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Study shows link between Alzheimer’s disease and gut health
Researchers found that people with higher levels of imidazole propionate (ImP), a compound produced by certain gut microbes, were more likely to show signs of Alzheimer’s disease.
Scientists discover a promising blood sugar–regulating compound in red alga
It is a dietary staple found in sushi, rice wraps and ramen toppings. Commonly known as nori in Japan and gim in Korea, red seaweed is especially popular across Asia. Yet, despite its widespread consumption, ...
No. 1 Exercise To Boost Bone Density, According to a Doctor
In TODAY.com’s Expert Tip of the Day, a doctor shares his favorite compound exercise to boost bone density and protect against bone loss in midlife.
Could This Centuries-Old Seafood Delicacy Hold Clues to Better Brain Aging?
Sea pineapples, a type of sea squirt known as meongge in Korea and hoya in Japan, contain compounds with potential anti-aging benefits. A study found that plasmalogens extracted from these marine animals improved memory, reduced brain inflammation, and promoted black hair growth in aging mice. But could eating this seafood offer similar benefits to humans?
Novichok Nerve Agents: What Science Actually Knows About the Deadliest Weapons
A new review finds that while Novichok agents potently inhibit acetylcholinesterase and modern forensics can verify exposure, many claimed properties of these weapons remain unvalidated by experiments on authenticated compounds.
Marshmallow Root’s Chemistry Revealed: The Science Behind an Ancient Cough Remedy
A new review in Pharmacia compiles the chemical compounds and pharmacological effects of Althaea officinalis, the marshmallow plant long used for coughs, wounds, and inflammation.
Magic mushroom ingredient takes the fight out of aggressive fish
A psychedelic compound found in magic mushrooms appears to have an unexpected effect: calming highly aggressive fish. Researchers discovered that low doses of psilocybin significantly reduced aggressive attacks in mangrove rivulus fish without disrupting their normal social interactions. The findings suggest psilocybin may selectively calm escalating aggression rather than simply suppressing all behavior.
Lower GLP-1 costs are here. Mochi cuts prices and adds lab testing
Mochi Health lowers costs for compounded semaglutide and tirzepatide while adding new blood testing services.
'I found the biggest ever haul of organics on Mars.' Meet the scientist at the centre of the search for life on the Red Planet | BBC Sky at Night Magazine
Dr Amy Williams and her team discovered the largest collection of organic compounds on Mars in a sample collected by the Curiosity rover.
Worth the squeeze - College of Arts and Sciences
Alecia Septer is pinching the cheeks of sharks and rays to uncover new compounds that could help fight infections.
Effective Governance in Behavioral Healthcare Organizations
As pressures on behavioral healthcare organizations mount, operational complexity compounds with it. With added payer scrutiny, increased regulation and
Proof Stacking — Or, the Compounding Value of Credibility in Business
It's not becoming the person with the strongest argument. It's becoming the person whose accumulated evidence makes the argument unneeded.
New sensor developed at Oregon State shows promise for fast, low-cost food-quality testing
CORVALLIS, Ore. – Researchers in the Oregon State University College of Science have developed a new electrochemical sensor for rapidly and accurately detecting a naturally occurring compound widely used in the food, beverage and fragrance industries.The compound is eugenol, which gives cloves their telltale flavor and smell, and measuring its presence in commercial products is important for manufacturers and regulators.
Vanilla Could Hold the Key to New Wound Treatments, Scientists Say
Vanilla is best known for its place in kitchens, desserts, and fragrances. But scientists at Australia’s Flinders University are exploring whether vanillin, the compound responsible for vanilla’s fami...
Americhem Opens New Clean Compounding Facility in Suzhou, China
SUZHOU, China--(BUSINESS WIRE)--Oct 12, 2026--
Service providers address mental health in homeless
(COLORADO SPRINGS)–Mental health struggles, substance use, and homelessness often compound one another, creating complex challenges for individuals seeking stability. Service providers in Col…
Scientists discover vanilla’s hidden healing potential
Scientists have discovered that vanillin, the compound that gives vanilla its distinctive flavor, has powerful properties that could help fight infections, reduce inflammation, and promote wound healing. The inexpensive, widely available ingredient could one day become an important component of advanced wound treatments and regenerative medicine.
U.S. Department of Health and Human Services (HHS) Recommends Science-Based Thresholds to Target Dangerous Enhanced Kratom Products
Kratom products credit: CDPH DEA takes action based on updated recommendation from HHS October 11, 2026 - WASHINGTON - On Friday, the U.S. Department of Health and Human Services relesed the following: The U.S. Department of Health and Human Services (HHS) provided a new recommendation to the Drug Enforcement Administration (DEA) that establishes science-based thresholds for 7-hydroxymitragynine (7-OH) and mitragynine pseudoindoxyl (MGPI), potent opioid compounds associated with products marketed as kratom. The Department of Justice today announced that DEA issued new Notices of Intent reflecting HHS’ updated scientific analysis and recommendations, including a new Notice of Intent for 7-OH and MGPI incorporating HHS’ recommended concentration and ratio thresholds. Following a review of available scientific data and comments, HHS Assistant Secretary for Health Admiral Brian Christine, M.D., recommended that DEA use concentration or ratio-based thresholds to determine which products containing 7-OH and MGPI are subject to Schedule I control for purposes of temporary scheduling of these substances under the Controlled Substances Act. The recommendation is designed to target concentrated or chemically altered products while distinguishing them from natural botanical kratom products, which may contain trace amounts of 7-OH and MGPI. “We are drawing a clear line between natural kratom and dangerous, enhanced opioid products,” said HHS Secretary Robert F. Kennedy, Jr. “We listened to the public, followed the science, and developed a clear recommended threshold for temporary scheduling that targets concentrated 7-OH and MGPI without sweeping natural botanical kratom into Schedule I. The Trump Administration will continue taking decisive action against dangerous products that fuel addiction while making sure our policies are grounded in rigorous science.” Under the recommendation, 7-OH and MGPI would be controlled in Schedule I for purposes of temporary scheduling when either substance alone, or their combined amount when both are present: Exceeds 1 milligram per gram in solid powders, encapsulated material, or other solid forms, or exceeds 1 milligram per milliliter in liquid preparations; or When the mass of mitragynine present divided by the mass of 7-OH, or MGPI, or the combined amount of 7-OH and MGPI if both present, is less than 100. The ratio-based approach reflects the alkaloid composition of natural kratom products and provides a way to identify products intentionally enhanced or concentrated with 7-OH or MGPI. Available scientific data indicate that 7-OH occurs naturally in botanical kratom at relatively low or trace levels, while some evidence reviewed by FDA suggests MGPI may also occur at trace levels in some natural or kratom-derived products. FDA's scientific review found that 7-OH is substantially more potent than morphine in preclinical studies, with available data indicating approximately two to nine times greater potency depending on the study. FDA also identified evidence supporting a meaningful risk of opioid-like physical dependence and withdrawal from MGPI. “Our recommendation gives DEA a scientifically supportable framework to distinguish natural botanical kratom from products that have been concentrated or manipulated to deliver dangerous levels of potent opioid compounds,” said Assistant Secretary for Health Admiral Brian Christine, M.D. “This approach allows us to focus on the products that pose the greatest threat to public health.” In July 2025, following an FDA scientific and medical evaluation, HHS recommended that 7-OH above a specified threshold be placed in Schedule I of the Controlled Substances Act. In July 2026, DEA announced its intent to temporarily schedule 7-OH above a specified threshold, and HHS simultaneously sought public comment on the proposed threshold. DEA subsequently temporarily placed MGPI and two synthetic 7-OH derivatives, MGM-15 and MGM-16, in Schedule I. Since then, questions have emerged about how scheduling could affect natural botanical kratom products potentially containing trace amounts of MGPI. The new HHS recommendation responds to those concerns by providing DEA with a more precise threshold based on both the concentration of 7-OH and MGPI and their relationship to mitragynine, the predominant alkaloid in kratom. HHS and FDA will continue working with DEA to protect Americans from dangerous concentrated and synthetic opioid products while ensuring federal policy is grounded in the best available science. Source: HHS
FDA may allow some toxic chemicals to be added to food without safety review. Experts are alarmed
Regulator looks to expand loophole to allow dangerous compounds in food as long as they’re not carcinogenic
House of the Week: A Colorful Compound With a Treehouse and Mini Golf
Eschewing typical 30A beach homes, an architect created a vibrant property packed with whimsical features.
Vanilla could help heal wounds
A compound in vanilla pods has anti-inflammatory, antibacterial, and antioxidant properties.
Brazil: Lessons from a Disaster
By Antonio Martins (Outras Palavras) Defeats become deeper and more prolonged when we misunderstand what caused them, avoid correcting course, and embrace “solutions” that only compound our mistakes. Lula’s government and the Brazilian left suffered a disaster in Sunday’s election. Contrary to every poll, the president finished the first round 2.2 million votes behind Flávio Bolsonaro—and, more significantly, 3.4 million votes below his total four years ago, when the machinery of the state was working against him and in favor of his opponent. His vote share declined in 98 percent of Brazil’s municipalities. The PL, the main party of the far right, elected 121 deputies and 28 senators, becoming the largest caucus in both houses of Congress. The parties aligned with the Centrão—Brazil’s bloc of transactional center-right parties—were somewhat diminished, but will still hold roughly 250 seats in the Chamber of Deputies and 35 in the Senate. That will make it easier to assemble the majorities needed to amend the Constitution or impeach Supreme Federal Court justices. If elected, Flávio Bolsonaro could appoint four members of the Court, substantially altering its internal balance of power. What produced these results? How can the far right be prevented from consolidating them into a prolonged political hegemony? And what is the essential change of direction the left now needs? Explaining the Disaster Across the commercial media and the exuberant chaos of digital platforms, interpretations are multiplying. Some focus on specific episodes: Lula’s absence from the Globo debate, his very close relationship with Alexandre de Moraes, or his emphasis on issues supposedly remote from most people’s everyday concerns, such as rare earth minerals. Among the more systemic interpretations, three seem especially questionable. One argues that the principal defeat was not the left’s, since its congressional representation declined only slightly. The decisive movement captured at the ballot box, according to this view, was a shift within the right itself—from the more moderate and transactional forces of the Centrão toward the more ideological and radicalized forces of the PL and Novo. A second interpretation holds that the nature of electoral and political processes has changed. The material interests and aspirations of society, it argues, no longer play the central role they once did; they have given way to forms of subjective self-identification that the left has yet to understand. And a third concludes that, because of these two developments, we should expect a political winter: a prolonged period in which the far right and the broader right dominate Brazilian political life. There are important elements in all three interpretations. The problem lies in what they deny or leave out: Lula’s third government was a small-bore government. It offered the majorities that elected it neither a clearly better life nor reasons to believe again in politics and its power to transform society. These failures flowed from two fatal accommodations, which I will examine below. As a result, the government suffered a slow but steady erosion of support. And, as has happened in so many Western countries, it gave the far right the opportunity to present itself as anti-system and to benefit from popular frustration and distress. The interpretation that emphasizes the migration of votes from the center-right and traditional right toward the far right has been advanced, among others, by the courageous journalist Leonardo Sakamoto. In his UOL column on Monday, October 5, he highlights the miserable behavior of the traditional conservative parties. Over the past four years, they repeatedly joined forces with the “neo”-fascists, helping to “normalize” them—a criticism that could equally be directed at almost the entire corporate media. Believing they could use the far right as a stepping stone, they instead ended up partly devoured by it. This was especially true in the Senate, where the PL’s gain of 13 senators and Novo’s gain of two came at the expense of the PSD, which lost nine; the MDB, which lost two; the PSDB, which lost two; and the PP, which lost one. Sakamoto’s observation is accurate and necessary, but it leaves uncomfortable questions unanswered. Why did the erosion of the Centrão benefit the far right rather than, for example, producing growth for the left—as has happened so many times before, both in Brazil and elsewhere? The answer is not difficult. Throughout its four years in office, Lula’s third government was almost invariably associated with the Centrão. Here lies its first accommodation: accepting the limits imposed by conservative institutions; avoiding, as much as possible, any attempt to strain those limits through popular pressure; and believing only in the modest changes that could be squeezed through openings in Congress. The failure of the campaign to end the six-day workweek is emblematic. Lula could have electrified the presidential race by pairing it with a popular campaign for passage of the measure. Instead, he chose to place his hopes in the hands of Senate president Rodrigo Alcolumbre. He generated no mass mobilization, did not force his opponents onto an uncomfortable defensive, and won no victory. In September 2025, the government squandered the greatest of its many opportunities to shake up conservative power in Congress. Popular opposition to the so-called Shielding Amendment—which, if approved, would have restricted criminal proceedings against members of Congress—brought crowds into the streets, mobilized primarily by artists and social movements. This opened the possibility for a broader political education: a campaign that could begin exposing the limits and dysfunctions of Brazil’s political system while putting Bolsonaro’s movement on the defensive for its predictable support of political privilege. The amendment was defeated. But the executive branch then backed away from the fight. It remained associated with an institutional world widely seen as corrupt, elitist, and indifferent to ordinary people’s struggles. In doing so, it forfeited its credibility as a vehicle for the protest vote. On Sunday, it reaped the bitter fruits. Are We Doomed? Taking a different approach from Sakamoto, the philosopher Moysés Pinto Neto and other writers have drawn attention, in their first analyses of October 4, to the fragmentation of the public sphere produced by Big Tech platforms. Through their algorithms, these platforms present each person with a different view of social reality. As a consequence, it becomes much harder to identify common material problems and demands—for example, the fight for labor rights or for a properly funded public health system. Voters no longer embrace such demands, these authors argue, because they no longer see themselves as part of a collective. Instead, they tend to value the identities assigned to them by neoliberal subjectivity—the role of the entrepreneur, for example. On this interpretation, the left’s possible error lies in clinging to outdated illusions. Moysés’s warning is highly relevant and resonates with arguments such as Naomi Klein and Astra Taylor’s “Apocalyptic Fascism and the Billionaires’ Bet.” Unlike a century ago, the far right no longer promises a radiant future. It concentrates instead on resentment—especially that of young men. “They belong to a generation that fears it may never own a home, but compensates with the pleasure it gets from constantly provoking progressives online. Convinced their future has been stolen, they share memes romanticizing historical authoritarian regimes,” the authors write. But Moysés seems to confuse this danger with inevitability. He fails to see that the left’s answer cannot be adaptation. On the contrary, it must strengthen the possibility of politics as collective action. Nor does he recognize that precisely such a reversal is already becoming possible in some of the most promising mobilizations of the twenty-first century: the election, at the end of 2025, of the young Muslim Zohran Mamdani as mayor of New York, on a platform centered on the intensely material fight for an affordable city; the Left Party’s victory in Berlin two weeks ago, built around the demand to expropriate private real-estate corporations; and the very recent wave of demonstrations in Spain—including an occupation of Madrid’s Puerta del Sol—in which tens of thousands of young people mobilized by the Tenants’ Union have demanded limits on rents. By putting itself in the straitjacket of the “fiscal framework” in the first months of 2022, Lula’s third government adopted the second fatal accommodation of its term. Faced with conservative institutions and a country devastated by four years of Bolsonaro, increased public investment was the government’s remaining weapon for offering a more dignified life to the majority and forging an anti-conservative pact with them. The same state that disburses 1 trillion reais a year to enrich a small class of rentiers could instead spend money to extend the Family Health Strategy to every Brazilian, at a cost of 30 billion reais; provide full-day public schooling and childcare to all adolescents and children—and, especially, relief to their mothers; achieve universal sanitation while cleaning up polluted urban rivers; multiply metro systems; begin transforming the urban peripheries; and undertake many other urgently needed projects. In April 2023, an article in Outras Palavras warned that the fiscal framework could “shrink the Lula government and preserve the forces that condemn the country to inequality and regression.” A year later, another article showed that restraints on public spending were strangling policies vital to ordinary people and undermining the president’s popularity. In November 2024 came a reality check, in the form of the government’s humiliating defeat in the municipal elections. Even then, the fiscal lock was neither removed nor loosened. On the contrary: throughout the government’s four years, fiscal restraint remained central to its political narrative. The administration proudly proclaimed that it had “put the state’s accounts in order,” without grasping either how misleading that phrase was—given the payment of 1 trillion reais in interest—or how badly the message was hurting it politically. Lula finally woke up in September 2026. The increase in Bolsa Família benefits, after four years of being frozen; the announcement that anti-obesity drugs would be offered through Brazil’s public health system; and the ban on online betting showed that the state has the power to act decisively on behalf of the majority when those in government are willing to confront obstacles. The huge marches that closed the campaign in Fortaleza, Salvador, Rio de Janeiro, and São Paulo on the eve of October 4 showed how such initiatives can mobilize activists and the broader public. But it was too late—and too little to change the outcome of the first round. History has not ended The possibility of a turnaround in the three weeks leading up to November 25 cannot be ruled out. It will not be simple or easy. Lula must not only make up a deficit of 2.2 million votes; he must also offset the movement of voters who backed other right-wing candidates in the first round, most of whom are likely to move toward Flávio Bolsonaro. Pulling that off will require a broad, grassroots effort to win over voters, potentially reinforced by new initiatives from Lula. The coming hours and days will be decisive. If Bolsonaro’s movement also wins the presidency, the result will create a high-risk situation for Brazilian sovereignty and democracy. The enormous challenges posed by such an outcome would require the left to reexamine, in depth and with a genuine willingness to engage in self-criticism, its political projects—or its lack of them—and its practices. But would that mean we are condemned to the long winter of far-right hegemony that some analyses are beginning to forecast? It is far too early to say, suggests a recent text by Álvaro García Linera, the thinker who served as vice president of Bolivia under Evo Morales. His central hypothesis is that this political current will prove short-lived. At a moment when the entire world is once again talking about sovereignty and protecting national economies, the far right offers a stale, recolonizing neoliberalism. Its submission to the United States is as blatant and pathetic as Flávio and Eduardo Bolsonaro’s overtures to Donald Trump. Its project amounts to something like every man for himself: greater inequality, capitalism without limits, devastation, and supremacism. Will it work? In the United States, just two years into his second term, Trump himself is reaching record levels of unpopularity and may be on the verge of losing Republican control of both the House and Senate in November. Every new beginning is difficult. Whatever the outcome of the second round, the defeats of October 4 show how profoundly the Brazilian left will have to rethink and rebuild. But just as it would be foolish to underestimate the seriousness of its mistakes, it would be equally foolish to conclude that rebuilding a political project is no longer possible. History has not ended. The times are moving faster than ever. Originally published in Portuguese by Outras Palavras. English translation by Eric Blanc; I’ve added the subtitles. More We can’t stop the far right at home or abroad without a revitalized labor movement, which is yet another reason why you should become a sustaining supporter of the Emergency Workplace Organizing Committee (EWOC) — one of US labor’s pivotal bright spots. Relatedly, Jacobin published a short piece of mine reflecting on a decade of Bernie Sanders inspiring a whole new generation of young worker organizers.
Remaking scents: could fragrance tech help take pressure off endangered plants?
Firms working on reproducing compounds without need for repeated harvesting but conservationists are sceptical
Search for life on Mars takes major leap forward. Scientists detect longest organic molecules on planet to date | BBC Sky at Night Magazine
Scientists make discovery analysing rock pulverised for study by Curiosity rover. Largest organic compounds found on the Red Planet to date.
RosCept Capsules Introduces Ros Cept Multi-Ingredient Dietary Supplement for Brain Health, Memory and Concentration
RosCept dietary supplement features Magnesium Beta Hydroxybutyrate, Calcium Beta Hydroxybutyrate, and Sodium Beta Hydroxybutyrate in a focused BHB formulation.Wilmington, DE, Oct. 05, 2026 (GLOBE NEWSWIRE) -- RosCept has announced the introduction of RosCept, a multi-ingredient dietary supplement formulated with three mineral beta-hydroxybutyrate (BHB) compounds: Magnesium Beta Hydroxybutyrate, Calcium Beta Hydroxybutyrate, and Sodium Beta Hydroxybutyrate. Official Website: https://roscept.shop/
Coffee-Rich Diet May Be Linked to Better Breast Cancer Outcomes, But Experts Urge Caution
A new study is again drawing attention to a popular morning beverage: coffee. Researchers found that women with breast cancer who consumed higher amounts of polyphenols, naturally occurring plant compounds abundant in coffee and many plant-based foods, experienced lower rates of breast cancer-related death over a long-term follow-up period.
Pomegranate Compound Improves Heart Function Up to 80% in Mice With Heart Failure
A juicy development.
AI Could Turn U.S. Media And Entertainment Into A $48 Billion Market
Scripts, storyboards, trailers, thumbnails, voiceovers and rough cuts are all becoming part of AI’s entertainment-industry résumé. A Research and Markets report projects the U.S. AI media and entertainment market will grow from $9.70 billion in 2025 to $47.95 billion by 2034, with a compound annual growth rate of 19.43 per cent from 2026 through 2034. […]
Your gut may be making a molecule that raises Alzheimer’s risk
Scientists have linked a gut bacterial compound called ImP to greater Alzheimer’s risk, harmful brain protein buildup, and faster cognitive decline. The finding raises the possibility that reducing ImP in the blood could one day help slow or prevent dementia.
A Hidden Compound in 'Healthy' Plant-Based Foods May Be Fueling Gut Inflammation
You may have never heard of it.
A Hidden Compound in 'Healthy' Plant-Based Foods May Be Fueling Gut Inflammation
You may have never heard of it.
A Hidden Compound in 'Healthy' Plant-Based Foods May Be Fueling Gut Inflammation
You may have never heard of it.
9 Best Fruits to Help Reduce Blood Pressure, Cholesterol and Heart Disease Risk
The soluble fiber in fruit can improve cholesterol, a cardiologist says. Certain fruits show “potent cardiovascular protective action” thanks to their beneficial plant compounds.
A New Agenda for Small Business Support in an Age of Uncertainty
Entrepreneurship requires accepting uncertainty. Yet today’s small businesses face multiple, compounding, and, at times, unprecedented sources of uncertainty,
A popular GLP-1 provider just made its weight loss medications cheaper
Mochi Health has lower starting prices for compounded semaglutide and tirzepatide, plus a new lab testing service designed to help patients monitor their health.
From wild rice to tarwi, researchers are exploring the health potential of Indigenous foods
A conference paper reviewed North American and Andean Indigenous foods, including Three Sisters crops, wild rice, native berries, tarwi, quinoa, and amaranth, and described their nutrients and bioactive compounds. Evidence for health effects remains limited for many of these foods, and the authors call for research developed with Indigenous communities that also supports traditional knowledge and food sovereignty.
The ice blasting from Saturn's moon Enceladus is stranger than scientists realized
Enceladus may naturally separate and concentrate chemicals from its hidden ocean as droplets slowly freeze and shatter on their way into space. The process could explain Cassini’s puzzling ice-grain chemistry while giving future spacecraft a powerful advantage in searching for organic compounds and clues to life.
What Marketing Science Can Teach Us About Making Compound Branding Work
Little Black Book, Brenda Imeson, director of strategy at Brave Bison, reflects on what brands need to make compound branding work
Saturn’s moon offers clues in search for extraterrestrial life
With a global ocean of liquid water below a thick crust of ice, Saturn’s moon Enceladus is one of the most promising places to search for life beyond Earth. A new study suggests the moon itself may aid in that search by making some ocean compounds easier for future spacecraft to detect.
Falcons division rival falling apart already after 3 games
Baker Mayfield injury compounds problems for Buccaneers
Shift4 Payments (FOUR): A Stock Priced for Trouble, a Business Still Compounding Underneath
Back in August, Shift4 Payments, Inc. (NYSE:FOUR) lowered its full-year outlook, cutting expected gross revenue less network fees to $2.48 billion – $2.53 billion from $2.5 billion – $2.6 billion and adjusted earnings per share to $5.15 – $5.35 from $5.50 – $5.70, citing roughly $25 million from Middle East travel disruption and $20 million […]
Intel Panther Lake Teardown, 18A, BSPD, GAAFET, SemiAnalysis STEEL
Panther Lake debuts the first commercial implementation of backside power delivery (BSPDN), introduces Intel’s first iteration of gate-all-around (GAA) transistors, and showcases their advanced packaging capabilities with its Foveros-S assembly. With Panther Lake, Intel’s manufacturing arc has shifted from nebulous roadmaps to shipped silicon, a significant milestone on their long road back to competitive semiconductor manufacturing. To evaluate the extent of Intel’s comeback, we tore down Panther Lake. The SemiAnalysis STEEL teardown lab breaks down advanced datacenter and AI hardware. To learn more about our pipeline or to commission a teardown, contact sales@semianalysis.com. WE’RE HIRING: Architecture, floorplan, packaging, manufacturing, and labs experts. Opportunities from system to transistor and everywhere in between. Check out our Careers page. Our teardown traces 18A from its four-sheet RibbonFETs (Intel’s marketing name for GAAFETs) and gate stacks through contacts, frontside and backside wiring, and the bonded carrier. We explain how these material and integration choices improve gate control and reduce resistance, while adding capacitance, thermal resistance, and process complexity. Our measurements put Panther Lake’s 18A compute logic and TSMC N3E GPU logic at similar logic density. However, 18A does not lead TSMC N3P, N2 or Samsung SF2 in peak density. Panther Lake’s CPU cores are incremental updates, and the high-end GPU still uses TSMC N3E. Panther Lake assembles one compute tile, one GPU tile, and one I/O tile atop a passive base tile using Intel’s Foveros-S advanced packaging. Both compute tile variants use Intel 18A. The Xe3 GPU options are a 4-core GT1 tile on Intel 3 and a larger 12-core GT2 tile on TSMC N3E. Both I/O tile variants use TSMC N6. [1], [2] Our analysis centers on the PTL-U compute tile, both the 4-core and 12-core GPU tiles, as well as the 12-lane I/O tile. In conventional chips, power and signal are routed through the same frontside metal stack towards the device frontend. Power rails consume scarce routing resources near the transistors, while tall via stacks carry VDD and VSS from the coarse upper wires to local rails. Backside power delivery (BSPD) moves the main power network behind the transistor layer, to the backside, separating it from frontside signal routing. We covered BSPD and its impacts in 2024. [3], [4], [5] Intel’s BSPD implementation, branded as “PowerVia”, routes power through dedicated backside metals to nano-TSVs, which connect those rails to local source/drain (S/D) contacts. Implementing that separation requires Intel to build the interconnect stacks from both sides of the wafer. The frontside comprises the M0-M14 signal stack, while the backside comprises the BM0-BM5 power stack. M0 and BM0 are closest to the transistors. The nano-TSVs connect the two sides, but Intel patterns and etches each via from the front after forming the contacts. A narrow via runs from the side of the contact deep into the silicon substrate. Intel then completes the frontside signal metal stack, bonds the wafer to a carrier, flips it and removes the original substrate until the buried via tips are exposed. The backside metal stack is then deposited directly on the revealed vias. The nano-TSV and backside-via profiles taper in opposite directions because Intel forms them from opposite sides of the wafer. The transistor structures form the FEOL. Local contacts and nano-TSVs connect them to the wiring. M0 begins the frontside interconnect stack. The silicon carrier remains attached above the frontside interconnects. It supports the device wafer during substrate removal and backside processing and remains part of the finished chip’s thermal path. PowerVia removes the main power distribution from the congested frontside metals, routing supply through shorter and wider backside wires. Its lateral landing still occupies area in the standard cell, so it recovers less cell area than a direct backside contact. [3] Nano-TSVs beside the logic devices carry VDD or VSS from the backside power network, while signal connections continue upward through the frontside metals. Backside Interconnects Samsung SF2 data is included for comparison to Panther Lake’s within this article. SF2 is the incumbent GAA foundry node but lacks BSPD, serving as a useful reference to evaluate 18A. A full teardown of Samsung’s S26 products, processed on SF2, will be shared soon.Nanosheet-cut EDS comparison. The PowerVia supply path runs from the backside Cu rails through Mo-lined W nano-TSVs to the local transistor contacts. In this cross section, the tapered connection spans roughly 150 nm from the contact level to BM0. The Ta liner confines Cu and promotes adhesion to the surrounding stack; the AlOₓ etch stop controls the next dielectric etch above the rail. Dielectric beneath the ribbons electrically separates the devices from the backside wiring and removes the conducting silicon body below the channel. [6] AlOₓ serves as an etchstop (ES), enabling endpointing and protecting the underlying layers. Low-volatility aluminum fluoride reaction products resist the fluorinated plasma, allowing a thin AlOₓ film to protect the metal while the surrounding low-k dielectric is removed. [6], [7]. While the BM0 and layers above the M1 lines show double AlOx layers, Our SMIC N+3 teardown showed single AlOₓ layers. SMIC uses a simpler local AlOₓ substack, while the remaining cap and etch sequence provide the required landing protection. So why double layers? The closely spaced AlOₓ doublets provide two protected endpoints in the etch sequence. Intel documents an AlOₓ/SiN/AlOₓ stack that explains the benefit. The main dielectric plasma etch stops on the first AlOₓ film; a selective wet clear opens that film; a second plasma etch removes the intermediate SiN and stops on the second AlOₓ film. The final wet clear exposes the metal landing surface. SiN is the intermediate dielectric in Intel’s published example. [8] The second stop protects the metal through a cap breakthrough. Wide openings can etch faster than narrow ones, and etch depth varies across the wafer. Metal under an early-clearing opening would otherwise be exposed while other openings still need more etching. Staged protection widens the process window and reduces metal erosion, corrosion and void formation. [8] TSMC documents AlN/AlOₓ/SiOC/AlOₓ above Cu, with AlN blocking Cu diffusion, and a simpler AlN/SiOC/AlOₓ variant that omits one AlOx film. [9] Levels with different opening sizes, aspect ratios, pattern densities and cap materials need different etch margins. A double AlOx stop is useful where another protected endpoint justifies the added processing. The extra film adds formation, selective opening and cleaning steps, plus another set of interfaces to control adhesion, moisture, and stress. These blanket films are opened through the existing via pattern, so each film does not require another lithography mask. AlOₓ adds parasitic capacitance when it replaces lower-k dielectric; two thin AlOₓ films can nevertheless contain less AlOₓ than one thick film. Total thickness, placement, and theintermediate dielectric determine the electrical cost. Deposition chemistry also changes AlOx permittivity and residual hydroxyl content, which can oxidize the underlying metal. [7], [8], [10], [11] The backside stack separates into relatively fine BM0-BM2 wiring near the devices and coarser BM3-BM5 power distribution. The largest pitch increase occurs between BM2 and BM3. BM0’s pitch closely matches the logic-row height, fitting local power delivery to the cell rows. Higher levels aggregate current through larger conductors: routing density becomes less important than low resistance and current capacity as the network approaches the package. This hierarchy provides wide power wiring for the power delivery network without consuming scarce frontside signal-routing resources. [3] The SemiAnalysis STEEL teardown lab breaks down advanced datacenter and AI hardware. To learn more about our pipeline or to commission a teardown, contact sales@semianalysis.com. WE’RE HIRING: Architecture, floorplan, packaging, manufacturing, and labs experts. Opportunities from system to transistor and everywhere in between. Check out our Careers page. Frontside Interconnects Intel 18A combines Mo-lined W contacts and nano-TSVs with a separate backside Cu power network. Samsung SF2 keeps power on the frontside, using Ti-based contact interfaces and Ta-based barriers and Co liners around Cu wiring. In 18A standard-cell rows, backside power rails supply the devices through nano-TSVs within the cells, freeing frontside routing resources. Samsung’s M0 accommodates both power and signal connections. From the device toward M0, the connection runs through a Ti-based S/D interface, W contact fill, a Mo-lined W via, and the Cu M0 wire. Mo supplies a conductive nucleation and adhesion layer for W, replacing the resistive TiN liner used in conventional W integration. This increases the effective conduction volume within the feature while retaining W fill and its established polishing, cleaning and etching processes. Intel’s Mo/W patent describes this integration tradeoff. The nano-TSV uses the same Mo-lined W construction in the backside supply path. [12] The move from TiN to Mo is an incremental change. While a full Co or Mo fill can also reduce the volume lost to liners in very small features, it requires new integration schemes that increase complexity and risk. Cu remains attractive for wider wires due to its low resistance. As wires and vias shrink, the diffusion barrier consumes an increasing fraction of their cross-section. [12], [12], [14] Intel uses Co/Ru liners at M0-M1, Co at M2-M4, and Nb at M5-M9. The lower-level liners help Cu adhere and reduce void formation during trench fills. Applied Materials’ Endura has new thermal control that facilitate wetting process, so the thin film continuity is good enough that good capillary pressure will drive Cu atoms to the via bottom without voiding. Intel’s choice to use Nb is particularly interesting. Intel’s Nb patent describes a conductive diffusion barrier intended to reduce the barrier’s contribution to resistance relative to conventional Ta-based barriers, particularly at via bottoms where all current crosses the barrier. The patent pairs Nb in coarser levels with the option of lower-cost PVD processing. [15], [16] The upper metal layers support thicker barriers formed through physical vapor deposition (PVD) despite its worse coverage and uniformity. Meanwhile, the lower metal layers require thinner barriers deposited through conformal atomic layer deposition (ALD). Co/Ru adds another material interface and requires controlled deposition and Cu fill. Changing liners and barriers by metal layer allows Intel to optimize interconnect resistance, process complexity, and reliability. [15, 16] RibbonFET, Intel’s name for its gate-all-around FETs (GAAFETs), replaces the FinFET’s vertical fins with four stacked horizontal silicon nanosheets, allowing the gate to surround the channel on every side. The path to GAAFET begins with the planar transistor. A planar MOSFET places the gate above the channel between its source and drain. Pairing an NMOS with a PMOS transistor creates a CMOS inverter, in which the NMOS pulls the output low for a high input, and the PMOS pulls it high for a low input. The gate must retain electrostatic control of the channel to ensure clean switching. As gate lengths shrank, the drain began to compete with the gate for that control, increasing off-state leakage. Electrostatic control was restored through an architectural evolution that raised the channel into a vertical fin and wrapping the gate around three sides. Called “FinFET”, this new architecture packed more effective channel width into a smaller footprint. Further scaling made it harder to maintain both drive current and leakage within smaller cells, and reintroduced the same problems planar MOSFETs faced. Nanosheet GAAFETs close the fourth side by replacing the vertical fin with a stack of horizontal nanosheets, each surrounded by the gate. The tighter electrostatic control suppresses leakage at shorter gate lengths while stacking adds effective channel width within the cell footprint. In a FinFET process, channel width changes in discrete steps as designers must add or remove whole fins. Nanosheet width can instead be adjusted continuously within the process’s design rules. Wider sheets increase drive current, while narrower sheets reduce capacitance at the cost of drive current. Intel 18A uses stacks of four nanosheets each and varies their widths across logic and SRAM. At the process level, adding more sheets to each stack increases effective channel width and drive current, but complicates fabrication. RibbonFET vs MBCFET Samsung began GAAFET production in 2022 with SF3E, following with SF3 and now SF2. Its ‘MBCFET’ provides a useful structural comparison with Intel’s first RibbonFET implementation. [17] STEEL is digging deeper into SF2, used in the Exynos 2600, and TSMC’s GAAFET N2, used in Apple’s A20 Pro, in upcoming newsletter articles. We’re throwing some teasers on X. Let’s compare Samsung SF2’s MBCFET with Intel 18A’s RibbonFET. Subscribe Even to the untrained eye, Intel’s extra nanosheet is obvious. Intel stacks four ribbons to Samsung’s three. Samsung’s sheets are much wider in these fields, so both sheet count and width matter to the available channel perimeter. Sheet width also changes which silicon surfaces carry current. On conventional (001) silicon, wide nanosheets emphasize the broad top and bottom surfaces, favoring electron transport; the larger sidewall contribution in a narrow sheet favors hole transport. Thinner sheets improve gate control but increase confinement and scattering. This makes width and thickness part of the NMOS/PMOS balance, alongside strain and threshold voltage. [18], [19] GAAFET designs like 18A use different work-function-metal (WFM) stacks for NMOS and PMOS. Around each ribbon, a thin SiOx interfacial layer separates the silicon channel from the HfOx high-k dielectric, with La providing dipole tuning and the WFM wrapping the dielectric. NMOS uses a TiAl-based stack, while PMOS uses TiN WFM. W fills the remaining gate trench, providing a lower-resistivity path where the work-function layers are no longer needed. In this field, the PMOS stacks leave room for W between ribbons, while the NMOS stacks occupy more of those gaps. A silicon-based dielectric marks the P/N boundary, allowing the PMOS and NMOS gates, sharing the same gate trench, to be processed sequentially. Fast logic paths, retention circuits, and SRAM need a family of threshold options. Changing threshold without substantially changing device dimensions, capacitance or fabrication complexity is valuable. FinFET processes typically use different work-function-metal stacks. In a four-ribbon GAA stack, the narrow sheet-to-sheet gap limits how much WFM can fit around each channel. La in the gate dielectric creates interfacial dipoles at the SiOx/HfOx boundary, shifting effective work function and tuning threshold voltage. This gives Intel another control alongside its NMOS and PMOS WFM stacks. Low-threshold devices improve critical-path drive; higher thresholds reduce leakage elsewhere. Dipole tuning is especially useful in GAA because it changes threshold without consuming the narrow intersheet gap with thicker WFM. Precise control of La incorporation, diffusion and interface quality has long been a challenge, limiting viability in high volume production but is now seen from every leading-edge foundry. Intel’s patent describes depositing a dipole-forming oxide above HfOx and annealing it toward the interfacial oxide before completing the work-function and fill metals. This separates threshold tuning from the space available for metal. Newer research addresses the thermal cost: imec’s 2026 dipole-middle research inserts the shifter between two HfOx depositions, shortening the diffusion path while protecting SiOx during patterning. [20], [21]Matched-cut EDS, Intel 18A (left) vs. Samsung SF2 (right). Intel retains raised source/drain epi beneath its contacts, while Samsung recesses W deep into the epi to form a V-shaped Ti-lined interface. The deeper contact increases metal-to-semiconductor area and shortens the current path from the lower sheets, reducing contact and spreading resistance. It also removes epi volume and brings the contact etch closer to the channel ends. Retaining more epi preserves the material available for strain transfer, especially from SiGe into PMOS. These geometries balance contact access against stress engineering and etch margin. [22], [23] Samsung stacks three sheets to Intel’s four ribbons, and both processes use sheet width to tune drive strength. In our Samsung cross-sections, widths range roughly from 19 to 30 nm in the NPU rows and 37 to 50 nm in the CU cell. The Samsung nanosheets taper, with the widest sheet at the bottom and the narrowest at the top. Both processes use HfOx gate dielectric and Ti-based work-function stacks, with Al in the NMOS stack. In the Samsung devices shown here, the dielectric and WFM occupy the intersheet gaps, leaving W above the top sheet. Intel’s PMOS stack leaves more room between ribbons, and W fills those gaps while the thicker NMOS stack leaves W mainly in the upper trench. Gate-stack EDS maps. The W between Intel’s PMOS ribbons provides a conductive path close to the lower gates. Where WFM fills the entire gap, the gate still surrounds the channel, but voltage reaches it through the more resistive work-function films. Thinner WFM and dipole tuning preserve room for low-resistivity fill; Mo and Ru are alternative fill metals being developed for further scaling. [24] A masked, sequential WFM flow explains the different gate heights and inter-nanosheet fill. The proposed sequence below shows how separate NMOS and PMOS work-function steps produce that geometry. Enabled by the BSPDN process, Intel replaces the dense-logic silicon subfin with dielectric, removing the parasitic conduction path below the ribbons and reducing substrate-related capacitance. A retained silicon body as in classical, non-SOI, planar and FinFET designs needs junction and punchthrough-stop engineering to suppress leakage. Dielectric isolation makes that leakage less sensitive to the subfin doping profile but adds removal and fill steps. It also weakens the direct thermal path through silicon, making the contacts, metal stacks and package more important for heat extraction. [24], [26] Fluorine is concentrated around selected Intel device structures in the maps. WF6 is a standard precursor for W nucleation and fill, while barrier films protect adjacent dielectrics from fluorine attack. Low-fluorine W processes reduce the residual-F burden. Chloride-based precursors avoid introducing F during W deposition, but require control of chlorine attack, nucleation and fill quality. The integration target is a continuous, low-resistance W path with a thin protective liner and minimal chemical damage to the surrounding stack. [20], [27], [28] The SemiAnalysis STEEL teardown lab breaks down advanced datacenter and AI hardware. To learn more about our pipeline or to commission a teardown, contact sales@semianalysis.com. WE’RE HIRING: Architecture, floorplan, packaging, manufacturing, and labs experts. Opportunities from system to transistor and everywhere in between. Check out our Careers page. We measured cell height, gate pitch, metal geometry, and ribbon dimensions at the XTEM sites shown below. The tables group these dimensions by site and device polarity. Our “sheet cuts” cross the silicon channel and show the ribbons end-on. “gate cuts” run along the channel through successive gates. The 18A logic cell dimensions point to a five-track logic library while the N3E and Intel 3 cell dimensions evidence a seven-track logic library. The DDR-PHY uses wider M0 wires and much larger spacing than core logic. That trades routing density for lower wire resistance and weaker coupling between neighboring nets. The geometry suits the current delivery and coupling requirements of analog, clock, and I/O circuitry. PowerVia lets 18A combine a compact cell height with wider M0 geometry by moving the main power rails off the signal-routing tracks. That relaxes local wire scaling while preserving a small cell footprint. Cell height and gate pitch set the geometric density; pin access and routability determine how much of it a real block can use. [29] The biggest takeaway from our gate-pitch measurements is that Intel 18A compute logic and TSMC N3E GPU logic have similar density in the Bohr representative-cell model. The 18A example is 18.6% denser than the Intel 3 GPU example. Gate pitches are nearly identical across the three sites, so cell height drives most of the difference. The Bohr model combines a four-transistor NAND2 spanning three gate pitches and a 32-transistor scan flip-flop (SFF) spanning nineteen pitches, weighting their densities 60:40. The sensitivity column shows how independently changing cell height and gate pitch by ±1 nm changes the result. This compares representative cell geometries; whole-die density also depends on cell mix and placement. The 18A P-core gives M0 substantially more metal cross section than the N3E vector engine. Treating each profile as a trapezoid gives 2.63 times the area per line and 1.84 times the area after normalization by routing pitch. The larger section reduces the geometric contribution to line resistance and lowers current density for a given current. Taller and wider wires also add capacitance, so circuit delay depends on the balance of resistance and capacitance. The DDR-PHY has less metal area per routing width than the 18A core fields, while remaining above N3E. [30] Area = height × (top CD + bottom CD) / 2, including liners. Area/pitch normalizes by routing width. Taper is the symmetric sidewall angle from vertical, with the largest angle belonging to the DDR-PHY. Compute tile The measurements show how ribbon dimensions and gate-stack geometry vary across the compute tile and between NMOS and PMOS to balance channel drive, gate load and the space needed for the dielectric/WFM stack across logic, SRAM and the DDR-PHY. Width mainly changes available channel perimeter; thickness also changes electrostatic control and carrier confinement. Gate-stack thickness then determines the space left for low-resistivity fill P-core and LP E-core logic Both the P-core and LP E-core use multiple nanosheet widths. Widths are measured on high-magnification XTEMs while wider-field images demonstrate additional width choices within the LP E-core. Multiple widths are expected even within an LP E-core. Timing-critical paths, buffers and cells with different fanout need different drive strengths. The lower-magnification fields show this width diversity beyond the sites quantified in the table. L2 and L3 SRAM GAA gives SRAM designers another way to balance the pull-up (PU), pass-gate (PG), and pull-down (PD) transistors. FinFET bitcells set device strength through fin count while GAA adds nanosheet width as a sizing knob. In a 6T SRAM cell, a strong pull-down relative to the pass-gate limits read disturbance, while a strong pass-gate relative to the pull-up improves writability. During a write, the pass-gate and write driver pull the node storing “1” below the inverter trip point. During a read, the pull-down holds the node storing “0” low. Bias, threshold voltage, mismatch and assist circuitry set the remaining margin. FinFET high-current cells commonly use a PU:PG:PD fin-count pattern of 1:2:2, a device-sizing ratio rather than a current ratio. Ribbon width lets Intel balance SRAM strengths without adding whole fins. The L2 cell uses its narrowest ribbons for PU and widest for PD, improving writability and read stability respectively. Intel’s disclosed HCC operates without assist; its denser HDC uses negative-bitline write assist. Pulling the selected bitline briefly below ground increases pass-gate overdrive so it can overpower the pull-up at lower supply voltage. That buys density and low voltage writability at the cost of boosting circuitry, switching energy, and additional voltage stress that must be controlled. [31], [32] Four rectangular ribbons give the perimeter = 8 × (width + thickness), before corner rounding. PG/PU is 1.49 and PD/PG is 1.16. The L3 structures closely resemble L2 in layout and cell height. Fewer L3 nanosheet widths are tabulated because fewer high-magnification images were available. DDR PHY The DDR-PHY trades density for controlled analog behavior and reliable off-chip signaling. It contains drivers, receivers, delay circuits, and calibration logic that set drive strength, sampling time, and voltage margin. Repeated four-sheet devices with similar widths fit the use of regular transistor units for matching and programmable drive. Its wider local wiring provides room for current delivery and separation of sensitive signals, while consuming more area than a dense core-logic grid. The layout serves the memory channel’s electrical requirements as well as digital logic density. [33] The SemiAnalysis STEEL teardown lab breaks down advanced datacenter and AI hardware. To learn more about our pipeline or to commission a teardown, contact sales@semianalysis.com. WE’RE HIRING: Architecture, floorplan, packaging, manufacturing, and labs experts. Opportunities from system to transistor and everywhere in between. Check out our Careers page. Intel 3 GPU devices Vector engine logic Intel 3’s XVE logic uses two-fin PMOS and NMOS devices with power rails in M0. Its cell height and M0 pitch give a seven-track geometry, two tracks more than the 18A logic. One-fin groups also appear among the two-fin devices. Intel 3 L2 SRAM The Intel 3 L2 SRAM uses the familiar HCC sizing pattern: one PU fin, two PG fins, and two PD fins. N3E GPU devices Vector engine logic The N3E XVE field contains repeated two-fin devices with seven-track cell geometry. N3E remains a FinFET process, giving Panther Lake a direct FinFET-to-RibbonFET comparison. N3E L2 SRAM The N3E L2 SRAM uses the same PU:PG:PD fin-count pattern of 1:2:2. Panther Lake-U follows Lunar Lake’s floorplan quite closely. Both pair 4 P-cores with 4 LP E-cores and NPU, media and display engines in similar locations. Lunar Lake also uses Xe2, the direct predecessor to Panther Lake’s Xe3 GPU. This makes Lunar Lake the most direct basis for our comparisons. Arrow Lake differs in core count and uses the older Xe-LPG GPU architecture, so we only use it where it offers a more direct component-level comparison. Compute tile Panther Lake compute-tile floorplans remain sparse even months after launch. Intel 18A’s backside metal and dielectric stack must be removed without damaging the underlying structures before a clean transistor-level floorplan can be imaged. Most published die shots hide or heavily process the background, but we are quite proud of the die shot we achieved and are excited to show the work we have done. We measured the areas of the key components on the compute tile and compared them with their Lunar Lake predecessors on TSMC N3B. These help us to capture changes in block area and compare the two chips across process nodes and designs. Our total tile areas exclude the scribe-line area. The compute-plus-GPU subtotal below uses the PTL-U compute tile and GT1 GPU; it excludes the I/O tile and passive base. Individual block areas use the boundaries marked on the floorplans The compute-plus-GPU row is recomputed from the displayed PTL-U and GT1 areas. Component rows use their stated per-region counts and are not an additive partition of the whole tile. The P-core area remains almost unchanged between Lunar Lake and Panther Lake, despite L2 capacity increasing from 2.5 MiB to 3 MiB. Arrow Lake uses the same Lion Cove core as Lunar Lake but also has a 3 MiB L2. Cougar Cove fits 20% more L2 into the same P-core area. The larger private cache keeps more of each core’s working set close to its execution units, reducing access to shared L3 and DRAM. Extra capacity adds storage leakage and lookup energy, so designers balance it against avoided lower-level accesses. The shared P-core L3 cache also shrank by 14.8%. [2] Cougar Cove combines a similar footprint with Intel’s reported power-efficiency improvements. RibbonFET’s tighter channel control reduces leakage, while PowerVia reduces supply droop and allows tighter voltage guardbands. [1] Darkmont’s four-core LP E-core cluster is 5.0% smaller than Skymont’s on Lunar Lake, with most of the reduction in its L2 regions. The 1 MiB region shrank by 8.4% and the 1.5 MiB region by 14.9%. The tag arrays also use one fewer visible row. Tags identify which memory addresses the data array holds, so rearranging them changes the cache’s layout and wiring without requiring less data capacity. [2] The LP E-cores share one L2. This pools capacity and avoids duplicating all the cache machinery, but the four cores contend for its banks and bandwidth. Their separate cluster also keeps light work away from the performance cluster and its L3, allowing that larger domain to sleep. [1], [2] Cache area includes more than the storage cells. Tags identify each line, decoders select rows, sense amplifiers read the small bitline signal, and wires connect to the banks. Splitting an array into smaller sections shortens wordlines and bitlines, improving access speed, but duplicates peripheral circuits. Panther Lake’s smaller cache regions therefore reflect the complete memory implementation, including how much of each region is devoted to storage. [34] Unlike Meteor Lake and Arrow Lake, Panther Lake has no separate SoC tile. The NPU, LP E-cores, memory controllers, PHYs, media and display engines now share the compute tile. This removes an active die and keeps CPU memory traffic on one die. The cost is moving PHY and I/O-related circuitry onto 18A: drivers, receivers and analog circuits must still meet external voltage, loading and signal-integrity requirements, so their area does not shrink like dense digital logic. [1], [2] The biggest shrink comes from the NPU, which occupies 36.9% less area. NPU 5 consolidates the same total INT8 MAC count into half as many neural compute engines. Each of the three NCEs has a larger MAC array to make the complete NCE envelope 22.6% larger than an NPU 4 engine. Consolidation also halves the number of scratchpads and SHAVE DSPs, from 12 to 6. The MAC array handles matrix multiplication and convolution, while SHAVE executes vector and custom operations that fit the array poorly. [1], [2], [35] The paired floorplans identify each NCE envelope and its scratchpad, MAC, and SHAVE regions. Each measured MAC polygon is counted once per NCE in the area accounting below. The scratchpads store weights, activations, and intermediate results near the MAC arrays, allowing repeated use without fetching them again from DRAM. Halving their number delivers the largest measured area saving but leaves less local storage for the same total MAC count. Layers that no longer fit locally require smaller working tiles or more transfers of intermediate data. The benefit depends on keeping the enlarged arrays busy while managing that tighter storage budget. [36] NPU 5 also adds native FP8. Using half the operand width of FP16 reduces storage and transfer demand, helping workloads fit the smaller local memory budget. Lower precision and format-dependent range make scaling and model validation part of deployment. Hardware activation functions further reduce work that would otherwise occupy the programmable DSPs. [1], [2] Microsoft requires an NPU to deliver at least 40 TOPS for Copilot+ PCs. Both Lunar Lake and Panther Lake meet this threshold, but Panther Lake uses significantly less silicon. GPU tiles Panther Lake is Intel’s first product with Xe3, its latest GPU architecture. It offers two different GPU tiles: a smaller GT1 tile with 4 Xe3 cores on Intel 3 and a larger GT2 tile with 12 Xe3 cores on TSMC N3E. Panther Lake allows us to compare the same GPU architecture across both Intel 3 and TSMC N3E. Wildcat Lake adds a third Xe3 implementation on Intel 18A. A future newsletter will detail Xe3 and its implementation differences across all three process nodes. GT2 scales Xe3 to a different physical layout, with render slices arranged vertically instead of GT1’s horizontal arrangement. Slice placement sets the distances to shared cache banks and the D2D interface. Those wires consume area and add delay, so scaling the number of Xe cores also requires a new balance of cache placement, routing and timing. [1] What’s immediately obvious is that the GT2 tile on TSMC N3E has much smaller Xe cores than GT1. These block areas include logic, caches, and routing. An Xe core on the GT1 tile is ~69% larger than one on Lunar Lake, and ~55% larger than one on GT2. Intel 3 therefore uses substantially more area per Xe core. The block-area gap exceeds the measured logic and SRAM density gaps, bringing routing, timing targets, cell mix, and floorplan allocation into the comparison. The measured vector/matrix engine region is almost unchanged between Lunar Lake and Panther Lake’s GT2 tile. Xe3 retains eight 512-bit vector engines and eight 2048-bit XMX engines per core. Its gains also come from feeding those engines more effectively: more resident threads hide stalls, and variable register allocation lets shaders trade registers per thread against the number of threads kept active. [1] The shared L1/SLM capacity increased by 33% from 192 KiB to 256 KiB, while its area increased only 5%, raising effective density by 27%. L1 retains reused cache lines, while software-managed SLM lets a thread group share data locally. Both reduce traffic to more distant memory. Allocating more SLM per group can also limit how many groups reside on a core at once. [1], [37] The GT1 tile carries 4 MiB of L2 against 16 MiB on the GT2 tile. GT1 divides its L2 cache into four 1 MiB banks, while GT2 uses eight 2 MiB banks. Each bank contains 128 macros, but each N3E macro stores 16 KiB, twice the Intel 3 macro’s 8 KiB capacity. The N3E macro is only 54% larger while holding twice as many bits, giving it 30% higher density: ~23.7 Mbit/mm² versus 18.3 Mbit/mm². Including bank-level circuitry, the gap widens to ~16.9 Mbit/mm² on GT2 versus ~10.4 Mbit/mm² on GT1. GT2 gains density with its macros storing more bits per unit area, and those macros occupy more of each cache bank. Larger macros spread decoder and sense-amplifier overhead across more storage, while a more compact bank layout reduces the share spent on control and routing. The compromise is longer wordlines and bitlines that carry more capacitance. [34] I/O tile Panther Lake uses two I/O tile variants, both fabricated on TSMC N6. The smaller one provides 4 PCIe 5.0 and 8 PCIe 4.0 lanes and serves lower-tier systems as well as those without a discrete GPU, while the larger one adds 8 PCIe 5.0 lanes, bringing the total to 20 lanes, for discrete-GPU connectivity. Panther Lake SKUs with the larger 10- or 12-Xe GPUs use the smaller I/O tile. [38] The smaller I/O tile adds a PCIe 4.0 block and a Thunderbolt block to Lunar Lake’s I/O layout, providing four additional PCIe 4.0 lanes and another Thunderbolt 4 port. Its repeated N6 blocks retain nearly identical areas and layouts. Reusing these proven PHYs and controllers avoids porting and requalifying external interfaces on 18A, where faster digital logic offers less benefit to circuits constrained by the off-chip link. [38] SemiAnalysis’s teardown lab (STEEL) dives deep into the world’s advanced datacenter and AI hardware. To learn more about our pipeline or to commission a teardown, contact sales@semianalysis.com. We’re hiring technical experts from system to transistor and everywhere in between. Check out our Careers page. Panther Lake offers scalability and modularity through its disaggregated packaging that partition compute, GPU, and I/O silicon into separate tiles allowing for a suite of tile configurations. This partitioning makes the package part of Intel’s node economics as it determines how much leading-edge wafer area each product consumes, which functions can remain on other processes, and how much configuration freedom Intel can offer from a shared set of tiles. Furthermore, fabricating the compute and GPU tiles separately confines the new 18A process to the compute tile and allows graphics and I/O to use other, more established, and more cost-effective processes. For Panther Lake, the GPU and I/O tiles are assembled alongside the compute tile on a passive silicon base using Foveros-S. Intel’s current technology brief lists a nominal 36 µm pitch for Foveros-S. Through-silicon vias (TSVs) in the base connect the fine wiring above to the larger package connections below. The functional tiles sit side by side on that passive base in a 2.5D configuration. [39] Our cross-section through the compute and GPU tiles shows the package’s wiring hierarchy. Microbumps connect each active tile to the passive silicon base; its fine redistribution layer (RDL) carries the short, dense tile-to-tile links. TSVs carry connections through the base to the package substrate, which fans them out to the much coarser motherboard solder joints. The base supplies interconnect, while computation remains in the active tiles above it. [39] At the compute-tile edge, the higher-magnification inset shows a local microbump spacing of approximately 25.24 µm and a feature width of 12.33 µm. These local spacings are finer than Intel’s nominal Foveros-S value. The X-ray fields further confirm tighter neighboring bumps, consistent across every die-to-die area found on each tile. Additional X-ray analysis is offered after the paywall. Putting the memory controller beside the CPU removes the D2D transfer that CPU memory requests required in Meteor Lake and Arrow Lake. This avoids the extra transmitter, receiver, and link traversal, saving interface energy and latency. Panther Lake’s separate GPU still crosses a D2D link to reach DRAM, so its larger local caches also help contain package traffic. [1], [40] Smaller dies are less likely to contain a random fatal defect, and screening them before assembly prevents one bad tile from consuming a complete package of good silicon. Reuse also spreads design and qualification work across more products. Against those gains, Intel pays for the passive base, D2D circuits, extra bonding and test steps, and losses during assembly. Cost per working product across the portfolio captures the combined effect of wafer yield, reuse, test, and assembly. [29] Wildcat Lake packaging Intel launched Core Series 3, formerly Wildcat Lake, on 16 April 2026 for value mobile and edge systems. Wildcat Lake keeps 18A but removes the passive base and combines more functions on one die to simplify the package. The two products therefore reveal two distinct ways to commercialize the same leading-edge process. [41] Wildcat Lake’s 18A die combines up to two Cougar Cove P-cores, four Darkmont LP E-cores, two Xe3 cores and a smaller NPU. A separate platform-controller die supplies I/O, connected through UCIe, Intel’s first processor implementation of the standard. Consolidating graphics remove a tile boundary and the passive base, reducing assembly complexity for a modest-bandwidth value product. It also ties CPU and graphics scaling to the same die, giving up Panther Lake’s ability to swap in a much larger GPU. [42], [43] In July 2021, Intel CEO Pat Gelsinger set out an ambitious process roadmap aimed at regaining performance leadership by 2025, later described as five nodes in four years. Five years and one CEO later, Intel’s comeback story is not as unambiguously positive as Pat may have hoped. [44], [45] Intel once set the pace for process technology, bringing high-k metal gate technology and FinFETs into volume production years ahead of the rest of the industry. Its 22 nm FinFET process reached consumers with Ivy Bridge in 2012. [46] Intel’s integrated device manufacturing (IDM) model allowed its architects and process engineers to co-optimize products and processes. Starting with Sandy Bridge, Intel dominated x86, while AMD struggled with Bulldozer. That lead faltered at 14 nm and broke at 10 nm. Intel targeted a massive 2.7× density increase, but the node arrived years late and required several revisions before it could support Intel’s full lineup. This delay forced Intel to stretch 14 nm across six generations, while TSMC moved ahead in process technology and AMD recovered in x86. By 2019, Intel was still shipping 14 nm across most of its product stack, with its 10 nm client ramp focused on Ice Lake mobile processors. Meanwhile, TSMC was shipping N7 and N7+, and AMD’s Zen 2 compute chiplets used N7 to raise core counts and improve efficiency. Intel’s process failures were central to its decline, but unsound business decisions furthered their downward slide. Product delays compounded product mistakes, pushing client, server, and FPGA roadmaps off schedule. Several attempts to enter AI (Nervana and Gaudi) and networking (Tofino) also failed to establish lasting businesses. Intel’s recovery has focused on consumer CPUs and advanced packaging. Tiger Lake, Alder Lake, Lunar Lake and now Panther Lake have restored Intel’s consumer roadmap. On the process side, Intel 4 shipped with Meteor Lake, Intel 3 with Granite Rapids and Sierra Forest, and Intel 18A with Panther Lake. Intel has also made advanced packaging part of its foundry offering. However, Intel is still playing catch-up in servers. Several Xeon generations arrived years late and trailed contemporary AMD and Arm server CPUs in performance, efficiency, and core count. The process roadmap is back, but Intel does not hold the same process-technology leadership position it held prior to 10 nm. The introduction of gate-all-around nanosheets and backside power delivery are two of the biggest changes to transistor integration in a decade. Intel took on both changes at once: 18A paired its first RibbonFET with PowerVia in Panther Lake. Panther Lake is a substantial manufacturing milestone. Our cross-sections show how RibbonFET and PowerVia reshape local contacts and wiring, while the floorplans show where architectural consolidation and process choices save area. A sustained competitive lead depends on product performance, cost, yield, and the next implementation. The SemiAnalysis STEEL teardown lab breaks down advanced datacenter and AI hardware. To learn more about our pipeline or to commission a teardown, contact sales@semianalysis.com. WE’RE HIRING: Architecture, floorplan, packaging, manufacturing, and labs experts. Opportunities from system to transistor and everywhere in between. Check out our Careers page.. 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The Big Holes in Wearable Heart Rate Variability And Readiness Scores
On September 9th, Apple announced it was revamping its Apple Watch Health Sensing System, rolling out a Readiness score (0 to 10), and increasing the frequency of heart rate variability (HRV) outputs 24-fold. This can be viewed as upping its competition with various other consumer wearable sensors. These “readiness scores” as a composite of multiple metrics, with heart rate variability (HRV) being front and center for most. The majority of Americans are now using wearable sensors, which equates to well over 100 million adults. HRV and Readiness scores are increasingly being marketed as a measurement of autonomic nervous system health, a digital marker for future disease, a clock for biological age, and a holistic metric to promote healthspan and even longevity. (Apple also introduced a new longevity tab and “Health Age”.) None of this has been proven. In this edition of Ground Truths I am going to review what we know about heart rate variability and readiness scores. Heart Rate Variability HRV is the variation in normal heart cycle timing. The variability of the heart rate, the barely perceptible millisecond changes in time between consecutive heart beats (see R-R intervals in the Figure below, left panel), is due to interplay between the sympathetic and parasympathetic (vagal nerve) inputs. Distinct from heart rate, individuals with the same heart rate can have very different HRVs. It is a rough reflection of the autonomic nervous system (ANS) activity, inadequate to say whether a person’s ANS function is abnormal. For more than three decades, heart rate variability (HRV) has been measured and several studies have found an association of low HRV and clinical outcomes, particularly a link with higher all-cause and cardiovascular mortality. There have also been less well established links of low HRV to risk of early cognitive impairment, dementia, mental illness, Type 2 diabetes and substance abuse. An important reminder is that HRV is a surrogate marker without any established cause-and-effect relationship. If you increase your HRV, that doesn’t mean it will improve health outcomes. In fact, there is no hard evidence for that. All that work linking to health outcomes was done with electrocardiogram (ECG) derived HRV. Now, in the era of consumer wearables, this is getting assessed differently, by optical pulse (yes, the lights you see) plethysmography (PPG) or what is called pulse rate variability (PRV). They are not the same, as shown below (right panel) and only concordant when the delay between the ECG and pulse is kept constant, which basically means at rest. I should mention there’s also what I will call MPV, a mattress mechanical movement sensor, a derived heart rate variability, that companies like Eight Sleep use, even further away from directly measuring HRV. HRV has not one uniform measurement but many different types of quantification, such as RMSSD, the magnitude of difference between successive R-R intervals of normal sinus beats (N-N) or SDNN, the standard deviation of NN intervals, both in milliseconds. SDNN is one of the so-called frequency domain HRVs (others are LF, HF, LF/HF). Different wearable sensors use different metics; Apple has relied on SDNN and nearly all of the others use RMSSD, which is generally considered the more accurate metric. There’s also the different length of time measured, such as for a matter of minutes, all day, or an overnight’s sleep. Short measurements are especially problematic since they don’t capture enough of respiratory modulation and other factors that influence HRV. Share Ground Truths How well does HRV correlate with PRV? There are very limited studies, especially independently done. One that is commonly cited was conducted by Air Force researchers in only 13 healthy adults assessing Oura ring 3 and 4, Whoop 4.0, and Garmin Fenix 6 and showed a correlation coefficient of 0.88 to 0.97 and a mean absolute percentage error from 6 to 10%. The correlation is not a perfect 1.0, but there’s at least a fairly high level of correlation. HRV is supposed to increase during the night due to takeover of the parasympathetic nervous system, and higher during deep sleep. A recent example of my 1 week, all day “HRV,” and one during sleep is shown below. As you can see, the N of 1 data are inconsistent for the same days from different sensors (Oura, AppleWatch, Fitbit Air, and Eight Sleep) by patterns, absolute numbers, and comparison with prior days and weeks. The largest study in over 8 million Fitbit users (the old version, not Google Fitbit Air, introduced in May 2026) gives you a sense of the effect of age, sex, and the 2 different main HRV (here PRV) metrics, with RMSSD on the left and SDRR (=SDNN) on the right below. That study, from data collected in 2018, is a major outlier, since all the more recent ones are tiny with respect to sample size. Many of the companies have not had independent evaluation of their HRV, such as Eight Sleep, but have published a low standard error on their website. There are some other published studies on the correlation between HRV and PRV, but they are all small and only in healthy adults. A scoping review emphasized the lack of study in underrepresented individuals, including the aged, people of color (which affects the PPG signal), and individuals who are underweight or obese. Add the typical adult age 60 plus with one or more chronic diseases. For example, one study in over 900 adults found poor correlation of HRV and PRV, non-uniformly underestimated across many chronic diseases (cardiovascular, endocrine, neurological, respiratory, and others), concluding PRV is “an invalid surrogate for HRV.” A recent systematic review of 43 studies comparing HRV and PRV found reasonable pooled absolute standardized error (HRV as gold standard) but only 10 of the studies provided quantitative synthesis in ideal conditions. Their main conclusion was similarly cautious: “PPG-derived HRV [PRV] should not be regarded as universally interchangeable with ECG-derived HRV across all devices, populations, and recording contexts.” Factors Affecting HRV and PRV That gets me to the long list of factors that affect HRV (and PRV) besides the device, the type of measurement (RMSSD, SDNN or others), the person’s signal, the sensor site, the duration of data capture, if weighting by sleep stage is used, how artifact is processed and corrected. And this list is not complete!: Oura puts out data from their community of users (who input data) on what affects their overnight HRV. The factors currently provided are: no alcohol (increase 8%), melatonin (increase 2%, float tank (increase 2%), wine (decrease 4%), and party (decrease 14%) in overnight HRV. Must be some big parties! Subscribe What is a PRV measurement good for? It has been falsely characterized as an index of “autonomic balance” and a specific indicator of stress. A 2018 review of the studies available for HRV and its relationship to stress, not using any of the current wearables, found that stress can lower HRV. But so can many other factors. The non-specificity of the signal, indexed to the table above, is striking. Evidence from a UK Biobank study of over 46,000 participants with actual HRV looked at genetically predicted HRV, a genetic risk score, that failed to show the expected HRV-mortality link, indicating that _HRV is likely not causa_l, but rather a reflection of person’s physiologic state. A review of consumer wearable HRV data from 5 longitudinal studies showed that nighttime PRV was not associated with perceived stress, and surprisingly higher HRV, in the largest cohort (N=717 participants), was correlated with higher stress. An Oura ring cohort of 525 first-year college students found a link between overnight PRV and perceived stress, but that was also seen with resting heart rate, sleep, and respiratory rate. Several very small studies have examined the relationship of HRV and athletic injuries or guiding training with mixed, and predominantly negative results. HRV biofeedback training with paced breathing had no significant effect on reducing stress or raising HRV, as demonstrated with sham controlled trials. When HRV for multiple days showed a decline in conjunction with body temperature, the Oura ring published data for prediction of Covid. The WHOOP company sponsored an observational study, published in 2026, of 30,000 users for 72 weeks, without a control group, that reported reduced alcohol intake (5.8 % points) by self-report. That doesn’t tell us much, and particularly about the merits of HRV for behavioral change. If you use the same device and conditions as longitudinal trends for multiple (at least 2-3) weeks that may be the one way to get something useful from the measurements. Data for overnight sleep with minimal motion and using RMSSD is the best proxy for real HRV. The reason to look at trends rather than any given night is that it more likely represents something, even though you won’t know with certainty what the “it” is. Keep in mind there are no data, no peer-reviewed evidence, to show that HRV fluctuation in-person has any correlation with health outcomes. Share Readiness Scores These are proprietary scores that integrate different metrics for each of the wearables: no algorithms have been disclosed. They are unvalidated against health outcomes. In a review of 14 composite health scores of readiness and recovery, HRV contributed 86% to the scores, followed by reading heart rate (79%), physical activity and sleep duration (both at 71%). That review noted the substantial variability in measurement protools and lack of standardization. Sleep staging is notoriously inconsistent and inaccurate by these sensors, which adds further to the HRV uncertainties for what the scores, which use sleep stage data, mean. Only resting heart rate has been shown consistently across devices to be extremely accurate. I’ve made a Table to summarize what we know about which metrics are included, the scores, any peer-reviewed studies that compared the readiness score with health outcomes, and the corresponding (if any, NA-not available) citation. You will note that some companies do not use the term “readiness," such as WHOOP for recovery, and Garmin, which has 2 different scores, one of which is Body Battery. Eight Sleep uses the term “Fitness Score.” They all include HRV; Apple includes a new metric they call “Recovery HRV” which among other components uses 7-days of sleep, but it is unclear what this means or how it is differentiated from other scores (there are clearly no data for outcomes). We have no knowledge of how the different components are weighted or whether any of these scores are better than resting heart rate, HRV alone, physical activity, or any other single metric. Since none of these are standardized, they are not interchangeable, so if you get a 90 for Oura that has no relationship to a 90 on a Google Fitbit Air. Notably, the company can update its algorithm for readiness score at any point without notification to device users. Without any useful evidence of actionability for these scores or established relationship with health outcomes, it is hard to make a case for their value. At the Apple recent announcement they showed their Readiness score (0-10) on the watch (Figure below) but there are no published data on this score, not even on their website. It’s available only on their new Watch Series 12 or Ultra 4 [of course, ;-)]. That exemplifies the problems with these scores, lack of data and evidence for being meaningful to promote health. Perhaps the best study (which isn’t saying much) is the WHOOP Recovery for golfer performance, because it did correlate with an objective outcome, even though there was no control group and the authors were all from the company. Among the 389 pro golfers, an absolute 10-per cent point increase in Recovery score was associated with about 0.5 fewer strokes per round. But that’s hardly a health outcome! WHOOP is also conducting a study in over 2,700 runners to see if their recovery score will be linked to less injuries and improved performance, but that is not yet published and has no control group or randomization. Putting This in Context For two decades I’ve been enthusiastic about the potential for digital health and particularly wearable biosensors. Over the years, we’ve seen some great progress for their ability to promote physical activity and accurately detect atrial fibrillation (the first FDA cleared deep learning AI for consumers). That work was the subject of rigorous research. But there are holes in the data and evidence for other metrics. One notable one is the “VO2 max” story that I wrote about earlier this year. At that time many subscribers asked me to cover heart rate variability, which I finally got to here. When I dived into the research and publication for HRV and readiness scores, I expected to find at least some that were of high quality and demonstrated their utility by linkage to health outcomes. To my surprise, I found none. The wearable sensor measurements for HRV (PRV) are, for the most part, accurate, but that validation work has only been done in small studies of healthy adults and does not take into account the long list of factors, from the device, software side, and the user side, that affect HRV measurements. Moreover, this metric chiefly relies on optical sensing and, as we have learned for heart rate PPG sensing, may be less accurate in people of color. Keep in mind that all of the health outcome association evidence comes from ECG-derived HRV; none are from wearable sensor data. I will repeat the key point: there's no peer-reviewed evidence to show that in-person HRV fluctuation—or efforts to raise your HRV— has any correlation with health outcomes. For those of you who look at your HRV on awakening, or even 2+ week trends of it being low, I hope this context helps to relieve any anxiety. Yes, low HRV (not PRV) has been shown to increase risk of some diseases as summarized above. But efforts to raise your HRV—a surrogate metric— has not been established for improving any health outcomes. HRV does not have any evidence of causality (the genetic evidence actually goes against this possibility). In this summary, I have not included data for other wearable sensors such as Polar, Samsung, Withings, Suunto, Amazfit, Coros, Ultrahuman, or additional mattress sensors. These are beyond my first-hand experience, and as far as I know from my in-depth review none have any peer-reviewed published data that differ from the 6 sensors I’ve reviewed here. From the points I’ve gone over above, we’re not ready for readiness scores. Besides being proprietary, they are predominantly based on metrics that have their own issues. It’s compounding the problem, like building a house without a solid foundation that has never undergone a rigorous inspection, and then selling it. Like I mentioned for PRV, you can look at trends over weeks rather than any single day, to get a handle, but even that may not be helpful. There’s simply no evidence that these scores meaningfully relate to health outcomes. I’d emphasize they might, but that requires doing prospective or randomized studies to prove it. None exist. There’s great promise for HRV/PRV utility_. For example**,**_ Prof Maiken Nedergaard, who discovered the brain glymphatics that are essential in eliminating metabolic waste products from the brain during sleep, has posited that HRV could be a non-invasive marker for neuromodulator oscillations, brain-body regulatory circuits, and brain clearance. That would be extremely useful, but like everything else on HRV and readiness scores it requires solid research and validation. The lay media isn’t helping much to get the story straight. Earlier this year The Economist published a piece entitled “The most useful indicator of your overall health” which ordained HRV as an “accumulated stress score.” That’s akin to the false assertion about VO2max: “V02 max is the singular most powerful marker for longevity.” As I’ve summarized here, that is not established. The fact is that so many things can lower HRV, including physical exercise (especially an intense workout), reduced sleep quality, stress, the list above, no less the device, signal, and software. Whatever fluctuations observed have not been correlated with any health outcome. Sadly, “datamaxxers” are widely using HRV and readiness scores that have never been validated to mean anything. We already know that for some people using the sensors for sleep metrics, it can induce “orthosomnia,” an obsession to get high sleep quality, with associated high levels of anxiety. In an experiment done by a company to promote sleep quality for its employees, “For those employees who did use the trackers, many reported feeling perfectly rested until their tracker told them they had had a terrible night. Others were told that they had slept like a baby when they had actually been lying awake worrying about the quality of their sleep. “ The same problem can result from preoccupation with HRV or readiness scores, with anxiety that would lead to further reduction in both. It you are using a wearable like >100 million American adults, it’s OK to look at these data, but contextualized with the major caveats reviewed here. If you are one to require evidence that HRV or readiness scores are linked to health outcomes, you may not even want to look. The companies make it hard to turn them off! Let me end with the companies that make and sell wearables. Apple’s doubling down on HRV (24-fold more reporting and heart rate very 5 seconds) and introduction of a Readiness score tells us that consumers have bought into these metrics and they are joining the club. However, all of this is occurring with a backdrop of tens millions of users, claims about the data that are not backed up by adequate evidence, marketing way out in front of whatever limited data exists, and not being transparent about their readiness score algorithms. The companies can well afford to do the research that is needed to connect these metrics with health outcomes show, once and for all, that increasing HRV or using readiness scores promotes our health. If they believed and invested in the products they are selling, we’d not be in this position of not knowing. That’s essentially where we are with HRV and readiness scores. Perhaps someday this will change and we’ll have good reason to embrace them. NB: I wrote this post. No AI. I have no conflicts of interest with any of its content. Loading... Ground Truths has 215,000 subscribers from every US state and 214 countries. There are over 300,000 followers of Ground Truths so more than 90,000 folks who can easily convert to be free subscribers. Your subscription to these free essays and podcasts makes my work in putting them together worthwhile. If you’re not a subscriber, please join! If you found this interesting PLEASE share it! Share Ground Truths The proceeds from all voluntary paid subscriptions go to support our summer internship program. It enabled us to accept and support a record number of 62 summer interns that joined us in 2026! These are high school, college and medical students selected from thousands of applicants. We couldn’t do this expanded program without the funds coming in through Ground Truths. Thank you!
Science Vs on the 49ers Substation: Anatomy of a Hatchet Job
In August, Pablo Torre Finds Out and Science Vs released an episode about my theory that electromagnetic fields from the electrical substation beside the 49ers facility may be contributing to the team’s run of soft-tissue injuries. As the originator of the theory, I was also a subject of the episode. I sat was interviewed by Wendy Zukerman and Rose Rimler of Sciene Vs. I sent them research, connected them with scientists, and spent hours digging through the City of Santa Clara’s and Silicon Valley Power’s records to help clarify critical details. Both Wendy and Rose came off as affable and professional, showing curiosity during the interviews, with Wendy going out of her way to question the “conspiracy theory” framing itself. Then they titled the episode We Solve the 49ers Viral Conspiracy Theory. I was familiar enough with their catalog that I never expected them to agree with my theory, but I did expect them to give it a fair hearing and to deliver their findings honestly. On both counts they came up short. They were not directly dishonest in anything they said, but rather in what they left out, in how what remained was cut, and in the picture painted by those two things in combination. They asked me to recorded the interview on my phone for better audio quality, and I held on to my copy for reference later. That turned out to be a fortuitous decision. Here is the raw audio of my first interview, unedited*. Only my side was recorded, so their questions aren’t on it, but you can generally infer them from the answers, and every claim I make below about what I said can be checked against my statements in this clip. (Note: Wendy had connection trouble at the beginning of the interview and was cutting in and out, which accounts for the false starts.) 0:00 -1:19:13 Audio playback is not supported on your browser. Please upgrade. Science Vs is a fun show. It is pitched at roughly a high-school understanding of science, for an audience that is skeptical, Snopes-oriented, and worried about misinformation. Take a claim circulating online, interview a supporter of the claim, interview consensus scientists, and then tell people which side of the line it lands on. I have listened to their episodes on raw milk, seed oils, 5G and other contested issues in the wellness space. I have problems with all of them, but each at least made an honest attempt to represent the actual range of scientific opinion by talking to credentialed scientists with differing perspectives. Dissenting researchers were heard from, answered, and often given a chance to respond. This episode did not do that. This article is not a relitigation of the science. I have written extensively about that already. This post is for the record. It is simply an accounting of what was wrong with their episode. Contents Is there a power plant next to the 49ers practice facility? — the clearest single example of getting something objectively wrong For the record — a high-level overview of all of the problems with their investigation Draw your own conclusions — why they had to make this episode at all What they left out about childhood leukemia — the exposure threshold, and playing games with statistics to minimize sick children What they left out about the mechanism — the body of literature they refused to cover, and evidence for the mechanism used against it The scientists Science Vs interviewed and did not air — four credential scientists who support myhe theory, recorded and cut, or not even called How they misrepresented me and my case — an answer severed from its question, and three telling edits How you would actually study the injuries — it doesn’t actually matter which team is the most injured, overall The theory: magnetic fields, oxidative stress, and collagen Since the episode never states my theory, here it is below. Those who are familiar with my work can skip this section. Electrical equipment produces magnetic fields, and those fields induce faint electrical currents in anything that passes through them, including people. My argument goes further than induced current. Mitochondria — the structures that generate a cell’s energy — run on continuous flows of electrons and protons, and those flows carry faint electromagnetic fields of their own. Maxwell’s principle of superposition shows that when two fields share the same space, they add together. An external field does not need to be strong to alter an internal field, it only needs to be present. The electron transport chain inside the mitochondria leaks a small fraction of its electrons by design, and those become reactive oxygen species — free radicals, which healthy cells use as signals. External magnetic fields cause the rate of leakage to change, increasing free radicals. When free radicals accumulate faster than the cell’s antioxidant systems can clear them, the result is oxidative stress. Oxidative stress is a recognized driver of chronic illness, including cardiovascular disease, neurodegeneration, diabetes and cancer, and it is in every medical school curriculum. One of its ordinary effects in connective tissue is that it switches on matrix metalloproteinases — MMPs, the enzymes that break collagen apart — while suppressing new collagen synthesis. Tendons are made of collagen. An athlete loading his soft tissue heavily six days a week is already creating oxidative stress in the tendons, so the addition of magnetic field exposure compounds the damage and inhibits repair, making him more susceptible to injury when enormous force lands on a tendon in a fraction of a second. That is the theory. We know that EMF causes oxidative stress, and we know that oxidative stress degrades collagen. The only thing missing is a study showing that direct connection. I have never claimed certainty that the substation is contributing to the elevated injury rate. I do believe it is likely, and I believe it warrants caution, and that a revenue machine like a major NFL team can easily afford to remove the exposure out of precaution. Is there a power plant next to the 49ers practice facility? Here is the clearest single instance of the problem with this episode. It requires no knowledge of electromagnetic fields at all. This story first came to me through Jon Feliciano, a former 49er, in an interview on Willard & Dibs on 95.7 The Game. Asked about why the 49ers are always injured, he said players used to joke that it was the power plant behind the practice fields. Wendy Zukerman corrects him on air. “It’s important to say that it’s not a power plant near the 49ers site.” Torre then asks her to explain the difference between a substation and a power plant. Her answer: a power plant generates electricity and transmits it to a substation, which converts the voltage into something your house can use and sends it on to your home or your business. There are two problems with that. The first is that there is a power plant on that site. The Gianera Generating Station is a natural-gas-fired peaker plant owned by Silicon Valley Power, and it has been there since 1986. I have published aerial photographs of the location from 1987 in which the gas plant is the only thing standing, before the practice facility was even there. I even mentioned the gas plant in my first interview. (Feliciano has since gone on record about this issue, and it is clear he had the substation in mind rather than the gas plant.) The second is that her definition describes a distribution substation, and the facility beside the 49ers is not that. It is the Northern Receiving Station, which takes in bulk power from outside the city’s grid and delivers it to distribution substations. Silicon Valley Power’s own map distinguishes receiving stations from substations, and Rose Rimler even reads the label out loud in the episode when she walks through that map on air. A few minutes before the map segment, Zukerman tells Torre: “like I said, we fact check everything.” Well, maybe not everything. I made a mistake On the morning of July 6th, at 10:20, I sent Rose and Wendy two studies. During the interview I had been asked which human studies show oxidative stress from electromagnetic fields, and I had not been able to name one on the spot. Rose emailed asking for the studies, I quickly searched for a couple, and I wrote that I thought these were the most relevant from that search. Unfortunately, I was busy and did not read either one closely at first. I picked them because they were topically relevant — one on substation workers, one on power plant workers. Neither were great studies, and their problems go past the ones raised in the episode. That was careless on my part. There is context that did not make the episode, though. Before that email I had been on a Zoom call with Rose talking about EMF and oxidative stress, and I pointed her to Dr. Henry Lai at the University of Washington, who has spent years aggregating the literature on this question. His tallies show that roughly 90% of studies since the late 1990s find oxidative effects from electromagnetic field exposure — hundreds of studies, systematically counted. Rose told me she was already aware of his work. So when she asked for studies, I understood her to have the aggregate view already and that she would report anything within that context. Not reading those two carefully was still a mistake, but the larger mistake was assuming the episode would be based on a thorough review of the actual body of literature, rather than on whatever I happened to send that morning. The second email At 1:49 that same afternoon — three hours and twenty-nine minutes after the first — I sent them a second email that I had been preparing for a while. It was a structured document in six numbered sections, written in response to a request they had made two weeks earlier, laying out my entire argument with citations attached to every link in the chain. The episode aired on August 13th, five weeks later, and not a single item from the second email is in it. Here is how it opens: The full email is included at the bottom of this post in Appendix B. Nearly 1,500 words in total. It contains two named mechanisms with the physics behind them. Occupational studies in humans. The literature on oxidative stress and collagen. A section addressing the strongest counter-evidence against my own theory, which I raised myself. And a closing section stating plainly what the theory cannot yet show. My entire argument, in writing, with detailed citations for every claim, provided to them five weeks before broadcast, and none of it made it into the episode. That is the single largest omission, but it is not an isolated one. The whole episode is riddled with similar problems, and the conclusion they came to is not merely a difference of opinion about the scientific evidence. Through omission and through strategic editing, Science Vs misinformed its audience — about what the evidence shows, about what I argued, and about who they spoke to. That is a notable outcome for a show whose stated purpose is correcting misinformation. For the record I am not going to tell you that Science Vs set out to discredit me, or that they had come to their conclusion before they reported the story, or that they used misleading editing to make me look like a man retreating from his own theory. I cannot know what was in anyone’s head, and I am not going to pretend otherwise, either. What I can tell you is what is on the record. They asked me for evidence and aired the weakest thing I sent. They interviewed three scientists who supported my theory and aired none of them. They discussed childhood leukemia without ever saying the exposure level at which it appears. And they took an answer I gave weeks before Ken Karipidis, the one EMF scientist who was put on air, was interviewed, and placed it directly after his critique, where it comes off as a major concession. A friend of mine who has worked as a journalist for thirty years read that last one and called it sleazy. I agree with her. Those are just the four issues that are impossible to defend as pure editorial decision, but they are not the only issues. The most glaring issues stem from what they left out: The exposure level at which the childhood leukemia association actually appears — three to four milligauss, a number the episode never states despite it being much lower than what I measured. The mechanism itself: The episode gets as far as “oxidative stress could weaken collagen,” which leaves it sounding like speculation, rather than a known pathway. The second email, and all the studies in it. Dr. Paul Héroux at McGill, whose work my proposed mechanism rests on, whose contact details I supplied, and who was never called. Dr. Beatrice Golomb at UC San Diego, who runs a research group on oxidative stress and mitochondrial function and has specific expdertice in collagen, interviewed and not aired. Dr. David Carpenter at Albany, the most prominent academic voice on the harm from magnetic field exposure, interviewed and not aired. Dr. Joel Moskowitz at Berkeley, interviewed and not even credited. The specific, testable condition I put in writing that would make me abandon the theory. My own unprompted statement of the theory’s evidentiary gap. My caveats about my own measurements. My ranking of EMF as one factor among several rather than the only one. The new equipment installed at those facilities between 2010 and 2014, and the sharp rise in system load from 2013 onward. But that is not all. What they kept, they selectively edited to serve a narrative that was not served by the raw transcripts of the interviews. A description of thousands of commercial routers in a workplace, reduced to the Wi-Fi in your house. My own acknowledgment, multiple times, that "I'm not a scientist" clipped in an episode that spends considerable energy pointing out that I am not a scientist. And a qualification I volunteered about my own measurements, cut from my answer and delivered later by their EMF expert as a correction. Together their edit produce a portrait of a wellness guy with Wi-Fi phobia and two bad studies, backing away from his theory the moment a “real” scientist looked at it. A practice facility where nothing changed because no new substation was built. Injuries written off as random because the 49ers were not quite the single most injured team in the league over the period in question. That portrait is false even though almost no individual statement made in the episode is. Draw your own conclusions At the top of the episode, Pablo Torre says his show had been flooded with requests to investigate the substation — that it was the thing they were asked to look into over and over again. Neither show went hunting for this story. It arrived from their own audience, in volume, and it could not be waved off. A thread I posted on X reached twenty-two million people. A guy with a gaussmeter and a brand-new Substack obligated a Pultizer prize winning program to spend an hour on a question about player health, that is considered fringe enough that most media operations won’t touch it. Pablo Torre Finds Out could not ignore it. So Science Vs came in and ran a “debunking” operation instead of an investigation. Everything below is what had to be left on the cutting room floor to deliver the “debunking”. They could not ignore it. So they tried debunked it instead. The demand was strong enough to force an episode, and since the episodes release the 49ers have sustained more injuries, including season ending ones, and interest has only grown. Demand from fans and playets is strong enough to force a better investigation from someone else. An omission is not a lie until you find out what was omitted. What follows is the detailed record so you can see the full picture. Draw your own conclusions. I have drawn mine. I am going to keep publishing. A note about Pablo Torre Finds Out After the episode aired I posted publicly, calling out Pablo Torre Finds Out for concerns I had about the integrity of their investigation, and about an interview directly with Pablo Torre which had been offered but never happened. I have since spoken with a producer at PTFO. The offer had rested on a misunderstanding about where things stood between us, and it fell away as the Science Vs part of the production widened past the science. He apologized for the miscommunication and I accepted. The producer also confirmed to me that they did essentially hand off the entire investigation to Science Vs for narrative purposes — so Pablo would be genuinely curious or potentially surprised by their findings — while still taking responsibility for what went out under their name. I appreciated the candor and the accountability, and I am comfortable with where we left things. So this post is not about PTFO. My disagreement is with Science Vs. What they left out about childhood leukemia Childhood leukemia appears at three milligauss. They gave no number at all. 1. They built an EMF ruler, then discussed childhood cancer without it. The sequence on air went like this: First I measured almost 9 mG, then I measured up to 50 milligauss. Torre reacts with concern — “that sounds high.” Cut to Karipidis: the public limit is 2,000 milligauss. Torre reacts again — “What happens at 2,000?” Karipidis explains that nothing happens at 2,000, that safety factors are built in. Then: at more than 50,000 milligauss you get flickers of light in the retina, and higher still, nerve stimulation. The listener now has a ruler (their ruler) to measure these numbers with. Fifty is nothing by their ruler. Then the episode turns to childhood leukemia and states, accurately, that there is a real association — but tellingly, they never give the exposure level at which that association appears. Childhood leukemia appears at three milligauss. They conveniently left that out. The pooled analyses that produced the World Health Organization’s carcinogen classification found roughly a doubling of childhood leukemia risk above three to four milligauss. That is the number that belongs in that segment, and it is more than ten times below the reading that had just been dismissed as trivial. I gave them that number myself, on tape, in the interview. Describing my own threshold, I said my comfort level for long-term chronic exposure is three to four milligauss, but preferably one. 2. Six children in thirteen million. The episode reports that these fields might explain one to four percent of childhood leukemias, then reframes it as a German estimate of perhaps six cases among thirteen million children. Torre, to his credit, is uncomfortable. What never gets explained is why that number is small. Almost no children lives above three milligauss in Europe. Fewer than two children in a hundred, in the Italian data. So even if the risk to those children doubles, the number of additional cases across an entire country stays small — not because the hazard is small, but because hardly anyone is exposed to it. Count the whole population and the few who are exposed disappear. And the reason hardly anyone is exposed is that siting rules keep housing away from transmission lines. In Europe, at least. The Dutch government has a standing precautionary policy against building new homes in any zone where the annual average magnetic field exceeds 4 milligauss — the same number the episode never mentioned. Denmark and Norway treat 4 milligauss as the level that triggers a look at mitigation. That is five hundred times below the ICNIRP figure quoted on air. The United States has no federal equivalent. That is evidence of infrastructure siting policy working. It is not evidence that there is no hazard. It is evidence that we already act as though there is one. If you listen to the raw audio you will hear that my proposed solution is EMF exposure is to build better infrastructure. What they left out about the mechanism 3. They accused me of cherry-picking, and then cherry-picked themselves. On air, Zukerman tells Torre that people who worry about electromagnetic fields dismiss the studies showing null results and collect the ones showing harm, and that this is why you have to be careful not to cherry-pick. They had two papers I had rattled off in a hurry, and a second email containing a carefully chosen set. They ran the two weakest, graded them on air, and presented the result as the state of the evidence for not only my theory, but the whole question of oxidative stress from magnetic fields. That is cherry-picking from my emails. The bigger picture is what they did with the literature as a whole. Zukerman acknowledges it exists, dismisses it, and disposes of it in a single stroke. You can go online right now, she tells Torre, and find scores of studies showing these fields increase oxidative stress. The issue, she says, is that they are not studies in people. Many of them are in people. The occupational studies in my second email are in people. That email had been in her inbox for five weeks. She waved off the literature on a factual claim that the documents in her possession contradict. (I have written separately about the evidentiary standard at work here). The effect was that they essentially baited me: ask the subject to supply the evidence, take the weakest thing he sends, and let that stand as a proxy for the whole argument. Wendy has been doing this show for ten years and clearly knows how to extract what she needs for her desired narrative. 4. They presented the collagen-improvement research as a gotcha, but I had already addressed it. The episode treats the existence of studies showing that EMF can improve collagen as a surprise that undercuts me, but I had pre-emptively addressed that five weeks earlier in the email they ignored. Those studies use measured, high-intensity pulsed dosing. The mechanism by which they work is oxidative signalling. The cell reads a controlled rise in reactive oxygen species as a warning, upregulates its antioxidant defenses, mounts a repair response, and the therapy stops before the system is overwhelmed. The key point is that it induces an oxidative response, which means those studies are actually evidence for my proposed mechanism, not against it. A field that produces a therapeutic effect cannot be biologically inert (which is the implication when they say “Nothing happens at 2,000 milligauss). Chronic ambient exposure is the same pathway with no off switch, and it is most consequential during the evening and while sleeping, when the body is in repair mode and the exposure does not stop. Section 5 of my email is titled What about the study showing improved collagen synthesis. I raised the counter-evidence myself, explained why I did not think it refuted the theory, and wrote that I was disappointed the question had not come up in the interview. That is worth holding against the cherry-picking charge in the item above: the studies they presented as inconvenient for me were studies I had gone out of my way to put in front of them. 5. Section 1 of my email stated a critical argument that was never put to the expert directly responsible for it. My email says the exposure limits exist to prevent acute effects and do not address chronic exposure at all, and that my dispute is with the entire framework. Zukerman gestures at this once. After Karipidis gives the 2,000 milligauss figure, she tells Torre that I would object because those levels do not capture “more subtle effects.” That is not my argument, and “subtle” is doing a lot of work here. My argument is that the limits are built to prevent acute effects — nerves firing, muscles twitching, etc — and were not designed to address chronic exposure at all. In fact, ICNIRP’s own documents state as much themselves. Mine is a structural objection to what the standard measures, reduced as a concern about subtlety, it becomes a matter of degree, rather than a categorical difference. They interviewed Ken Karipidis, vice chair of ICNIRP — the body that writes those limits. He was asked what the limit is, but he was never asked how it applies to chronic exposure. The scientists Science Vs interviewed and did not air 6. They interviewed four officials of the standards body. The episode credits roughly a dozen researchers. Four of them are associated with ICNIRP. Ken Karipidis is the vice chair. Rodney Croft chaired ICNIRP from 2020 to 2024 and led the development of its current guidelines. Dan Baaken is ICNIRP’s scientific secretary. Frank de Vocht sits on the Main Commission. One of them speaks in the episode. Their institution’s position is more than adequately represented — the 2,000 milligauss figure, the safety factors, the assurance that nothing happens below the line. 7. The four who were left out. Dr. Beatrice Golomb is Professor of Medicine at UC San Diego — a physics undergraduate degree, a PhD in biology, an MD. She directs a research group whose stated focus is the relationship between oxidative stress, mitochondrial function and health. That is the mechanism the episode spent its first half dismissing. Her published work includes the fluoroquinolone case series behind the FDA’s black box warning on an antibiotic class that ruptures tendons, where the accepted mechanism is oxidative stress and mitochondrial toxicity — the back half of my chain, already on a drug label. She is in the credits. She is not in the episode. She has told me she finds my theory biologically plausible, and that she has a recording of her interview. Dr. David Carpenter directed the Institute for Health and the Environment at the University at Albany for decades and is the most prominent academic voice arguing these fields cause harm. Childhood leukemia is the reason these fields carry a WHO classification at all, and Carpenter is the person you call if you want that case made by someone who has spent a career on it. He is in the credits. He is not in the episode. He has told me that when he was interviewed they could not have been less interested in what he had to say. Dr. Joel Moskowitz directs the Center for Family and Community Health at UC Berkeley’s School of Public Health. He told me directly that they interviewed him and that he thought it went well. He does not appear in the episode, and unlike Golomb and Carpenter, he does not even appear in the credits. Dr. Paul Héroux at McGill is the researcher whose work provides the foundation for the oxidative stress mechanism my theory rests on. I gave Rose his email address and phone number. He was never interviewed. They never even called him. 8. “He’s not a scientist.” The episode leans hard on the fact that I am not a credentialed scientist. Zukerman says it. Torre repeats it. “At all.” Having built a segment on that, they then left out the physicist-biologist-physician, the professor of public health, the director of a university environmental health institute, and the McGill researcher whose work the primary mechanism comes from. They spent the episode telling their audience I am not a scientist, and then kept four actual scientists who support the theory off because their argument does not survive otherwise. How they misrepresented me and my case 9. They played my words as a response to an interview I had never heard. Near the end of the hour, Zukerman says she went to me and told me the evidence was lacking. Then she plays me saying I am not wedded to it being an EMF, that I have staked my reputation on it needing more study, and that I am not certain of anything. That segment was placed immediately after Karipidis had finished taking the cherry-picked papers apart. It plays as a man folding under expert scrutiny. Commenters have used it against me since, but it is incorrect. Here is the sequence as it happened. I was interviewed. Karipidis was interviewed weeks later. I was never told what he said, or even who he was. I was never asked to respond to it. I did not know his name until the episode aired. That is not a simple editing decision. That is a quote from one interview, moved to follow a critique from a different interview it was not a response to, so that it would land as a concession. A friend of mine who has spent thirty years as a journalist read that sequence and called it sleazy. She is right. The full passage is reproduced in Appendix A, and it is worth reading. What airs is the preamble. Four paragraphs later I say “to directly answer your question” — and that answer, about what would change my mind if the team relocated, is not in the episode. Neither is the sentence two paragraphs on, where I say the EMF might turn out to be ten percent of the problem. I will say the underlying point again, though, because I meant it and I still do. I am not wedded to my theory that magnetic fields from the substation are contributing to the 49ers injuries. I could be wrong. What I am wedded to is the process of scientific inquiry, and the fact that we should be cautious around these exposures and we need more independently funded studies. 10. Three telling edits. They cut “I’m not a scientist” mid-sentence. What I said: “...and I am not certain of anything. I’m not a scientist. To me, I find the mechanisms compelling. I will go back to the fact that I got into this not because of the 49ers, but because of clients I was working with who suffer from EDS...” What aired: “...and that I am not certain of anything. I’m not.” The clip ends on the first two words of the sentence in which I say I am not a scientist, in an episode that spends considerable energy establishing that I am not a scientist. The full sequence is in Appendix A. They cut my own description of my work. Asked what I do, I said I run a wellness business, that I am focused on writing software to help people navigate environmental stressors, that environmental health is my focus, and that I also do independent journalism and research. What aired is the wellness business and the environmental health, with the software and the journalism removed from my own answer. The software engineering does come up later — narrated by them, as a hacker who grew up to write firmware — but my current work, in my own words, arrives as “wellness guy.” Thousands of commercial routers became home Wi-Fi. What I described: working at a wireless networking company surrounded by thousands of Wi-Fi routers, and a stress-induced health collapse afterward that working in that environment contributed to. What aired: Wi-Fi, the kind you have at home — reinforced by a clip of Christian McCaffrey talking about turning his router off at night. Three cuts, and every one of them makes me seem less credible. That is not a coincidence. 11. I gave them my own caveats and the test that would disprove me. In the first email I wrote that a well-designed chronic, ambient-level exposure study in tendon showing no collagen degradation, run over many months, would undercut my confidence in the theory. That is a specific, testable condition, stated in advance and in writing. There was a second interview, weeks later, which was not used in the episode, but in that I asked again for the falsification criterion to be included. What the episode presents instead is a man saying “we need more study,” which reads as a hedge, an open-ended request for the benefit of the doubt. It is the opposite of a hedge. Section 6 of my second email says, unprompted, that as far as I am aware there is not a single study showing EMF-driven oxidative stress degrading collagen in a human in vivo or in human tendon in a lab. I wrote that because it is true and because it is the first thing anyone should check. Under their standard it becomes the hinge of the entire first half, framed as something they had to surface without my cooperation. I had handed it to them five weeks earlier. And in the interview I said that my 25 to 50 milligauss readings were taken at knee level, and that these fields attenuate quickly, so by the time it reaches your head it is not that high anymore. That did not air either. The qualification arrives later, from Karipidis, as a correction. How you would actually study the injuries 12. They measured the wrong thing. The episode spends its final act on whether the 49ers are the most injured team in the NFL, finds no clean ranking, and lands on “injuries are random”. That is the wrong test. You would define the exposure — measured field levels at the facility — and the outcome narrowly: soft-tissue injuries, not a single MSK injury count that a broken finger and a ruptured Achilles both land in. Then you would compare the 49ers to themselves before and after the exposure changed, and compare that change against every other team over the same window. That controls for league-wide shifts in rules, turf and training load. It is a difference-in-differences design, and it is standard. I sent them that argument on July 28th, in writing, along with the fact that in eleven of the past twelve seasons the 49ers had finished top ten in Adjusted Games Lost. And by the episode’s own reporting, the 49ers are second in games lost to injury over the past decade, with FTN’s Aaron Schatz confirming that once you adjust for starters they come out second worst in the league — after having been one of the healthiest teams for years before that. A finding like that is where an investigation starts, not where it stops. 13. I did a lot of substation research for the episode that was never aired. I had reported that the substation next to the facility was expanded in 2014. That was wrong, and Rose Rimler and I sorted it out together. They gave me credit on air, which I appreciated, but framed it as a concession on my part to something they had found. In fact I had been investigating it myself, was uncertain before they asked, but was waiting for clarification from Silicon Valley Power. The uncertainty centered around a substation named “Esparanca” that was proposed right behind the facilities as part of the stadium construction, but now appears to never have been built. I spent days in Silicon Valley Power’s records, and did eventually reach Silicon Valley Power for confirmation and indentified the mistake myself. I also gave them highly detailed documents on what we do know about those facilities: new equipment installed between 2010 and 2014, and load growth across the system with an inflection around 2013–2014, with the Northern Receiving Station carrying the highest capacity in the system and sitting closest to the data center corridor. None of that is in the episode. I have a separate piece about it coming out soon. *I cut 2 seconds from the raw audio to remove personal information that had no connection to anything in the episode. Appendix A: the passage the clip was taken from This is the sequence from my first interview, in full. The episode uses one fragment of it. It’s tricky because my understanding is that there’s something like a 15-year half-life on collagen remodeling issues. They’re going to get a new crop of players. What I really need, though, is for the injuries to be broken down so we can see the soft tissue injuries. Right now, they’re categorized as MSK injuries, but let’s say we can actually identify them more specifically. Is that right? He was able to do that? Oh, cool. I wasn’t able to find that information. Interesting — I didn’t know that data existed. I tried so hard to get it, and I didn’t know it was available. Maybe you could connect me with that person. That would be amazing. I’m not wedded to it being an EMF, honestly. I’m not. I would say that, to a certain extent, I’ve staked my reputation on the fact that it needs more study. It’s important to look into it, and I am not certain of anything. I’m not a scientist. To me, I find the mechanisms compelling. I will go back to the fact that I got into this not because of the 49ers, but because of clients I was working with who suffer from EDS, Ehlers-Danlos Syndrome, a tendon hypermobility issue. This condition is documented to be partially caused by oxidative stress. I’ve worked with them to mitigate their EMF exposure and have seen people improve. I think it’s a bigger story. In a way, the 49ers represent an occupational cluster with specific exposure risks. If someone would conduct a study on this, I believe we could learn a lot. Perhaps we would discover that it’s like, okay, maybe it’s 10% of the problem. I don’t know the exact number, but I think either way, conducting the study would provide valuable insights. To directly answer your question, it’s challenging for me because it’s part of a bigger story. If the 49ers move and stop having injuries, I might conclude that it was related to the substation. However, if they move and still experience injuries, I would want to analyze the nature of those injuries. Are they primarily soft tissue injuries? I don’t think it’s necessarily a case closed, but the story might lose traction at that point regardless. Three things are worth noting. The aired fragment stops immediately before the sentence in which I say I am not a scientist — the cut described in item 10. It also stops four paragraphs before the words “to directly answer your question.” What the episode plays is the throat-clearing. The actual answer, about what would change my mind, never airs. And two paragraphs in, I say the EMF might turn out to be ten percent of the problem. That is the ranking the episode says I never gave. Appendix B: the full email, July 6th, 1:39 PM Hi Rose, You asked me to send you some studies a couple of weeks ago. I apologize for the delay. I have been incredibly busy. I also wanted to give you a chance to dig in yourself, and get your own perspective before I influenced you too much with mine. That said, I do want to make sure that the actual argument is abundantly clear, so here it is! One note before I begin, there are really two separate questions here: Does the substation cause the soft-tissue injuries? That was my specific claim, and what the podcast is about. Is the theory biologically sound? Can 50/60 Hz fields at these levels do anything biological below the safety limits? Question two is why people have been calling me a conspiracy theorist. The regulatory and advisory bodies (ICNIRP, etc) maintain that anything below their exposure limits is biologically inert, and that position is broadly accepted within the mainstream, but the actual science paints a different picture. To defend my theory I’ve had to defend a much larger claim: that the advisory bodies have the biology wrong. I can’t honestly answer question 1 without first addressing that. Here’s is a simplified outline of my theory, with links to studies: 1. Advisory body thresholds for biological effects The ELF magnetic-field limits (ICNIRP’s ~2,000 mG public / 10,000 mG occupational) exist to prevent acute effects from exposure. If a magnetic field is strong enough, it makes nerves fire and muscles contract. Muscles twitch. You can see faint flashes of light in your vision. People can even feel tingling or even a shock. That happens due to Faraday’s law, which states that a time-varying magnetic field induces an electric field inside the body via the creation of Eddy currents.The standards assume that those currents do nothing below the twitch threshold. They do not consider chronic effects at all. My argument is that they are biologically active and do have chronic effects. 2. There are multipe ELF-EMF mechanisms for inducing oxidative stress. This is basic biophysics. Below are the two primary mechanisms. Simplest first. Dr. Paul Héroux of McGill has the most intuitive explanation, which rests on Maxwell’s principle of superposition: because Maxwell’s equations are linear, two sets of electromagnetic waves sharing the same space simply add together. In the interview I pictured a pebble dropped into a pond, sending out clean ripples. Then a boat motors past at distance, sending larger waves, and where they meet the ripples, the two add together and the original pattern gets distorted. In our cells, the mitochondria run on continuous currents of electrons and protons that carry their own faint electromagnetic fields. An external field from a substation, by the principle of superposition, adds to those internal currents and shifts the pattern. The electron transport chain in the mitochondria leaks a fraction of its electrons by design as reactive oxygen species (ROS), which act as signalling molecules in a healthy cell. Distorting that field increases that electron leakage, creating oxidative stress. A tiny electromagnetic interference results in a large downstream effect. https://www.sciencedirect.com/science/article/pii/S2405844025006474 The more complex pathway is Dimitris Panagopoulos’s Ion Forced-Oscillation / Voltage-Gated Ion Channel (IFO-VGIC) mechanism. Weak, polarized, low-frequency fields force the ions (calcium, potassium, sodium) next to an ion channel’s voltage sensor to oscillate; because that force scales with the inverse cube of the distance involved, fields far below the stimulation threshold can still force the channel open, disrupting the cell’s ion balance and driving ROS overproduction (Nitric oxide and superoxide interact and produce peroxynitrite, a highly unstable cytotoxin that breaks down into free radicals). https://www.researchgate.net/publication/366088934 https://www.spandidos-publications.com/ijo/59/5/92 https://www.mdpi.com/1422-0067/22/18/10041 https://www.frontiersin.org/journals/public-health/articles/10.3389/fpubh.2025.1585441/full https://pmc.ncbi.nlm.nih.gov/articles/PMC3772193/ 3. Evidence of oxidative stress, in vivo, in humans from ELF-EMF There are many studies, and the strongest are occupational, which applies to the 49ers situation. 115 power-plant workers vs. 145 office controls. Serum malondialdehyde (MDA, the standard lipid-peroxidation marker), superoxide dismutase, and catalase were all significantly higher in the exposed group, and the markers rose with increasing field exposure. https://journals.sagepub.com/doi/abs/10.3233/WOR-203244 A follow-up where they reversed the oxidative stress in power plant workers. A double-blind randomized controlled trial: 91 power-plant workers given vitamin E, vitamin C, both, or placebo for 90 days. The antioxidant groups showed reduced lipid peroxidation and raised antioxidant capacity versus controls. https://pubmed.ncbi.nlm.nih.gov/32191586/ A spot-welder study: 46 welders occupationally exposed at 50 Hz, showed significantly altered red-blood-cell antioxidant enzyme activity and concluded ELF-MF “might act as an oxidative stressor… even at the recommended levels of exposure.” https://pubmed.ncbi.nlm.nih.gov/18504600/ A substation-specific study found oxidative stress and DNA damage https://pubmed.ncbi.nlm.nih.gov/24460415/ 4. Oxidative stress degrades collagen This half isn’t controversial at all. Oxidative stress activates the matrix metalloproteinases (MMPs) that break collagen down and suppresses its synthesis. Here are three example studies: Siwik et al. 2001: Oxidative stress raises MMPs and lowers collagen synthesis in cardiac fibroblasts. https://pubmed.ncbi.nlm.nih.gov/11121376/ Fisher et al. 2009: Collagen fragmentation drives oxidative stress and elevates MMP-1 in aged human skin. https://pmc.ncbi.nlm.nih.gov/articles/PMC2631323/ Varani et al. 2006: Decreased collagen production in oxidatively aged skin. https://pubmed.ncbi.nlm.nih.gov/16723701/ 5. What about the study showing improved collagen synthesis I’m glad you asked this question, and I’m bummed we didn’t get to it in the interview because it is a great question, and very important to understand. Superficially it may appear to be a refutation of my theory, but I would argue that it actually supports the underlying argument. That study used a short, high-intensity pulsed dose: therapeutic-PEMF, the same type of field used clinically to stimulate bone and tissue healing. The reason this works is because it triggers the very same biological pathways that can lead to oxidative stress. The exposure still stimulates ROS production, but done at a controlled dosage, for a limited duration it has a different effect. The cell reads the ROS as a warning signal and it upregulates its antioxidant defenses, and mounts a repair/proliferation response. The therapy is then stopped before the cell gets overwhelmed. That is essentially a hormetic response: a small dose of a stressor producing a beneficial adaptation. Two things follow: At the very least, this means the field is biologically active, which by itself undercuts the regulatory claim that these fields are inert below their thresholds. There is a wealth of literature on PEMF (pulsed EMF) bone regeneration and calcium channel signalling (which is the second mechanims in section one). Here is one. https://www.nature.com/articles/srep13856 At best, it leads us straight to my actual concern, which is that under chronic, chaotic and unregulated exposure, the cell’s antioxidant capacity gets overwhelmed, resulting in oxidative stress. There are plentiful examples of things that are beneficial at controlled doses, but harmful at uncontrolled doses. Excecise is one obvious, uncontroversial example. Botox is perhaps a more interesting example. 6. What about a study that shows EMF causing collagen degradation in humans? As far as I am aware there is not a single study showing EMF-driven oxidative stress degrading collagen in a human, in vivo, or in human tendon in a lab. There are studies involving isolated fibroblasts though, which secrete collagen. The most relevant one showed that human fetal scleral fibroblasts exposed to 50 Hz ELF-EMF showed a significant decrease in collagen synthesis and that MMP-2 expression was upregulated, which is the exact mechanism I described in section 2. https://pmc.ncbi.nlm.nih.gov/articles/PMC3626379/ That’s it! Thanks again for the interview. Best, Peter Anthony Cowan Environmental Health · Wellness Tech · Researcher & Journalist Publisher & Editor, Living Energy Bio: petercowan.comSocial: X · Instagram · TikTokApp: sunlightis.lifePhone: [redacted]
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The Cost of Cutting American Science: How Federal Cuts Diminish Public Health Capacity
Among the federal government’s many responsibilities is the work it does to protect public health. Federal agencies monitor our food supply to ensure safety, conduct research to better understand emerging health threats, provide funding for public health programs in communities and work to detect and respond to disease outbreaks. Americans rely on these efforts every day—in a 2024 online survey, 74% of respondents said that “if the federal government issued safety guidance about food you eat regularly,” they would follow it. Changes to Federal Public Health Capacity The Trump administration’s efforts to reshape the federal government have resulted in significant impacts on our nation’s public health capacity over the past 20 months, affecting the response to health concerns such as measles, Ebola and cyclosporiasis. Agencies with core public health, food safety and disease prevention responsibilities experienced large workforce decreases during the first year of the administration. At the Centers for Disease Control and Prevention, for instance, the workforce in February 2026 was 26.7% smaller than in September 2024 before the start of the Trump administration. The Food and Drug Administration saw a similarly steep decline of 21.6%. Agencies such as the National Institutes of Health, Substance Abuse and Mental Health Services Administration and Food Safety and Inspection Service also experienced large workforce decreases. (function(){function e(){window.addEventListener(`message`,function(e){if(e.data[`datawrapper-height`]!==void 0){var t=document.querySelectorAll(`iframe`);for(var n in e.data[`datawrapper-height`])for(var r=0,i;i=t[r];r++)if(i.contentWindow===e.source){var a=e.data[`datawrapper-height`][n]+`px`;i.style.height=a}}})}e()})(); Changes can also be seen in crucial public health occupations. The number of federal food inspectors, for example, decreased by more than half between September 2024 and February 2026, going from 1,035 to 473. This is the lowest number of food inspectors employed by the federal government since at least 2005. By February 2026, there were also 33.3% fewer federal public health program specialists, whose work includes advising federal funding recipients on public health activities and analyzing the effectiveness of public health programs. Government’s capacity is diminished as employees with specialized knowledge and experience in protecting the public and responding to health risks depart, leaving agencies less prepared to carry out their public health missions. There also have been vacancies in critical high-level leadership positions at public health agencies, most notably at the CDC, which had a permanent Senate-confirmed director for less than a month between January 2025 and early August 2026. Although the CDC has previously been led by acting directors at the start of an administration, the nearly yearlong gap since the departure of the administration’s first permanent director in August 2025 is without precedent. As of August 2026, the FDA is also currently without a Senate-confirmed commissioner following the previous commissioner’s resignation in May 2026. Additionally, public health agencies are experiencing increased politicization of their leadership ranks. In agencies such as the CDC and Food Safety and Inspection Service, the number of individuals in the Senior Executive Service—the most senior career leaders in government—has declined significantly, while at the same time the number of political appointees has reached record levels. (function(){function e(){window.addEventListener(`message`,function(e){if(e.data[`datawrapper-height`]!==void 0){var t=document.querySelectorAll(`iframe`);for(var n in e.data[`datawrapper-height`])for(var r=0,i;i=t[r];r++)if(i.contentWindow===e.source){var a=e.data[`datawrapper-height`][n]+`px`;i.style.height=a}}})}e()})(); (function(){function e(){window.addEventListener(`message`,function(e){if(e.data[`datawrapper-height`]!==void 0){var t=document.querySelectorAll(`iframe`);for(var n in e.data[`datawrapper-height`])for(var r=0,i;i=t[r];r++)if(i.contentWindow===e.source){var a=e.data[`datawrapper-height`][n]+`px`;i.style.height=a}}})}e()})(); At the CDC, for example, the number of career SES decreased 42.9% between December 2024 and February 2026, while the number of non-Senate confirmed political appointees at the agency was six times larger than the agency’s historical average from 2009 and 2024. Knowledgeable career leaders are integral to the ability of public health agencies to carry out their work with scientific integrity and professional judgment, and rapid leadership turnover and increased politicization threaten agencies’ ability to make evidence-based decisions to protect our health. The upheaval and politicization in public health agencies have also negatively affected employee engagement. Strong employee engagement is crucial to the ability of agencies to carry out their mission and successfully provide essential services to the public. In the 2025 Public Service Viewpoint Survey conducted by the Partnership for Public Service, the Department of Health and Human Services—which encompasses major public health agencies such as the CDC and FDA—had an employee engagement and satisfaction score of 20.4 out of 100, one of the lowest among large agencies. Only 2.8% of HHS employees indicated trust in their political leaders and only 8.7% reported confidence that they could report a suspected violation of law or regulation without retaliation. Employees at HHS also reported that the agency’s ability to provide services to the public had suffered. Nearly half of employees at HHS, 47.5%, said their work unit was worse at delivering quality services compared to its performance in 2024. In addition, 57.8% said their work unit was performing worse at fulfilling stakeholder needs. In addition to the work done within federal agencies, the federal government also distributes significant funding for public health and disease prevention work to state and local governments, nonprofits and small businesses—funding which has been significantly disrupted. At the CDC, for example, there was a 71.9% decrease in the amount of project grant funding issued in fiscal year 2025 compared to fiscal year 2024. The FDA also issued far less funding in fiscal year 2025—a 21.3% decrease from its fiscal year 2024 funding. Changes in federal funding include the ending of grants to community organizations that worked on HIV prevention and the cancellation of funding for research into improvements to patient safety and healthcare quality. These changes go beyond federal agencies to impact the broader public health ecosystem, including the state and local health departments responsible for much of the on-the-ground public health work in their communities. About 80% of the CDC’s domestic funding is directed towards state and local partners—meaning that cuts to CDC funding can ultimately result in cuts to state and local public health capacity. Federal agencies also provide expertise and assistance to state and local health agencies as they deal with particular health challenges, but workforce cuts have resulted in fewer federal employees available to help. The Impact of Changes to Public Health Capacity These changes to federal public health capacity are not abstract concerns. Disrupted programs, reduced funding and lost expertise at public health agencies across all levels of government threaten the public’s physical well-being and safety. In some cases, this has already led to harm. The most immediate impacts of federal cuts were seen in interruptions to ongoing public health programs and crisis responses. In one instance, when CDC grants were canceled during the 2025 Texas measles outbreak—the most severe measles outbreak in 25 years—public health officials in Lubbock, Texas were forced to pause parts of their measles response work supported by the frozen funding. Lubbock’s director of public health further said that a lack of available CDC experts to reach out to for advice “definitely” impacted the department’s response to the measles crisis. Cuts to federal funding also forced Dallas County Health and Human Services to cut staff and cancel 50 community vaccination clinics during the outbreak. Public health work outside of major outbreak responses was also disrupted. For example, in April 2025, the Milwaukee Public Health Department was unexpectedly unable to reach experts on lead poisoning due to firings at the CDC when responding to concerns about lead contamination in Milwaukee public schools. Due to federal workforce cuts, several programs at the CDC, including Alzheimer’s and epilepsy programs, have also become trapped in limbo—existing on paper, but without the staff necessary to operate. More recent crises reveal how federal cuts have weakened the public health infrastructure needed to prevent and respond to dangerous new outbreaks. Internationally, cuts at the U.S. Agency for International Development eliminated funding for disease testing and contact tracing abroad, which delayed detection of and responses to the 2026 Ebola outbreak in the Democratic Republic of Congo. While international outbreaks may seem far removed, the unchecked spread of disease in any country can quickly pose a danger to economic well-being, security and health around the world. Within the United States, public health cuts inhibited responses to the summer 2026 outbreak of the food-borne parasite cyclospora. At the federal level, cuts to funding for lab equipment and for CDC staff with expertise in parasitic infections—including 9 out of 11 staff members at the lab responsible for identifying parasitic outbreaks in 2025— contributed to the largest reporting delay in outbreak cases at the CDC in 15 years. Conflicting communications from the FDA about the source of the outbreak, which followed cuts to the agency’s communications department, additionally led to confusion among the public about how to best avoid infection. At the same time, cuts to HHS funding and support for local and state public health slowed some health departments’ responses to the crisis. The exact costs of these delays, constraints and confusion in public health responses are difficult to estimate. However, their message is clear: federal cuts have already made containing threats to public health even more of a challenge. Conclusion Protecting public health—from food safety to disease prevention—is one of the federal government’s most important missions. Dramatic and haphazard cuts to federal agencies and funding have already disrupted the public health system, impacting the response to challenges such as measles, lead poisoning and cyclosporiasis. The U.S. public health system needed improvement before these disruptions. Since 2022, federal leadership and coordination in response to public health outbreaks has been on the Government Accountability Office’s High-Risk List of areas in need of attention to improve government effectiveness and efficiency. Recent cuts only compound these concerns. The chaotic dismantling of government and resulting disruptions to crucial functions like public health and disease prevention highlight the need for meaningful reform and concrete policy proposals to reimagine how government can better serve the public and be more effective, responsive and accountable. To learn more about the impact of federal cuts to public health and science more broadly, visit The Cost of Cutting American Science. Learn more For more information on the Partnership for Public Service’s government reform initiative, visit Government for a New Era. View here In line with The Cost of Cutting American Science, federal workforce data in this brief is as of February 2026
The Cost of Cutting American Science: How Federal Cuts Diminish Public Health Capacity
Among the federal government’s many responsibilities is the work it does to protect public health. Federal agencies monitor our food supply to ensure safety, conduct research to better understand emerging health threats, provide funding for public health programs in communities and work to detect and respond to disease outbreaks. Americans rely on these efforts every day—in a 2024 online survey, 74% of respondents said that “if the federal government issued safety guidance about food you eat regularly,” they would follow it. Changes to Federal Public Health Capacity The Trump administration’s efforts to reshape the federal government have resulted in significant impacts on our nation’s public health capacity over the past 20 months, affecting the response to health concerns such as measles, Ebola and cyclosporiasis. Agencies with core public health, food safety and disease prevention responsibilities experienced large workforce decreases during the first year of the administration. At the Centers for Disease Control and Prevention, for instance, the workforce in February 2026 was 26.7% smaller than in September 2024 before the start of the Trump administration. The Food and Drug Administration saw a similarly steep decline of 21.6%. Agencies such as the National Institutes of Health, Substance Abuse and Mental Health Services Administration and Food Safety and Inspection Service also experienced large workforce decreases. (function(){function e(){window.addEventListener(`message`,function(e){if(e.data[`datawrapper-height`]!==void 0){var t=document.querySelectorAll(`iframe`);for(var n in e.data[`datawrapper-height`])for(var r=0,i;i=t[r];r++)if(i.contentWindow===e.source){var a=e.data[`datawrapper-height`][n]+`px`;i.style.height=a}}})}e()})(); Changes can also be seen in crucial public health occupations. The number of federal food inspectors, for example, decreased by more than half between September 2024 and February 2026, going from 1,035 to 473. This is the lowest number of food inspectors employed by the federal government since at least 2005. By February 2026, there were also 33.3% fewer federal public health program specialists, whose work includes advising federal funding recipients on public health activities and analyzing the effectiveness of public health programs. Government’s capacity is diminished as employees with specialized knowledge and experience in protecting the public and responding to health risks depart, leaving agencies less prepared to carry out their public health missions. There also have been vacancies in critical high-level leadership positions at public health agencies, most notably at the CDC, which had a permanent Senate-confirmed director for less than a month between January 2025 and early August 2026. Although the CDC has previously been led by acting directors at the start of an administration, the nearly yearlong gap since the departure of the administration’s first permanent director in August 2025 is without precedent. As of August 2026, the FDA is also currently without a Senate-confirmed commissioner following the previous commissioner’s resignation in May 2026. Additionally, public health agencies are experiencing increased politicization of their leadership ranks. In agencies such as the CDC and Food Safety and Inspection Service, the number of individuals in the Senior Executive Service—the most senior career leaders in government—has declined significantly, while at the same time the number of political appointees has reached record levels. (function(){function e(){window.addEventListener(`message`,function(e){if(e.data[`datawrapper-height`]!==void 0){var t=document.querySelectorAll(`iframe`);for(var n in e.data[`datawrapper-height`])for(var r=0,i;i=t[r];r++)if(i.contentWindow===e.source){var a=e.data[`datawrapper-height`][n]+`px`;i.style.height=a}}})}e()})(); (function(){function e(){window.addEventListener(`message`,function(e){if(e.data[`datawrapper-height`]!==void 0){var t=document.querySelectorAll(`iframe`);for(var n in e.data[`datawrapper-height`])for(var r=0,i;i=t[r];r++)if(i.contentWindow===e.source){var a=e.data[`datawrapper-height`][n]+`px`;i.style.height=a}}})}e()})(); At the CDC, for example, the number of career SES decreased 42.9% between December 2024 and February 2026, while the number of non-Senate confirmed political appointees at the agency was six times larger than the agency’s historical average from 2009 and 2024. Knowledgeable career leaders are integral to the ability of public health agencies to carry out their work with scientific integrity and professional judgment, and rapid leadership turnover and increased politicization threaten agencies’ ability to make evidence-based decisions to protect our health. The upheaval and politicization in public health agencies have also negatively affected employee engagement. Strong employee engagement is crucial to the ability of agencies to carry out their mission and successfully provide essential services to the public. In the 2025 Public Service Viewpoint Survey conducted by the Partnership for Public Service, the Department of Health and Human Services—which encompasses major public health agencies such as the CDC and FDA—had an employee engagement and satisfaction score of 20.4 out of 100, one of the lowest among large agencies. Only 2.8% of HHS employees indicated trust in their political leaders and only 8.7% reported confidence that they could report a suspected violation of law or regulation without retaliation. Employees at HHS also reported that the agency’s ability to provide services to the public had suffered. Nearly half of employees at HHS, 47.5%, said their work unit was worse at delivering quality services compared to its performance in 2024. In addition, 57.8% said their work unit was performing worse at fulfilling stakeholder needs. In addition to the work done within federal agencies, the federal government also distributes significant funding for public health and disease prevention work to state and local governments, nonprofits and small businesses—funding which has been significantly disrupted. At the CDC, for example, there was a 71.9% decrease in the amount of project grant funding issued in fiscal year 2025 compared to fiscal year 2024. The FDA also issued far less funding in fiscal year 2025—a 21.3% decrease from its fiscal year 2024 funding. Changes in federal funding include the ending of grants to community organizations that worked on HIV prevention and the cancellation of funding for research into improvements to patient safety and healthcare quality. These changes go beyond federal agencies to impact the broader public health ecosystem, including the state and local health departments responsible for much of the on-the-ground public health work in their communities. About 80% of the CDC’s domestic funding is directed towards state and local partners—meaning that cuts to CDC funding can ultimately result in cuts to state and local public health capacity. Federal agencies also provide expertise and assistance to state and local health agencies as they deal with particular health challenges, but workforce cuts have resulted in fewer federal employees available to help. The Impact of Changes to Public Health Capacity These changes to federal public health capacity are not abstract concerns. Disrupted programs, reduced funding and lost expertise at public health agencies across all levels of government threaten the public’s physical well-being and safety. In some cases, this has already led to harm. The most immediate impacts of federal cuts were seen in interruptions to ongoing public health programs and crisis responses. In one instance, when CDC grants were canceled during the 2025 Texas measles outbreak—the most severe measles outbreak in 25 years—public health officials in Lubbock, Texas were forced to pause parts of their measles response work supported by the frozen funding. Lubbock’s director of public health further said that a lack of available CDC experts to reach out to for advice “definitely” impacted the department’s response to the measles crisis. Cuts to federal funding also forced Dallas County Health and Human Services to cut staff and cancel 50 community vaccination clinics during the outbreak. Public health work outside of major outbreak responses was also disrupted. For example, in April 2025, the Milwaukee Public Health Department was unexpectedly unable to reach experts on lead poisoning due to firings at the CDC when responding to concerns about lead contamination in Milwaukee public schools. Due to federal workforce cuts, several programs at the CDC, including Alzheimer’s and epilepsy programs, have also become trapped in limbo—existing on paper, but without the staff necessary to operate. More recent crises reveal how federal cuts have weakened the public health infrastructure needed to prevent and respond to dangerous new outbreaks. Internationally, cuts at the U.S. Agency for International Development eliminated funding for disease testing and contact tracing abroad, which delayed detection of and responses to the 2026 Ebola outbreak in the Democratic Republic of Congo. While international outbreaks may seem far removed, the unchecked spread of disease in any country can quickly pose a danger to economic well-being, security and health around the world. Within the United States, public health cuts inhibited responses to the summer 2026 outbreak of the food-borne parasite cyclospora. At the federal level, cuts to funding for lab equipment and for CDC staff with expertise in parasitic infections—including 9 out of 11 staff members at the lab responsible for identifying parasitic outbreaks in 2025— contributed to the largest reporting delay in outbreak cases at the CDC in 15 years. Conflicting communications from the FDA about the source of the outbreak, which followed cuts to the agency’s communications department, additionally led to confusion among the public about how to best avoid infection. At the same time, cuts to HHS funding and support for local and state public health slowed some health departments’ responses to the crisis. The exact costs of these delays, constraints and confusion in public health responses are difficult to estimate. However, their message is clear: federal cuts have already made containing threats to public health even more of a challenge. Conclusion Protecting public health—from food safety to disease prevention—is one of the federal government’s most important missions. Dramatic and haphazard cuts to federal agencies and funding have already disrupted the public health system, impacting the response to challenges such as measles, lead poisoning and cyclosporiasis. The U.S. public health system needed improvement before these disruptions. Since 2022, federal leadership and coordination in response to public health outbreaks has been on the Government Accountability Office’s High-Risk List of areas in need of attention to improve government effectiveness and efficiency. Recent cuts only compound these concerns. The chaotic dismantling of government and resulting disruptions to crucial functions like public health and disease prevention highlight the need for meaningful reform and concrete policy proposals to reimagine how government can better serve the public and be more effective, responsive and accountable. To learn more about the impact of federal cuts to public health and science more broadly, visit The Cost of Cutting American Science. Learn more For more information on the Partnership for Public Service’s government reform initiative, visit Government for a New Era. View here In line with The Cost of Cutting American Science, federal workforce data in this brief is as of February 2026
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Chartbook 464 The"China squeeze" - the politics of development counterfactuals.
There are three types of China shock discourse. Each has a distinct temporal register. China shock 1.0 was a phrase coined by US academics in the 2010s to retrospectively summarize the impact on particular US labour markets, which they identified through painstaking empirical investigation. China shock 2.0 on everyone’s lips in Europe in the mid 2020s is an alarm raised by trans-Atlantic policy thinkers warning of a coming disaster which they project onto Europe’s ailing car industry. The third type of China shock discourse - commonly known as the “China squeeze” launched most recently by Indian economists Shoumitro Chatterjee and Arvind Subramanian in the pages of Foreign Affairs - mobilizes a different, more speculative temporal register: the counterfactual realm of alternate history. The China squeeze argument asks not what has happened, or what is going to happen, but what might have been. Specifically, what options for economic development might have been open to Global South economies like India or the economies of sub-Saharan Africa, had it not been for China’s spectacular industrialization since the late 1990s and the persistent competitiveness of China’s manufacture in low-skilled segments. Chatterjee and Subramanian’s argument is that whilst China has built a powerful position in electrical machinery and other high-skill manufacturing, which is now delivering China Shock 2.0, it also continues to run a trade surplus in low-skill, labour-intensive manufacturing. This surplus is large and has remained largely unchanged in fifteen years. Indeed, in the 2010s, in trade with low-income countries, China’s surplus rapidly increased. On their reading, this squeezes low-income producers in low-skill sectors in which they “should” be able to compete. Source: “China’s Mercantilist Squeeze on Developing Countries” Shoumitro Chatterjee and Arvind Subramanian. Peterson Institute for International Economics 26-7 May 2026 Chatterjee and Subramanian’s wording is telling: (emphasis mine) The canonical trajectory of economic development in the post-World War II period is for countries to transition from agriculture to manufacturing, first in low-skilled manufacturing and then later on to high-skill manufacturing (Herrendorf, Rogerson, and Valentinyi 2013). At the global level, this implies that high-income countries (HICs) that once specialized in low-skilled activities cede manufacturing export space to poorer countries that come along to occupy that space. In 1965, advanced economies accounted for about 60 percent of global value-added exports in four key low-skilled manufacturing sectors, i.e., apparel, leather, textiles, and footwear. Over time this share declined and began to be occupied first by the East Asian tigers and, beginning in the late 1990s, by China. Today China accounts for about 50 percent of the global market. The question is whether China, with its rising prosperity, is continuing to behave like its richer counterparts and ceding export space to poorer followers or to behave unlike them and continuing to occupy space. In terms of the conceptual maneuvers it performs, of the three China shock discourses, the “China squeeze” argument is by far the most ambitious. After all, it bases its critique of China on a counterfactual imagining of the world. Like any counterfactual argument, to construct this alternative reality it must rely on a heuristic model. To make their argument Chatterjee and Subramanian mobilize two key claims. The first reference point is the actual history of rich-country industrialization, what they refer to as the “canonical path”. The idea is that countries transition from agriculture to light industry and low-skilled manufacturing and from there up the value chain. To make this useful as a standard of comparison and a means to construct a normative standard, they adjust sectoral export shares for two factors: 1. the underlying level of economic development of the exporting country, as measured by national income and 2. the degree to which the sector in question is internationalized. The idea being that for a high income country to have a high export share in low-skill sectors is anomalous and even more so if that particular product is highly internationalized and thus suitable for being “conceded” to lower-income competitors. Where should this process end? Here Chatterjee and Subramanian introduce their second benchmark. Their normative idea of a global development path is one in which, in due course, low-skill manufacturing exports are distributed in proportion to a country’s share in the global labour force. They imagine, in other words, a world of proportional, polycentric global development without much national specialization in low-skill manufacturing. A useful benchmark is that, in labor-intensive manufacturing sectors, a country’s share of world exports should be broadly commensurate with its share of the world’s low-skilled labor endowment. … In the Heckscher-Ohlin model, this would be true if value added per worker and export propensities, i.e., fraction of output that is exported, are the same across countries. It is this pleasant liberal vista of orderly global development, progressing towards a general distribution of low-skilled manufacturing against which they judge reality and conclude that the low-income countries are suffering a “China squeeze”. China is not exiting low-skill sectors fast enough Allowing for its gdp level and the degree of globalization, China’s share of low-skill manufacturing exports is far higher than it “should” be. Relative to population, its low-skill share of exports is far too high. That in turn yields the conclusion that huge numbers of jobs - the authors suggest tens of millions - are being hoarded by China. For the four sectors captured in figure 4, this excess in value-added exports is $110 billion in 2022. For all low-skilled sectors overall captured in appendix figure D.1, excess value-added exports amount to $365 billion. The crowding out of LMIC exports by China is therefore substantial. Both these claims have in common that they are strong structuralisms. The first is that development paths ought to resemble each other. The second is that broadly speaking as far as low-skilled manufacturing is concerned, all countries are alike. If the world currently diverges from the distribution of trade implied by these assumptions, if China is not following the advanced economy path and has huge exports, this must be the result of “policy”, which the authors then put in question as illegitimate or unfair. Thus the naturalistic construction of a canonical path leading to a “level” distribution of low-skilled manufacturing reveals itself to be a polemical tool. From the point of view of China shock polemics, this discourse is no doubt welcome. But as an account of economic history, it must surely be regarded as nothing short of bamboozling. Development paths do not follow a regular, natural sequence. As David Fishman put it aptly, “development is not a queue”. They are always and everywhere, through and through political. Development is not so much a process, as a project. Each such project is more or less well adjusted to its context. As Gerschenkron taught uneven and combined development implies differentiation rather than simple imitation on a single parth. It may be true that Europe and the US exited relatively early from low-skill work. But clearly technology has changed. As C&S themselves point out, China no longer enjoys a low wage environment. Do they really believe that such huge differences can be accounted for either by industrial policy, which as they admit does not operate powerfully in low-skill sectors, or by exchange rate manipulation? What is overwhelmingly dominant in explaining the persistence of “low-skill” manufacturing in China are surely the network effects of complex supply chains. Indeed the label of “low-skill” may miss the point. The degree of globalization which Chatterjee and Subramanian decide to conjure away in their model of the development path - to allow for the fact that Europe and American textiles exporters did not enjoy just-in-time logistics in the 1950s - obscures the point that the networks through which Chinese factories supply the world are themselves key parts of the low-skill industrialization project. China isn’t knocking out 1970s style “cheap”. It has redefined the entire product cycle. C&S’s casual reference to “T-shirts” is telling. In today’s “fast fashion”, there is weight on both terms. Fashion and fast. China’s success in delivering on both at unprecedentedly high speed and at unprecedentedly low cost, isn’t a low-skill operation at all. If we see development trajectories not as the serial repetition of the same, but as distinctive, crafted projects that cumulate in complex agglomerations of skill, technology and labor, then this explains why the assumption that low-skilled manufacturing should follow the distribution of population flies in the face of all experience. As countless cases attest, low-wage, low-income developed economies are not by themselves the makings of a competitive production base. As Leon Liao puts it quite fairly: “International trade has never been allocated according to population. A country’s population gives it no natural claim to an equivalent share of global exports." And the remarkable fact is that Subramanian alone and with co-authors has long been making this point, not to pillory China, as is the case of the tendentious _Foreign Affair_s and Peterson pieces, but to highlight the great counterpart to China’s industrial success, namely India’s relative failure. The much-quoted Foreign Affairs piece showed low-skill export shares only for China, not for India. If you put both countries in the picture as Chaterjee and Subramanian have done on other occasions, the picture looks like this. China is far above the line, but India, almost as large in terms of population, is no less anomalous, just in the opposite direction. As far as global populations are concerned, and the imagining of tens of millions of “squeezed” jobs, it is this Sino-Indian pair that account for a huge share of the action. What this graph reveals is not China’s cheating, but India’s “greatest development failure”, at least this is the argument made Arvind Subramanian, this time in co-authorship with Devesh Kapur, in their major book, A Sixth of Humanity. Independent India’s Development Odyssey which appeared with Oxford University Press earlier this year. In this highly critical work on India’s development, China is repeatedly evoked, not to criticize but as a benchmark against which to illuminate what India’s political economy has not delivered i.e. large-scale formal employment for hundreds of millions of citizens. Kapur and Subramanian leave no doubt, if you want to understand why China, not India was the main driver of manufacturing globalization from the 1980s, don’t look to slots opening up in the division of labour thanks to the liberal mindedness of advanced economies, look to the contrasting political economy of the Maoist PRC and India’s post-independence political economy. As Kapur and Subramian note: The great divergence between China and India did not begin in 1978 with the Deng reforms—it was well underway by then. In one of the great ironies of modern history, the conditions created by Maoism turned out to be a great launching pad for industrial globalization. As the comparison of India and China in 1980 makes clear, to imagine manufacturing would be equally distributed when populations are so differently endowed in terms of educational and nutritional is fanciful. Here is the data from Kapur and Subramanian, data which I explored back at the very beginning of Chartbook. As Kapur and Subramanian insist, the striking fact is that even as India’s growth accelerated from the 1980s, structural change has not. Formal employment in India lags woefully behind. Why? As Kapur and Subramanian note, the path-dependent impact of India’s poor early start was devastating. The list of factors they mention is long and weighty: We argue for a new five-fold explanation applicable at different stages of Indian history: in the initial stages, the legacy of two key pre-1980s policies, the neglect of agriculture and the strangling of the domestic private sector, were critical. The failure of broad-based agricultural growth militated against rural industrialization, which would have been devoted to satisfying local needs that would have necessarily been labour intensive. Then, when the boom came after 1980, the thicket of regulation and broader labour protections that were legislated prematurely in a nascent democracy, underpinned by a deep ideological aversion to private capital in general and big capital specifically, became a barrier to attaining the size that would be necessary to compete globally. Similarly, the reforms after 1991, while wide-ranging, did not quite encompass non-tradeable inputs critical to manufacturing, namely, land, logistics infrastructure and power. A combination of low investment (logistics infrastructure), regulation (land) and the continued monopoly supply by state governments (power), combined with residual socialism, kept costs at 75–100 per cent above efficient supply. These factors were compounded on the supply side by the government, which dominated the formal labour market and established exorbitantly high wages at the lower end of the skill spectrum. This made their employment in the labour-intensive sector by the private sector less attractive. Finally, when the services sector and its exports boomed, wages soared even further via a Dutch Disease effect: one successful tradeable sector killed and cannibalized another less-skilled tradable sector, namely, manufacturing. Thus, scarcity-inducing policies of the planning era, precocious democracy and a Gandhian aversion to size; inefficient, monopolistic supply of critical non-tradable inputs; the behemoth of government; and super-successful skill-intensive services successively undermined India’s unskilled labour employment opportunities. The employment failure seems to have been over-determined. … Less quantifiable but no less important are some of the sociological factors that have undermined manufacturing and factory jobs. Take the impact of the success of the IT sector—located in urban areas with better working conditions, such as air-conditioned offices, good schools for children and attractive entertainment options. It became a more attractive place for engineering and management graduates to flock to. … Consider manufacturing and female employment. Indian society makes it difficult for women to work, reflected in India’s unusually low female labour force participation (elaborated in Chapter XIII). Indian society, in particular the routine harassment of women in public spaces, makes it even more difficult for them to travel long distances to take up work.37 Combined with onerous regulations on creating hostels and dormitories for women—which, in turn, prevents multiple shifts of operation—factories need to be located in areas with a large female labour pool. While firms can take apparel plants to female labour or bring them to the plants by building large-scale dormitories, this raises costs. If there was a case for subsidies to encourage labour-intensive manufacturing, housing subsidies to build dormitories for women workers would be a good place to start. All of this meant, that when opportunities did open up, in part thanks to adjustments in China, India was in no position to take advantage. Here is the account of the 2020s from Kapur and Subramanian. It stands in dizzying contrast to the one-sided, “China squeeze” argument delivered in the Peterson and Foreign Affairs pieces: In 2022, for example, India’s share of global exports in clothing (the canonical labour-intensive sector) was 3.1 per cent compared to 32 per cent for China. This is extremely disappointing because China started vacating export space in this sector after the Global Financial Crisis as its wages started rising; it then vacated further space in the aftermath of geopolitical developments that led investors to seek alternative investment locations. Between its peak and today, China lost about 7.5 percentage points of global export share (worth about $43 billion in 2022); over this period, India’s export share remained stagnant at 3 per cent, while that of Vietnam and Bangladesh rose by 3.5 to 4 percentage points. China’s loss did not translate into any gain for India in terms of low-skill exports and employment. Put differently, when the conditions for dynamism and prosperity were established after 1991, and even more tantalizingly when the global export opportunities opened up, it was as if India was a high-wage economy and only skilled labour could benefit from the dynamism. It had converted its physically abundant unskilled workforce into an economically expensive resource, penalizing its use. It is not my mission here to argue for or against Kapur and Subramanian’s interpretation of India’s development trajectory. The point in this context is simply that the “China squeeze” such as it is can only be understood, in relation to the heavy burden of domestic constraints that Kapur and Subramanian so unsparingly enumerate. I am concentrating here on India because it is the great counterpart to China and the unspoken reference point of the “China squeeze” discourse. But the point is more general. Can anyone with a straight face suggest that the main problems afflicting the development of South Africa or Nigeria, the great centers of mass underemployment in sub-saharan Africa, are cheap competition from China driven by Beijing’s industrial policy and an undervalued RMB? Likewise, is the main problem of the American working-class the threat of Chinese competition or the manifest crisis of social reproduction in the United States itself? The point here, as in the discourse around China shock 2.0 in Europe, is to insist that we should not normalize the world and pathologize China, without actually investigating what is going on in America’s industrial wastelands, the German car industry, or India’s lopsided labour market. One-sided pathologization should be understood for what it is, a polemical gesture. Concepts like China shock and China squeeze are, what Reinhart Koselleck, following Carl Schmitt, would have described as “asymmetrische Kampfbegriffe”, or “asymmetrical counter-concepts” or “asymmetrical combat concepts”. If the function of arguments like the “China squeeze” is to alert elites in the rest of the world of the need to rejuvenate and energize their development projects, so be it. But let us see the resulting discourses as the mobilizing interventions that they are. Interestingly, a significant slice of China’s public sphere - the so-called industrial party - have been obsessed for the last twenty years with precisely these questions of counterfactual economic history. Since the mid 2000s, a massive online discourse developed around an alternative history in which Chinese techno-patriots were asked to imagine how they would proceed if they had the possibility of traveling back in time to transport modern technology into the Ming dynasty (1368-1644) thus averting the “great divergence” of the 18th and 19th centuries. It is a fantasy of course, but also a goad. The point was not directed at Westerners. The alternate history is dramatically nationalist, but few n the West had even heard of it until recently. The adherents of the industrial party are not liberal moralists. They don’t project natural ladders of international development and ask why others don’t cede space. They take the Realpolitik of global economic development for granted. Their pointe was directed against fellow Chinese. The rallying cry of the alternative narrative was this: Now that we are beginning to gain steam and push forward on our national development path, now that we are breaking out of the inferior position assigned to us even in the early years following WTO accession, do not lose yourself in humanistic imaginings about better futures. In the spirit of Deng, they called on China to embrace the hard truth of development. Perhaps one might of the Industrial Party as a cultural trend born out of desire for symbolic revenge against those who had inflicted the century of humiliation. In terms of the various temporalities of the “China shock” - retrospective, prospective and counterfactual - one might think of the Industrial Policy discourse as truly speculative, conjuring up the China shock that never was. Or perhaps one might better think of it as imagining a world in which a powerful China was no shock at all, but simply a defining fact of modern history. I love putting out Chartbook. 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The Beauty Of Settled Science
Commenters convinced me I made a subtle mis-step in my framing of Psychology Research Is Mostly Fine. My framing emphasized that social priming studies had failed to replicate, but that many other subfields of psychology hadn’t. This naturally led commenters to point to failed replications in other subfields. Although none of these were as bad as social priming, few or none were entirely problem-free. Instead of emphasizing the difference between social priming and other subfields, I should have emphasized the difference between settled science and novel research. Here are some of my favorite psychology findings: The brain is sculpted by reinforcement learning, and a key driver of this learning is a prediction-error-based algorithm located in the nucleus accumbens and implemented through dopamine. Psychedelic drugs exert their effects through 5-HT2A receptors, pointing to a role for these receptors in some sort of construct like the balance between priors and new evidence. Certain cognitive functions are localized to certain brain areas (for example, impulse control to the frontal lobes; linguistic structure to Broca’s area, linguistic meaning to Wernicke’s area. But injure one of these areas, or render a certain function useless (eg a blind person having no more use for their visual cortex), and these mappings can gradually shift - suggesting that neurons are general-purpose compute whose specialization is a contingent fact about convenience and efficiency rather than a necessity. Most personality traits and general capabilities are about 50% genetic and 50% random, with little role for family environment or childhood history, with a few notable exceptions like partisan preference. Recent research complicates this story, but the further you go from this basic picture, the gnarlier the chains of indirect causation you require. Neurons fire together in “brain waves”, whose exact frequency corresponds with the character of consciousness; These divide neurons into natural subpopulations and linked graphs. The gamma rhythm corresponds surprisingly well to items in conscious awareness. GABA receptors seem to be involved in something like relaxation. By hitting different GABA receptors in different ways, you can modulate the exact type of relaxation you produce. Hitting GABA-A directly is too powerful and can cause dangerous levels of sedation, but allosteric modulation of GABA is an incredibly fruitful strategy that underlies drugs from benzos to barbituates to alcohol. If you know your GABA-A subunits, you can target specific subtypes of relaxation; for example, Ambien hits GABA-A1 and induces sleep. Memory divides somewhat fuzzily into bins of immediate-sensory, short-term, and long-term, with separate retrieval and storage functions, and separate systems for declarative vs. procedural learning. These can be harmed selectively, usually by hippocampal injury, so that some patients can remember their life stories but not form new long-term memories, or learn new skills like bike-riding but not new facts. The exact substrate of memory is unclear but seems to involve new synaptic connections between neurons in at least some way. The ability of modern psychology and psychiatry to treat mental illness is real but limited. SSRIs work for half or slightly fewer than half of patients; antipsychotics work with extreme side effects; benzodiazpines work but produce addiction and tolerance in many (not all) people. Most supplements are stuck in Poor Quality Study Replication Crisis Hell, but melatonin and l-theanine stand out as especially promising. Psychotherapy works with moderate effect size, but (with a few exceptions) seems to be more about the relationship with the provider than the details of the therapy itself. Mental hospitalization can sometimes defuse immediate crises but work less well than mental hospitals would like, with some studies showing overall negative effects. Schizophrenia is mostly genetic, but risk also increases with prenatal infection (especially rubella) and obstetric complications; there is suggestive evidence for roles of social stress and drug use (with psychedelics and marijuana making things worse, and nicotine if anything making things better). Bipolar and schizophrenia are so closely linked on a pathophysiological level that it seems like they might be the same disease; on the clinical level, they do seem to follow two separate courses/prognoses but can sometimes surprise clinicians by eg someone who seemed condemned to permanent schizophrenia unexpectedly recovering. The brain’s native reinforcement learning algorithms cash out in the phenomena of classical and operant conditioning; different reinforcement schedules reinforce at different levels, which can be exploited by bad actors to make especially compelling products (eg slot machines). None of these are immune to doubt. A few are speculative; one or two are genuinely unorthodox. But they’re all a step above one p = 0.049 paper that might not replicate. If they get overturned, they’ll be overturned by the same sort of genuine scientific shift that replaced Ptolemy with Copernicus or Lamarck with Darwin, not some sort of sordid discovery about someone entering random numbers into a spreadsheet. In 2008, Eliezer Yudkowsky wrote about The Beauty Of Settled Science: If you only care about scientific issues that are controversial, you will end up with a head stuffed full of garbage. The media thinks that only the cutting edge of science is worth reporting on. How often do you see headlines like “General Relativity still governing planetary orbits” or “Phlogiston theory remains false”? So, by the time anything is solid science, it is no longer a breaking headline. “Newsworthy” science is often based on the thinnest of evidence and wrong half the time—if it were not on the uttermost fringes of the scientific frontier, it would not be breaking news. Scientific controversies are problems so difficult that even people who’ve spent years mastering the field can still fool themselves. That’s what makes for the heated arguments that attract all the media attention. Worse, if you aren’t in the field and part of the game, controversies aren’t even fun. Don’t be embarrassed to read elementary science textbooks, either. If you want to pretend to be sophisticated, go find a play to sneer at. If you just want to have fun, remember that simplicity is at the core of scientific beauty [...] A steady diet of science news is bad for you: You are what you eat, and if you eat only science reporting on fluid situations, without a solid textbook now and then, your brain will turn to liquid. Psychology isn’t centrally the new paper in Annals Of Recently-Breaking News saying that an n=5 study showing that large portion sizes increase support for terrorism. Psychology is centrally ideas like brain waves, GABA receptors, reinforcement learning, twin studies, and connectionism. People who think differently are worrying too much about BREAKING NEWS!!!, and should stop. The key distinction isn’t “recent research in social psychology” vs. “recent research in cognitive/bio/behavioral psychology”, as my essay last week unfortunately implied. It’s recent research in general vs. the deposit of settled science, battle-tested hypotheses, and carefully-earmarked speculation. And part of the reason social priming in particular was such a disaster was that it defied that heuristic, building itself up over hundreds of studies until it approached or even entered the pantheon of settled science - before collapsing (5-HTTLPR was also sort of like this). This isn’t a claim that settled science is always right - Freud was “settled science” for a long time - just that there’s an intuitive distinction between the level of credence you should have in the existence of power posing vs. the existence of Broca’s Area. (I compounded this error by calling the last post “Psychology Research Is Mostly Fine”, which suggested I was talking about the new research rather than the settled science. I actually meant to distinguish between research-psychology-the-field vs. clinical-psychology-aka-therapy, but this framing unintentionally pushed against the point I wanted to make) Some commenters on the previous article understood this point, but challenged its weight. It’s very cool, they said, to know how many neurons are in which brain lobe, but the main way that Psychology affected their lives was through bad clickbait studies used to buttress dumb policies; some p = 0.049 study says that exposure to microaggressions makes minorities’ brains shrivel into raisins, and now their company has to implement punitive DEI or be sued for hazardous work conditions. I won’t dispute this as an accurate description of how the sausage gets made, but it’s worth examining the trains of thought that connect this observation to a campaign against psychology in general: The dumb woke psychology was wrong and bad, and I don’t have good heuristics for distinguishing dumb woke psychology from other psychology, so I’m going to assume it’s all wrong and bad. The dumb woke psychology was wrong and bad; it seems useful to punish/discredit psychology as a whole to assist my campaign against it, so for propaganda purposes I will try to discredit psychology as a whole. To people in the first camp, my response is: come on, your heuristics aren’t that bad. “Microaggressions makes minorities’ brains shrivel up like raisins” is in the woke category; “the hippocampal theta rhythm seems to be associated with both memory and pathfinding, suggesting an unexpected yet surprisingly compelling relationship between the two” is in the not-woke category, don’t play dumb here. To people in the second camp, my response is: deliberately exaggerated propaganda campaigns are bad and this is a confession, not an excuse. Inability to view science through anything but a political lens was what got us into this problem; doubling down on it is a temporary solution but a recipe for permanent disaster. If you pronounce entire fields of science to be acceptable collateral damage in your campaign against bad political actors, you will alienate not just scientists but patients, clinicians, and general lovers of truth. Instead, you can say the thing you mean - that woke partisans shouldn’t try to occupy and exploit the otherwise-noble science of psychology for their own political gain - and wage the same campaign with a halo rather than a comic-book-villain goatee. From the font of oracular wisdom that is Weird Sun Twitter: [ Vessel Of Spirit@VesselOfSpirit i love you all conditionally but i love the good part of you unconditionally. even if it becomes a very small part 2:11 AM · Jan 22, 2015 1 Reply · 5 Reposts · 29 Likes ](https://x.com/VesselOfSpirit/status/558084551772471298) This is how I feel about psychology1, too, but with a touch more optimism. The good part of psychology is enormous, a hoard of endless treasures. You just have to look past the headlines! 1 To play devil’s advocate - should one always be so magnamious? Astrology? Phrenology? These seem different in that their entire orientation was flawed from the start; they didn’t simply fail to find the correct constellation-personality connections, the whole project of searching for connections between constellations and personality was doomed from the start. More difficult might be asking the same question about education research, which is notoriously bad. I don’t know enough about education research to know if there’s some settled science of correct and enlightening results lurking in the background beyond the day-to-day froth of poorly-conducted and politically-motivated studies. I think if it’s 90% bad, 10% good, it’s correct to call it bad as a compact way of communicating a useful truth; I think psychology is better than that, but admit it’s a tough judgment call.
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