bottom line Dewayne Johnson was exposed to glyphosate at levels most people will never encounter, and a jury decided he deserved compensation. That outcome is not evidence that the oatmeal in your pantry is dangerous. But it is a reminder that the dose, the context, and the person doing the exposing all matter enormously. Glyphosate is a chemical tool with benefits, trade-offs, and genuine open scientific questions. Learning to hold that complexity without collapsing into panic or dismissal is, honestly, one of the most useful and hardest things to do in navigating modern health science. Love, YLE Your Local Epidemiologist (YLE) is founded and operated by Dr. Katelyn Jetelina, MPH PhD—an epidemiologist, wife, and mom of two little girls. Hannah Totte, MPH, is an epidemiologist and YLE Community Manager. YLE reaches more than 425,000 people in over 132 countries with one goal: “Translate” the ever-evolving public health science so that people will be well-equipped to make evidence-based decisions. This newsletter is free to everyone, thanks to the generous support of fellow YLE community members. To support the effort, subscribe or upgrade below: Subscribe
Your Thymus and Your Healthspan
Our thymus gland plays a central role in the development or our immune system, specifically for supporting T cell development (how these cells got their name, maturation and differentiation in the thymus) and discriminating between self and foreign, non-self antigen proteins with production of dendritic cells. As we age, our thymus gland shrinks—the process known as involution—with progressive change from spongy to fatty tissue, with loss of functionality. But this process, with respect to timeline and extent, markedly varies from one person to the next. And to make things even more complicated, our thymus gland anatomy and precise location in the chest also is highly variable. So the famous Frank Netter diagrams from the 1960s (such as at left below) don’t capture the remarkable heterogeneity that a random set of 12 chest CT scans (below at right). What I consider as 2 landmark papers in Nature this week (here and here) used AI to quantify health of the thymus in 2 large cohorts, and then correlate the metric to a broad array of health outcomes. In this edition of Ground Truths, I’m going to cover three questions: (1) How was thymus health determined by AI?; (2) How is thymus health linked to key clinical outcomes? and (3) Are there ways we can promote a healthy (aka rejuvenate) thymus gland in our later years? Subscribe 1. How was thymus health determined by AI? This was accomplished by extensive work developing and validating an AI pipeline for 2 stages, the first for localization and segmentation of the thymus bed, and the second to quantify a digital marker, termed the thymic health score. There’s a lot to this algorithmic development, so I won’t go into all the details, but just provide a rudimentary outline of what was done. The 1st stage used supervised learning with 2 radiologists reviewing 2,461 chest CT scans. That work trained a 3D U-Net model to automatically identify the thymic bed’s 3D cropped region using center of mass coordinates, which reached 99.8% accuracy. The 2nd stage used a foundation model that was pre-trained with SwAV (which stands for Swapping Assignment between multiple Views), a self-supervised model, that generated a high-dimensional thymus representation of 4,096 features. That compares to the radiology reductionist and subjective scoring of 0 to 3 where 0 means the thymus is fully degenerated and fatty, and 3 is considered dense, intact glandular soft tissue. Notably, the self-supervised learning (SSL) performance was superior to supervised (AUC ~0.75 vs 0.55, respectively) reflecting the shallowness of the 0-3 classifier vs SSL’s holistic, self-taught AI. The thymic health score ranged from 0 to 100, with the highest number indexed to fully preserved thymic health. The algorithmic work extended to explainability with both Shapely value distribution, meaning the model was holistic not relying on any “magic” pixel, and occlusion sensitivity, demonstrating the model’s performance was not affected by ribs, sternum, lung tissue, but rather focused on the thymic bed directly. Below are a few saliency maps from the occlusion sensitivity that indicate the thymic bed focus, not affected by neighboring structures, using the jet color scale. Now the AI was ready for processing ~25,000 CT scans, each over 30 MB files, from the 2 large participant cohorts to provide a thymic health score, it did so in less than 14 hours, which is less than 2 seconds per scan! Share 2. How is thymus health linked to key clinical outcomes? The two cohorts were the National Lung Screening Trial, NLST (N=25,031) and the Framingham Heart Study, FHS (N=2,581) each with baseline demographics and long term follow up of >12 years for health outcomes. From the NSLT, you can see below that increased age and body-mass index were correlated to reduced thymic health. And, overall, men had reduced thymic health scores compared with women. There are a lot of graphs in the paper for outcomes, for both the NLST and FHS cohorts. To simplify the major outcomes, below is a composite Figure with striking reduction of all-cause mortality and for the different causes of death. The results were consistent between the 2 cohorts. For example, the cardiovascular mortality hazard ratio average was 0.57 in NLST and 0.38 in FHS (weighted to be 0.53 for the aggregate). The reduction of mortality also extended to digestive diseases and pulmonary disease (data not shown below). Lung cancer incidence was reduced by 36% for high vs low thymic health (Figure below, with a panel -incidence and b panel-mortality, adjusted for age, sex, BMI, smoking status). Notably, there was a smoker’s paradox: lower incidence and improved survival for lung cancer in smokers who had a high thymus health score. Smoking was associated with lower thymic scores whereas alcohol was not. Higher thymic health was linked to higher HDL cholesterol, lower triglycerides, lower fasting blood glucose, and lower systolic and diastolic blood pressure. Inflammation biomarkers, such as C-reactive protein and interleukin-6, were elevated in the people with lower thymic health scores. In their second paper, the same team looked at the relationship between thymic score and outcomes for 3,476 patients receiving cancer immunotherapy. The non-small cell lung cancer progression-free survival was reduced in patients with low thymic health score. A parallel relationship for survival was seen for other types of cancer including melanoma, breast, and kidney with a 44% lower risk among high thymic scores (Figure). A similar pattern was seen with different immune checkpoint inhibitors. The thymus health score outperformed programmed death ligand-1 (PD-L1)and tumor mutation burden (TMB) assay of the tumor and was an independent prognostic marker of progression-free survival. In this dataset, a direct connect with thymus score and adaptive immune function was noted with a correlation before cancer treatment for both T-cell diversity and thymus T-cell production (a metric known as T cell receptor excision circles). Thymus Removal Study There is a highly relevant citation about thymus function before moving onto ways to rejuvenate it. In 2023, a very important study of thymus removal during cardiothoracic surgery was published, with 1146 patients undergoing thymus removal vs 1146 matched controls (mean age 55 years). The adverse outcomes for thymus removal were striking, with a 2.9 higher risk of all-cause mortality and doubling of cancer incidence, 1.5 fold increase in cancer mortality, and 1.5-fold increase in autoimmune diseases. The immune function showed marked compromise after thymus removal, as reflected by CD4+ and CD8+ T cells (Figure below) Share Ground Truths 3. Are there ways we can promote a healthy (aka rejuvenate) thymus gland in our later years? In recent months we’ve learned a lot about the process of thymus involution and the pathways by which this may be modulated. Thymus involution is primarily due to loss to thymus epithelial cells (TECs) and there are 2 subtypes with different functions: the cortical, responsible for positive selection of T cells, and the medullary, for negative selection. When adipose tissue infiltrates the thymus, thymic adipocytes are pro-inflammatory, knocking out T-cell output. Likewise, systemic inflammation, or “inflammaging,” from smoking, obesity, and chronic stress promote thymic adipocytes. Now, from preclinical studies, we know about key pathways that account for these processes. Historically, back in 2014, FOXN1 was recognized as a single master transcription factor essential for TEC function, with studies in mice with forced FOXN1 upregulation leading to thymus regeneration. That laid the foundation for potential regrowth of quiescent thymus cells. It took awhile to find pathways to accomplish this goal and to even refute its role as the master regulator. The Liver-Thymus Axis Feng Zhang and his team recently showed that injection of an mRNA vaccine to the liver encoding DLL1, IL-7 and FLT3-L in combination, factors known to support thymopoiesis (Figure), successfully enhanced immune function in aged mice. However, the effect was transient. The FGF21 Story Two reports in 2025 addressed the thymus gland’s production of FGF21, a growth factor (fibroblast growth factor 21) and its control of thymus involution. This growth factor is also produced by the liver, but it doesn’t have impact on the thymus in aged rodent models. In contrast, The liver’s hepatocyte growth factor (HGF) has been shown to reverse senescent TEC structural changes. Growth hormone stimulates production of insulin growth factor-1 (IGF-1) in the liver and the thymus. Two small studies in human participants (TRIIM, for Thymus Regeneration, Immunorestoration, and Insulin Mitigation) of 6 and 50 people, respectively, treated with combined human growth hormone, metformin and DHEA, suggested the potential of slowing epigenetic aging and improving thymus mass and function. But the combination of drugs, small sample, and lack of controls make conclusions murky. Increased thymus FGF21 led to increased CD8 T cells in old mice and extended healthspan and improved physical performance. Building on the previous FOXN1 data, ablation of β-klotho, the obligatory co-receptor for FOXN1, accelerated thymic aging. The benefit to FGF21 was confirmed in a companion paper using an FGF21 knock-in mouse model showing thymus enlargement and increased TECs throughout the lifespan. (schematic Figure below). The accompanying editorial for these 2 papers speculated: “The proposed link between age-associated thymus involution and organismal aging is intriguing, and suggests we might seek to achieve systemic rejuvenation by counteracting thymic involution.” Other Factors Lessons from the Axolotl (Mexican Salamander) In an elegant set of experiments of the axolotl (Figure), known for its complete thymus regeneration after total surgical removal, mediators were identified. Surprisingly FOXN1 was dispensable. But midkine, a growth factor, appeared to be the driver, the initiator of thymus cell growth, survival, and repair. Other components that contributed were Postn+ (periostin-expressing mesenchymal niches) and Ccl19, a chemokine protein from the bloodstream. RANK and RANKL RANK (receptor activator of nuclear factor κB its ligand (RANKL) have been considered key regulators of medullary TECs. In a study of both aged mice and human thymus cell cultures, their key role was confirmed, with multiple benefits of resorting TEC function, recruitment of progenitor cells, and T cell development. Subscribe Summing Up This body of work strongly supports the health of the thymus gland as a critical regulator of human healthspan, not just a correlate or link. The new landmark studies are reinforced by the regenerative biology experimental models that have shown, via an array of mediators, that healthspan of aged mice is at least in part dependent on thymus gland function and its critical role for maintaining adaptive immunity. It sure seems that we’d be better off having an immune reservoir of naive T cells instead of a profile in older adults of exhausted, low quality, memory T cells, with a senescent phenotype. It is striking that we ignored the importance of the thymus gland for many decades. A wake-up call was the results of the thymectomy matched control study reviewed here, with the opposite of high thymic health score improved health outcomes. The convergence of AI and healthspan here is notable. The exceptional and laborious work for developing and validating (no less explaining) the AI to quantify thymus health set the foundation for probing the connect the major health outcomes in two cohorts with extensive follow-up. We’ve never had a way to meaningfully quantify the thymus gland before, so this represents important leverage of supervised, self-supervised, and transformer models. The study wouldn’t have been possible without AI. And it begs the question as to whether there are ways we can maintain our thymus at a high health score. But it’s not so simple to rejuvenate our thymus. There are multiple risks including the induction of autoimmunity, increasing the risk of cancer, and inducing a pro-inflammatory state. For example, factors that increase TEC proliferation could compromise the medulllary negative selection process and leak out auto-reactive (self-attacking) T cells. Thymic cells could be induced to proliferate, but we know, for example, that growth hormone and IGF-1 are associated with an increase risk of cancer. If thymus rejuvenation doesn’t clear out the accumulated senescent cells in older adults, then inflammation within the gland could block the production of TECs. Keeping these risks in mind, we now have identified many ways to keep our thymus healthy as we age that undoubtedly will be tested in clinical trials going forward. Ultimately, the benefit-to-risk tradeoffs will be defined. In the meantime, we have desperately needed an immunome. As I’ve stressed in multiple prior Ground Truths, we have no test in the clinic to assess a patient’s immune status! It was very encouraging for me to get an email from Hugo Aerts, the senior author of the landmark papers in the days after they were published: “I also wanted to say that your Substack on “Why We Need an Immunome” was inspiring for this work. We found it a very compelling perspective and greatly enjoyed reading it.” Just having an assessment of a person’s immune status via a chest CT scan, with millions of these performed per year, might help in guiding the right immunotherapy for cancer (e.g. more intensive, combinations for those with low thymic health scores) and help define people who are increased risk for age-related diseases of cancer, cardiovascular, and neurodegenerative. The main theme of Super Agers is that we now have many layers of data (genetics, proteins, biomarkers, organ clocks that can be integrated via multimodal AI) for us to define a person’s specific risk decades before one of these age-related diseases leads to symptoms, enabling prevention. From the new studies this week, we can add thymus health score as yet another way to understand a person’s risk, a window into their adaptive immune system and healthspan. And perhaps someday we will be able to safely rejuvenate the thymus, or maintain its health through one’s life, and use the thymus health score to monitor. NB: I wrote this post (No A.I.) A Quick Poll Loading... ********************************************************************* Thanks to Ground Truths subscribers (now > 200,000) from every US state and 212 countries. Your subscription to these free essays and podcasts makes my work in putting them together worthwhile. Please join! If you found this interesting PLEASE share it! Share Ground Truths Paid subscriptions are voluntary and all proceeds from them go to support Scripps Research. They do allow for posting comments and questions, which I do my best to respond to. Please don’t hesitate to post comments and give me feedback. Let me know topics that you would like to see covered. Leave a comment Many thanks to those who have contributed—they have greatly helped fund our summer internship programs for the past two years. 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