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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!
Florida Department of Health in Clay County expands services for student athletes
The Florida Department of Health in Clay County has expanded its clinical services to include school and sports physicals along with electrocardiogram screenings.
K-Air purification technology heads to India’s railway market to tackle extremely high fine-dust levels
A research team at the Korea Institute of Machinery and Materials (KIMM) – including Principal Researchers Dr. Sang Bok Kim and Dr. Inyong Park and Senior Researcher Dr. Younghun Kim of the Department of Urban Environment Research, Eco-friendly Energy & Environment Research Division – has begun developing a compact electrostatic precipitator-based air purification module for use in Indian trains. The project is a collaborative effort with THN Co., Ltd., a KIMM Family Company (partner firm), as part of KIMM’s flagship air purification brand, Air Five.
MAHA Gone Mild
This week’s summit featured Vice President J.D. Vance, electrolyte powder, and very few mentions of vaccination.
Studying Science in an Anti-Scientific Time
This Chronicle Review Deep Cut was first published in 2025. By Julianne Werlin Thanks for reading The Chronicle Review! Subscribe for free to receive new posts and support my work. Subscribe The last two decades have not been kind to science studies. Already bruised and battered by the “science wars” of the 1990s, by the 2000s sociologists of science — who had long argued that science had to be understood in its human context — were encountering the funhouse-mirror version of their own views in right-wing critiques of climate scientists. It was enough to give some prominent scholars pause. “Was I wrong to participate in the invention of this field known as science studies?” asked Bruno Latour, the most famous sociologist of science in the world, in 2003. “Should we apologize for having been wrong all along? Or should we rather bring the sword of criticism to criticism itself and do a bit of soul-searching here: What were we really after when we were so intent on showing the social construction of scientific facts?” In response, Latour proposed a change of method and attitude. Science studies, now chastened and contrite, would no longer seek to strip facts of their authority, but to enrich and enhance them. What this meant in practice was never fully clear. But his diagnosis of problems resonated, even if his solutions did not. Latour’s exercise in public hand-wringing signaled a shift in mood. By 2016, with the first election of Donald Trump, the idea that skepticism of science was a right-wing position, not a left-wing one, had become a commonplace, discussed eagerly in The New York Times. For liberals, vaccine denial during the Covid era and Trump’s second-term attacks on the funding of scientific research, covered extensively in these pages, added a new urgency to the defense of science on both practical and principled grounds. There was little appetite for a sociology or philosophy of science that emphasized the messiness and missteps of the scientific process rather than its integrity and triumphs. The distinguished historian of science Peter Dear’s new book, The World as We Know It: From Natural Philosophy to Modern Science (Princeton University Press, 2025), which seeks to tell the story of 18th- and 19th-century science for a general public, may seem comfortably remote from these bitter contests. In its 16 short chapters, Dear draws swift, sure sketches of major discoveries from Newton to Einstein, ably guiding the reader through debates on stellar nebulae, animal taxonomy, atomic chemistry, evolution, and other flashpoints in the history of science. But though a work of history, Dear’s book must still negotiate our polarized present. In a blurb on its back cover, the historian of biology Lynn K. Nyhart alludes to the “present moment, when scientific knowledge is being swamped by misinformation and its institutions are under siege.” Dear himself, in his conclusion, refers to the “yard signs” and “bumper stickers” that proclaim “Science Is Real.” One antidote to both anti-science propaganda and to reductive slogans in science’s defense is a robust history and philosophy of science: exactly what Dear’s scholarship has long offered. But his new book illustrates how difficult such work has become. Dear, an emeritus professor of history at Cornell University, is best known as a creative and philosophically minded historian of the Scientific Revolution. His edited volume The Literary Structure of Scientific Argument (1991) analyzed the rhetoric of Galileo’s thought experiments to brilliant effect. Discipline and Experience: The Mathematical Way in the Scientific Revolution (1995) was a major contribution to the analysis of scientific experiments in early modern Europe and beyond, while Revolutionizing the Sciences: European Knowledge in Transition, 1500-1700 (2001), now in its third edition, remains one of the best overviews of the profound epistemological upheavals of 16th- and 17th-century science. But Dear has also ventured into later periods. Nearly two decades ago, in The Intelligibility of Nature: How Science Makes Sense of the World (2006), he turned to the 18th and 19th centuries to sketch a history and theory of scientific knowledge. Aimed at a generalist audience, Dear’s simple prose belied serious philosophical ambitions. Science, Dear argued, has two aspects: “natural philosophy,” the quest to understand the true nature of the universe, and “instrumentality,” the applied skills and technologies that allow us to manipulate the world for human advantage. Both strands are ancient, but the innovation of the phenomenon we call “science” was to yoke them together. As Francis Bacon wrote, “Human knowledge and human power meet in one; for where the cause is not known, the effect cannot be produced,” an insight typically abridged to “knowledge is power.” Or, in Bertrand Russell’s characteristically blunt phrase, science has two functions, “1. to enable us to know things, and 2., to enable us to do things.” So far, so conventional. But Dear took issue with this familiar story in one respect. Bacon’s formula implied that theory and practice could be fused in a single method. In fact, Dear argued, the quest to understand nature and the desire to manipulate it were coupled only loosely. They could come together, but they could also pull apart. Focusing on natural philosophy, the “knowing” half of the scientific circle, he used a series of case studies from cosmology, taxonomy, chemistry, electromagnetism, and quantum theory to show how theories changed over time, in dialogue with practice, but never reducible to it. Take the case of matter, the basic substrate of the physical world. In the 18th and 19th centuries, scientists not only disagreed about what it was, but also about how well it could be known. In 1789, the chemist Antoine Lavoisier dismissed speculation about the atomic composition of chemicals as “discussions entirely of a metaphysical nature,” as he sought to orient chemistry away from philosophical abstraction and toward laboratory results. But in the 19th century, atoms returned with a vengeance in the atomic chemistry of John Dalton, who wanted to explain the underlying structure of nature. It was not just that Dalton and Lavoisier had a different set of experimental results, or even a different theory, Dear showed. What counted as an explanation had changed. In arguing that scientific theories depended on their intelligibility to human beings with complex arrays of beliefs and commitments, Dear was in sympathy with science studies. Key figures such as the sociologist Steven Shapin emphasized the importance of psychological mechanisms like trust in the formation and acceptance of scientific ideas. But in focusing on the scientific pursuit of knowledge, not its politics or economics, Dear resisted the more cynical perspective of some of his colleagues. The Intelligibility of Nature strikes a very different note than Shapin’s collection of a few years later, Never Pure: Historical Studies of Science as If It Was Produced by People With Bodies, Situated in Time, Space, Culture, and Society, and Struggling for Credibility and Authority (2010), to name just one example. Walking a very fine line, Dear depicted science as driven at once by complex social dynamics and by the intellectual power of real discoveries. It was a testament not only to his own acumen but also to the vitality of the field that he was able to do so. Nearly two decades later, The World as We Know It returns to the questions broached in The Intelligibility of Nature. Like Dear’s earlier study, it begins with the Newtonian cosmos and ends with debates between Einstein and Bohr on quantum physics. Beyond its terminal figures, many of the same characters appear in both studies, including the naturalists John Ray and the Comte de Buffon; the chemists Étienne François Geoffroy, Antoine Lavoisier, and John Dalton; as well as Charles Darwin and Michael Faraday, among others. Its subject is nearly identical: As in The Intelligibility of Nature, The World as We Know It considers natural philosophy as opposed to instrumentality, here defined as the “desire to create a picture of what the world is really like — the world as God knows it — rather than simply having instrumental or operational control over it.” The two books also overlap in insights — and sometimes even in language. The reader who has learned in The Intelligibility of Nature that Buffon’s method of classifying animals “reflected his belief in the importance of the senses and empiricism in learning about nature (a doctrine associated with Newton and the philosopher John Locke)” will experience a sense of déjà vu on reading, in The World as We Know It, that the classification “reflects Buffon’s commitment to the epistemological stance of Newton and his philosophical underlaborer John Locke, who stressed the role of the senses in creating natural knowledge.” Later in the passage, we read that, “because of its stress on understanding the ways of life of animals in their environments, Buffon’s approach could almost be labeled (anachronistically) as ‘ecological.’” And again, “an anachronistic way of putting it would be to say that Buffon recommends an ecological mode of understanding.” Likewise, in The Intelligibility of Nature we read of Dalton that he was initially drawn to meteorology, and that: He did a bit of experimental work on these things, especially having to do with the water-holding capacity of gases, but his real interest lay in understanding what, at an underlying natural-philosophical level, was really going on physically.” Whereas, in The World as We Know It: He did experimental work on these things, especially concerning the water-holding capacity of gases — although not at a very refined level quantitatively — but he was continually trying to develop a theoretical conception of what was happening physically. The final full chapter of each book closes on the same resigned note. Intelligibility: These days, most serious work on the natural philosophical underpinnings and implications of quantum mechanics is performed not by physicists but by philosophers of science. Among scientific practitioners themselves, Bohr’s attempt to use instrumentality as sufficient grounds for a respectable science has met with a high degree of success. And again, in The World as We Know It: Bohr’s and Einstein’s concerns are now questions that are mostly discussed by philosophers of science rather than by physicists themselves. The marginalization of these sorts of questions amounts to the demise of natural philosophy, at least in physics, in the 20th century. Quantum mechanics “works,” and that’s good enough for most scientists who encounter it. Examples could be multiplied. When handling the same subject matter, some echoes are inevitable. Scholars should not feel that because they have written “Isaac Newton died in 1727” in one book, in the next they must describe him as perishing, expiring, or meeting his maker. But the repetitions of language and arguments (not to mention six reproduced images) threaded throughout The World as We Know It are more extensive than that. They should have been caught by Princeton University Press or its reviewers, and revised. Because the two books have so much in common, it is easy to see where they diverge. The World as We Know It is a less theoretical work than its predecessor. The sociology of knowledge that organized The Intelligibility of Nature has been reduced in scale and folded into readings and examples. The taut interplay between history and theory, which gave the earlier study so much interest, is there, but it is subtle. In the earlier book, the case studies demonstrated theoretical claims about the character and development of science. In the later work, each narrative of discovery is an end in itself. Insights emerge from the history, but they do not control the organization of the study. With the theory muted, it can be hard to understand the logic uniting Dear’s sprawling history of more than two centuries of scientific knowledge. The 16 brisk chapters cover an enormous amount of material. But the closer the volume edges to comprehensiveness, the more obvious the missing elements become. A chapter on “Institutions and Pedagogy,” describing the birth of the research university, illustrates the problem. Inserted roughly halfway through the book, the unnumbered chapter is designed as an “entr’acte,” in acknowledgement that it does not fit the study’s organization around scientific discoveries. Yet as Dear is well aware, no general history of the development of modern science can bracket its 19th-century institutionalization and professionalization. It was the 19th-century university, after all, that gave us the “scientist,” a term coined by the Cambridge philosopher William Whewell. Dear’s history of scientific discoveries implies a wider social and institutional history, but it remains largely subterranean, only occasionally extruded under the pressure of the narrative. It must be said that the balance is not all on the side of the earlier study. There are some advantages to the more historical, less theoretical organization of The World as We Know It. Dear’s accounts of paradigm shifts are remarkably lucid, no small accomplishment given that they span fields and centuries. He makes excellent use of the wealth of new scholarship on Darwin and his influences, to which he has himself contributed. It is satisfying to see puzzle pieces from Buffon’s natural history, Georges Cuvier’s animal taxonomy, Thomas Robert Malthus’s demography, and Charles Lyell’s geology recombined seamlessly in the Darwinian jigsaw. Likewise, Dear’s discussion of stellar nebulae, divided between chapters two and 15, shows vividly how Newton, Kant, Herschel, and Hubble reimagined insights and observations as they sought to discover whether the diffuse light that filtered through early telescopes was a glowing, gaseous substance or discrete but distant stars. Yet despite such pleasures, the book remains a more modest work than The Intelligibility of Nature. Dear has clearly not changed his views about the history of science. But in the two decades that have elapsed, the discipline and the world around it have changed, making it harder to write a sociologically and philosophically ambitious history of science for the general reader. That is a shame, because in the age of Silicon Valley and biotechnology, both the reciprocity and the tensions Dear identified between the epistemological and instrumental ambitions of science are more evident than ever. In recent years, some of the most exciting new books on the history of science in early modernity have focused precisely on this pressure point. Important studies such as Pamela H. Smith’s From Lived Experience to the Written Word (2022), James Poskett’s Horizons: The Global Origins of Modern Science (2022), and Vera Keller’s The Interlopers: Early Stuart Projects and the Undisciplining of Knowledge (2023) all shed new light on how early modern science negotiated the relationship between its instrumental and epistemological ambitions, or in Russell’s phrase, knowing and doing. There is every opportunity for a philosophically informed approach to draw new insights from this wealth of material. Dear, unfortunately, has not done so in The World as We Know It. But for future scholars of the history of science, his body of work over nearly four decades may provide just the model. Julianne Werlin is an associate professor of English at Duke University. Thanks for reading The Chronicle Review! Subscribe for free to receive new posts and support my work. Subscribe
EFI and Agfa’s DPS Business to Combine and Form a Global, Full-Service Industrial Inkjet Company
September 28, 2026 – 7.45 AM CET Regulated information – Contains inside information EFI and Agfa’s DPS Business to Combine and Form a Global, Full-Service Industrial Inkjet Company Combination to Create a Broader, More Diversified Business with a Comprehensive Product Portfolio, Expanded Geographic Reach and Enhanced Capabilities to Serve Customers Across Key End Markets Mortsel, Belgium and Londonderry, N.H. – September 28, 2026 – 7.45 a.m. CET Electronics for Imaging, Inc. (“EFI”), a leading
Is Marvell The Broad Chip Business You Think You Own?
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Scientists are about to test Einstein’s gravity with exotic matter
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How do e-ink displays work? The science behind digital paper
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Ukrainian defence tech seeks new ways to scale up
Since Russia's full-scale invasion in February 2022, Ukraine's defence sector has expanded several-fold, becoming a significant source of military innovation, especially in unmanned systems, counter-drone technologies, electronic warfare and AI-driven combat systems. But finding the funds and personnel to scale up and to reach international markets remains a challenge.Spurred on by the demands of the front-line, Ukrainian defence companies say they can develop a minor component in a couple of weeks, or major hardware or software solutions within a year. This is several times faster than the usual development cycles in the sector. Tencore, founded in 2024, is now one of Ukraine’s largest providers of unmanned ground vehicles, well exceeding the production of NATO members in this category. Odd Systems, a Ukrainian combat cameras developer founded in 2023, launched its first thermal camera in 2024. Less than two years later, it is developing the fourth generation of the product, one that has evolved into a full vision system.According to Michael Singer, managing partner at Verne Capital, a venture capital fund supporting defence companies in Europe, this speed is down to the short feedback loop between the developer and the end user. “Ukrainian companies develop technologies in close interaction with soldiers and military units, test them under real combat conditions and rapidly incorporate feedback into the next generation of the product,” he says. “Sometimes we need to react to feedback and deploy an upgrade within hours,” says Polina Tymchenko, the spokesperson for Himera, which develops electronic warfare-resistant walkie-talkies. “It means that, as a company, you have to have a higher tolerance for risk, and also design your products in a way that fosters those quick changes.”Getting a product deployed by a combat command involves no paperwork other than a purchase order, says Perry Boyle, co-founder and chief executive of Mits Capital, a Ukrainian-US investment group focused on attracting capital for Ukraine's defence tech sector. “New weapons can be developed and deployed based largely on handshakes.”Nevertheless, the speed of development is largely subject to the level of funding, says Iryna Sukhomlyn, head of business development at RMachine, a developer of unmanned ground systems. “Financial support needs to start much earlier, particularly at technology readiness level 3-5, not only when most of the technological risk has already been removed,” she says.In 2025, Ukrainian defence tech companies attracted about $129 million in investment, with the true figure likely higher given the share of undisclosed security-sensitive deals, according to a report published by the Kyiv School of Economics. These investments were primarily concentrated in the AI and software segment, as they are considered a lower financial risk.Scaling production is a major barrierAccording to Iryna Supruniuk, business development director at Odd Systems, proving a defence product in Ukraine is not the end of the development process, but the beginning of a continuous evolution, since operational requirements change rapidly. “Continuous iteration remains our highest priority,” she says.It's also when production must scale up, which represents a major hurdle. “Scaling production requires capital, manufacturing capacity, components, certification, procurement access and reliable supply chains,” Singer says. Scale-up is also hampered by demographic pressures, especially a shortage of young specialists needed to expand engineering teams. Companies have reported struggling to replace specialists lost due to Russian attacks, mobilisation and emigration. In order to meet this scale-up challenge and finance arms production, begun allowing defence technologies to be exported, assuming it has an excess capacity. It has also announced the creation of ten defence and weapons export centres across Europe by the end of 2026.According to Singer, a technology that has demonstrated its value under real combat conditions has a fundamentally different credibility than a product that has only been tested in a laboratory or training environment. But combat validation alone doesn’t automatically create an international business. “Companies still need access to foreign defence ministries and procurement organisations, international certification, financing for production scale-up and, in many cases, local industrial partners,” he says.Already in 2026, the EU has signed several agreements with Ukraine that aim at joint defence technology development and production. These include allowing Ukraine to join the European Defence Fund, signing a financing agreement under the European Defence Industry Programme, and setting up the EU-Ukraine Drone Alliance.For Singer, it is important that European defence companies don’t just see their Ukrainian partners as technology suppliers, but rather as potential innovation partners. “Ukrainian companies bring speed, operational experience and an exceptional ability to iterate. European partners can provide industrial capacity, capital, established supply chains and access to European procurement markets.”Procurement possibilitiesWhen it comes to exports, the procurement and compliance processes involved require time, taking months or even years, and money. In other words, resources that small defence tech companies need if they are to improve and scale up their technologies. According to Sukhomlyn of RMachine, if the priority is to rapidly increase available defence capabilities, then the processes need to reflect that urgency. “If Europe wants defence innovation at wartime speed, its administrative processes also need to operate much closer to wartime speed,” she says, highlighting a need for support with certification, market access and mutual recognition of relevant testing. “Otherwise, we risk having excellent technology available but spending years making it administratively eligible to be purchased.”Related articlesRussia widens targeting of European research centresEU must support research managers in central and eastern Europe, says Visegrad fund headThis is a lesson Europe’s defence sector would do well to learn, Singer says. “Defence innovation needs to be organised around the speed and requirements of the end user, not around the speed of the bureaucracy.”Supruniuk says the European defence sector should rethink the balance between quality and quantity. “In many cases, a good-enough system available in thousands of units creates greater operational value than a perfect system available in dozens.”“For decades, everyone has been looking for that all-powerful, exquisite system that can protect everyone,” adds Tymchenko. “We see in crime that only scalable, dedicated, affordable solutions can actually defend democracies.”
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Yale School of Medicine On the Science of Childhood Anxiety, Say, Anxiety Disorders Are the Most Common Mental Health Challenges In Youth
Credit: Matt Bradbury October 5, 2026 - By Isabella Backman - Anxiety disorders are the most common mental health challenges in youth. Left untreated, they can disrupt the lives of both children and their families. The good news is that with intervention, most children will overcome these conditions. Across Yale School of Medicine, scientists are working to understand anxiety at every level, from common anxious behaviors to molecular biomarkers in the brain. They are using their findings to develop and disseminate new evidence-based treatments for childhood anxiety. Today, the go-to treatment for childhood anxiety disorders is cognitive behavioral therapy (CBT). This is a form of psychotherapy that teaches children skills for confronting anxious thoughts and helps them practice managing situations that cause anxiety. While it is the gold-standard treatment backed by considerable scientific evidence, up to 50% of children will not see sufficient benefit from CBT alone. Wendy Silverman, PhD, Alfred A. Messer Professor in the Child Study Center, co-directs the Anxiety and Mood Disorders Program alongside Eli Lebowitz, PhD, associate professor in the Child Study Center. One of their main interests is learning how to improve outcomes beyond CBT. “We’re developing cutting-edge, research-based knowledge that can reduce the suffering that anxiety causes children and their families,” says Silverman. Changing parent behavior YSM experts are investigating how to improve CBT outcomes for children by involving the parents. Silverman’s research has uncovered two main components of parent intervention that improve childhood anxiety: not enabling children to completely avoid the things that make them anxious and taking steps to enhance their autonomy. Parents may unintentionally reinforce their child’s anxiety by allowing them to avoid what makes them anxious. They also may unintentionally limit the children’s sense of autonomy by being overly intrusive. “One of the things that we take pride in is that we’ve focused on trying to understand what parents need to do, and to test our ideas and see if changing the parents’ behaviors is enhancing the effects of CBT,” Silverman says. “Our findings thus far suggest that they do." As much as CBT can be helpful, it can also be challenging to get one’s child to do the necessary steps for CBT to work. This is one important reason why Lebowitz created a novel intervention program for parents named Supportive Parenting for Anxious Childhood Emotions (SPACE). Existing intervention programs often teach parents to act as therapists for their child, such as training them on how to practice breathing exercises. “It makes sense, but this doesn’t work very well in practice,” says Lebowitz. “And part of the reason, I think, is that it’s not easy to get your kid to do things, especially if they’re not excited about doing it.” SPACE is unique because it focuses entirely on parent involvement and changing parental behavior—children are not involved in the sessions. For example, parents learn how to use supportive messages that convey confidence that their child can tolerate and manage distress. “It might sound like a parent saying to a child, ‘I get that this is really hard for you, but I know that you can handle it,’” Lebowitz says. The program also works with parents to identify the ways in which they are accommodating anxious behaviors. “We’ll pick one thing that parents are doing that is an accommodation and help them make a detailed plan for how they’re going to change that,” Lebowitz explains. Treating Anxiety in Children and Adolescents Much of the existing research on SPACE has focused on parents of children under age 14. Ongoing studies are now exploring its use with parents of older teens. “Both anxiety and accommodation can interfere with normative developmental shifts during the teen years, including increased autonomy and individuation from parents,” says Rebecca Etkin, PhD, associate research scientist in the Child Study Center. “In this sense, SPACE may be particularly well-suited for anxious teens and their parents. We want to see whether it is effective during this distinct developmental window.” Unfortunately, many families in need of CBT face barriers, including limited availability of services and geographic constraints. One way to improve access is digital interventions. Silverman and her team are developing an evidence-based digitized intervention program for parents that they can access directly from their computer or smart phone. “The work we’re doing will be one of the very few parent interventions that is digitized and importantly tested for effectiveness,” she says. Creating interventions for anxiety-related challenges Silverman and Lebowitz recently received a generous gift to develop and test other interventions that help parents reduce other child anxiety-related behavioral and emotional difficulties, such as restrictive eating and unexplained somatic symptoms. One of these projects in particular focuses on understanding the risks of social media and its potential benefits, including offering a sense of connection. “A lot of research has focused on the idea that social media is harmful and the less of it the better,” says Lebowitz. “But we actually see is that this is not quite right—there are negatives, but there are also positives. So, we’re trying to get a little bit more nuanced of a picture.” The team is working with teens with social anxiety and their parents over an extended period to better understand their social media habits and how their anxiety levels affect engagement with different platforms. The teens will answer questions sent to an app on their phones about mood and social media usage in an effort to capture emotional responses as they unfold. “We hope to develop interventions that can help make the best of social media while protecting against the more problematic effects,” Lebowitz says. The brain’s role in anxiety Researchers are also testing therapies to address anxiety at the neurological and molecular levels. In collaboration with Dylan Gee, PhD, professor of psychology in Yale's Faculty of Arts and Sciences, and Hilary Blumberg, MD, John and Hope Furth Professor of Psychiatric Neuroscience at Yale School of Medicine, Lebowitz and Silverman are using brain imaging to identify changes in a child’s brain before and after parents enroll in SPACE. In one study, children viewed anxiety-inducing images while undergoing magnetic resonance imaging (MRI); the researchers conducted scans with and without the children’s parents nearby. Before SPACE, children’s brains were better able to activate the regulatory circuitry needed to turn off an anxious response when their parents were nearby. But after SPACE, children could activate this circuitry even without the parent around. “As parents work on gradually reducing some of their accommodations, you can see a child get better at regulating their own fear system in the brain,” Lebowitz says. “It’s remarkable.” Research into the molecular underpinnings of anxiety can also inform new childhood anxiety treatments. In a recent study, Lebowitz, Silverman, and Flora Vaccarino, MD, Harris Professor in the Child Study Center, discovered that a protein known as fibroblast growth factor 2 (FGF2) could be protective from the toxic effects of stress. FGF2 levels in children and their parents were linked to the children’s risk of developing anxiety and depression, the study showed. The findings could help explain why some children who are exposed to early life trauma such as poverty or abuse are more prone to developing mental health disorders. And FGF2 could be a target for treatment. “This is very novel because it starts to give a clue to what is the molecular chain that connects those lived experiences to the actual psychological outcomes,” Lebowitz says. New ways to study and treat childhood anxiety Michael Crowley, PhD, associate professor in the Child Study Center, collaborates with Silverman and Lebowitz to study the role that attention plays in development and maintenance of childhood anxiety. There is a large body of research that shows that anxious children, like anxious adults, are prone to focus on threatening stimuli such as angry faces compared with neutral faces. This has led to innovative interventions that involve attention retraining. The idea is that if experts train children to look away from threatening stimuli, it may reduce their anxiety—especially children with social anxiety who are most prone to attend to threats. The researchers have just completed a clinical trial for attention retraining with 10- to 14-year-olds with social anxiety disorders and are currently analyzing the findings. Besides this innovative attention retraining research, as Crowly notes, “I like to design tasks that are engaging to kids,” Crowley says. “My goal is to assess something without the kids knowing what we are assessing.” With this goal in mind, Crowley has created a virtual game, named Boom, to study threat processing in children with anxiety disorders. The game is similar to that of hot potato—the child and three digital players take turns virtually passing a ball to each other’s gloves. At some point, the ball turns into a bomb, and as the bomb lands in each player’s glove, the outline of the glove turns yellow. The goal is to avoid having the bomb go off in your glove. What isn’t obvious is that the game is designed to measure different types of threatening stimuli, both ambiguous and direct. In the game, the direct threat occurs as the bomb is traveling towards your glove. The ambiguous threat is the yellow outlined glove as it is unknown where the bomb will travel next. While children play the game, Crowley’s team measures their brain activity using electroencephalography (EEG). The researchers have discovered that in kids with anxiety, the brain reacts more strongly to ambiguous threats than it does in their peers, but less strongly to direct threats. They believe that the initial abnormally large brain response to not knowing where the bomb is going impairs the brain's ability to properly respond when the threat is actually traveling the child’s way. “The brains of children with anxiety are unable to differentiate between threats you need to do something about and those that are not your problem.” Michael Crowley, PhD, develops innovative games for studying anxiety in children and adolescents.Credit: Matt Bradbury Based on these insights, Crowley hopes to study whether interventions like attention training could restore appropriate threat processing. Crowley’s team is also working on a test called the Balloon Risk Avoidance Task, which evaluates risk-taking and avoidance behaviors. It features a digital balloon that is full of air and about to burst. Kids have six seconds to let air out of the balloon. The more air they let out, the less risk they face that the balloon will pop. But at the same time, the balloon becomes less valuable as it deflates. “The more air you keep in the balloon, the more points you get,” Crowley explains. So far, the researchers have found that when the balloons pop unexpectedly, teens with social anxiety show distinct brain responses. Studying these responses can help psychologists understand the underlying pathways driving the various manifestations of anxiety. The genetics of anxiety When Thomas Fernandez, MD, associate professor in the Child Study Center and of psychiatry, was still in training, there was a lot of excitement about understanding the genetics associated with autism spectrum disorder. Since then, scientists have identified around 250 genes associated with autism. The genetic contribution to anxiety disorders, on the other hand, has historically received less attention. Anxiety is less heritable than autism, but the genetic contribution for anxiety disorders that emerge in childhood may be higher than for anxiety disorders overall. While scientists estimate the heritability of anxiety disorders in general to be around 30% to 50%, some studies suggest higher heritability for certain childhood-onset anxiety presentations. “I saw firsthand how researchers in the field went about finding vulnerability genes for autism,” Fernandez says. “So, we’re using a very similar playbook for childhood anxiety.” “I saw firsthand how researchers in the field went about finding vulnerability genes for autism. So, we’re using a very similar playbook for childhood anxiety.” Thomas Fernandez, MD Associate Professor In the Child Study Center and in Psychiatry Now, Fernandez and Emily Olfson, MD, PhD, assistant professor in the Child Study Center, are studying children and their parents to identify genetic changes that are present in the child but not the parents, known as “de novo mutations.” “All of us have some de novo mutations—maybe about 50 to 100 sprinkled throughout the genome,” Olfson says. “But when they occur within the coding regions of genes, they can be really disruptive.” Previous research shows that people with autism have higher rates of damaging de novo mutations than the general population. In 2022, Olfson, Lebowitz, Silverman, and Fernandez published a study on 68 children and their families that found that children with anxiety had similarly high levels of these mutations. Studying de novo mutations can help point the researchers to where they should be looking for genes associated with anxiety. “The end game is using the genes to steer us toward the right part of biology that we can then target to come up with better treatments,” Fernandez says. Building on those findings, the team is now studying more families to better understand how these de novo mutations, along with other genetic and environmental factors, shape pediatric anxiety disorders. They recently received a National Institutes of Health grant to enroll 750 new families over the next five years. Olfson is the principal investigator, with co-investigators Lebowitz, Fernandez, Silverman, and Shuangge Steven Ma, PhD, department chair and professor of biostatistics at Yale School of Public Health. Neurodevelopment, Risk Genes, and Mental Health Conditions - The Olfson Lab Joel Gelernter, MD, Foundations Fund Professor of Psychiatry, is interested in how different anxiety disorders differ genomically. “We are studying social phobia, panic disorder, and generalized anxiety disorder, working to understand why people differ in their risk to these specific anxiety disorders and evaluating various risk factors,” he says. Gelernter was recently involved in one of the largest studies to date of the genomics underlying anxiety disorder. The study included around 122,000 people with anxiety disorders and around 730,000 without. It found that some genetic differences associated with anxiety were linked to signaling that helps reduce overactivity in the nervous system. Many anxiety medications available today work by targeting this process. “It’s nice when the biology that you get out of a large genome-wide study ratifies things that we already know because that can help increase confidence in further findings from the study,” Gelernter says. Uncovering the neurobiology of psychiatric disorders John Krystal, MD, Robert L. McNeil, Jr. Professor of Translational Research and chair of the Department of Psychiatry, is interested in the neurobiology of psychiatric disorders, including post-traumatic stress disorder (PTSD), of which anxiety is a major symptom. In the late 1980s, Krystal’s team discovered that the drug yohimbine activated symptoms in patients with PTSD. “This was the first time we could link a specific biological mechanism to the symptoms of PTSD,” Krystal says. At the time, he adds, this finding was highly controversial. “A lot of people felt that PTSD was a purely psychological syndrome that didn’t have an underlying biology.” Since then, Krystal has dived deep into understanding the neurobiology of PTSD to learn how to better treat it. His team is evaluating the use of ketamine and psychedelics. These would be among the first treatments to be developed specifically for PTSD. They may also be applicable for other disorders including anxiety disorders, Krystal adds. An important gap in PTSD treatment is the absence of biological tests that inform how to best help patients manage their PTSD symptoms. A doctor doesn’t diagnose cancer based on how they feel. Rather, they use tests of the biology of the cancer to determine the best course of treatment. “And we can’t do that in any psychiatric disorder other than Alzheimer’s disease,” Krystal says. “But now we are building a foundation for this approach to the treatment of anxiety disorders for the first time.” Source: Yale School of Medicine
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Science Vs on the 49ers Substation: Anatomy of a Hatchet Job
In August, Pablo Torre Finds Out and Science Vs released an episode about my theory that electromagnetic fields from the electrical substation beside the 49ers facility may be contributing to the team’s run of soft-tissue injuries. As the originator of the theory, I was also a subject of the episode. I sat was interviewed by Wendy Zukerman and Rose Rimler of Sciene Vs. I sent them research, connected them with scientists, and spent hours digging through the City of Santa Clara’s and Silicon Valley Power’s records to help clarify critical details. Both Wendy and Rose came off as affable and professional, showing curiosity during the interviews, with Wendy going out of her way to question the “conspiracy theory” framing itself. Then they titled the episode We Solve the 49ers Viral Conspiracy Theory. I was familiar enough with their catalog that I never expected them to agree with my theory, but I did expect them to give it a fair hearing and to deliver their findings honestly. On both counts they came up short. They were not directly dishonest in anything they said, but rather in what they left out, in how what remained was cut, and in the picture painted by those two things in combination. They asked me to recorded the interview on my phone for better audio quality, and I held on to my copy for reference later. That turned out to be a fortuitous decision. Here is the raw audio of my first interview, unedited*. Only my side was recorded, so their questions aren’t on it, but you can generally infer them from the answers, and every claim I make below about what I said can be checked against my statements in this clip. (Note: Wendy had connection trouble at the beginning of the interview and was cutting in and out, which accounts for the false starts.) 0:00 -1:19:13 Audio playback is not supported on your browser. Please upgrade. Science Vs is a fun show. It is pitched at roughly a high-school understanding of science, for an audience that is skeptical, Snopes-oriented, and worried about misinformation. Take a claim circulating online, interview a supporter of the claim, interview consensus scientists, and then tell people which side of the line it lands on. I have listened to their episodes on raw milk, seed oils, 5G and other contested issues in the wellness space. I have problems with all of them, but each at least made an honest attempt to represent the actual range of scientific opinion by talking to credentialed scientists with differing perspectives. Dissenting researchers were heard from, answered, and often given a chance to respond. This episode did not do that. This article is not a relitigation of the science. I have written extensively about that already. This post is for the record. It is simply an accounting of what was wrong with their episode. Contents Is there a power plant next to the 49ers practice facility? — the clearest single example of getting something objectively wrong For the record — a high-level overview of all of the problems with their investigation Draw your own conclusions — why they had to make this episode at all What they left out about childhood leukemia — the exposure threshold, and playing games with statistics to minimize sick children What they left out about the mechanism — the body of literature they refused to cover, and evidence for the mechanism used against it The scientists Science Vs interviewed and did not air — four credential scientists who support myhe theory, recorded and cut, or not even called How they misrepresented me and my case — an answer severed from its question, and three telling edits How you would actually study the injuries — it doesn’t actually matter which team is the most injured, overall The theory: magnetic fields, oxidative stress, and collagen Since the episode never states my theory, here it is below. Those who are familiar with my work can skip this section. Electrical equipment produces magnetic fields, and those fields induce faint electrical currents in anything that passes through them, including people. My argument goes further than induced current. Mitochondria — the structures that generate a cell’s energy — run on continuous flows of electrons and protons, and those flows carry faint electromagnetic fields of their own. Maxwell’s principle of superposition shows that when two fields share the same space, they add together. An external field does not need to be strong to alter an internal field, it only needs to be present. The electron transport chain inside the mitochondria leaks a small fraction of its electrons by design, and those become reactive oxygen species — free radicals, which healthy cells use as signals. External magnetic fields cause the rate of leakage to change, increasing free radicals. When free radicals accumulate faster than the cell’s antioxidant systems can clear them, the result is oxidative stress. Oxidative stress is a recognized driver of chronic illness, including cardiovascular disease, neurodegeneration, diabetes and cancer, and it is in every medical school curriculum. One of its ordinary effects in connective tissue is that it switches on matrix metalloproteinases — MMPs, the enzymes that break collagen apart — while suppressing new collagen synthesis. Tendons are made of collagen. An athlete loading his soft tissue heavily six days a week is already creating oxidative stress in the tendons, so the addition of magnetic field exposure compounds the damage and inhibits repair, making him more susceptible to injury when enormous force lands on a tendon in a fraction of a second. That is the theory. We know that EMF causes oxidative stress, and we know that oxidative stress degrades collagen. The only thing missing is a study showing that direct connection. I have never claimed certainty that the substation is contributing to the elevated injury rate. I do believe it is likely, and I believe it warrants caution, and that a revenue machine like a major NFL team can easily afford to remove the exposure out of precaution. Is there a power plant next to the 49ers practice facility? Here is the clearest single instance of the problem with this episode. It requires no knowledge of electromagnetic fields at all. This story first came to me through Jon Feliciano, a former 49er, in an interview on Willard & Dibs on 95.7 The Game. Asked about why the 49ers are always injured, he said players used to joke that it was the power plant behind the practice fields. Wendy Zukerman corrects him on air. “It’s important to say that it’s not a power plant near the 49ers site.” Torre then asks her to explain the difference between a substation and a power plant. Her answer: a power plant generates electricity and transmits it to a substation, which converts the voltage into something your house can use and sends it on to your home or your business. There are two problems with that. The first is that there is a power plant on that site. The Gianera Generating Station is a natural-gas-fired peaker plant owned by Silicon Valley Power, and it has been there since 1986. I have published aerial photographs of the location from 1987 in which the gas plant is the only thing standing, before the practice facility was even there. I even mentioned the gas plant in my first interview. (Feliciano has since gone on record about this issue, and it is clear he had the substation in mind rather than the gas plant.) The second is that her definition describes a distribution substation, and the facility beside the 49ers is not that. It is the Northern Receiving Station, which takes in bulk power from outside the city’s grid and delivers it to distribution substations. Silicon Valley Power’s own map distinguishes receiving stations from substations, and Rose Rimler even reads the label out loud in the episode when she walks through that map on air. A few minutes before the map segment, Zukerman tells Torre: “like I said, we fact check everything.” Well, maybe not everything. I made a mistake On the morning of July 6th, at 10:20, I sent Rose and Wendy two studies. During the interview I had been asked which human studies show oxidative stress from electromagnetic fields, and I had not been able to name one on the spot. Rose emailed asking for the studies, I quickly searched for a couple, and I wrote that I thought these were the most relevant from that search. Unfortunately, I was busy and did not read either one closely at first. I picked them because they were topically relevant — one on substation workers, one on power plant workers. Neither were great studies, and their problems go past the ones raised in the episode. That was careless on my part. There is context that did not make the episode, though. Before that email I had been on a Zoom call with Rose talking about EMF and oxidative stress, and I pointed her to Dr. Henry Lai at the University of Washington, who has spent years aggregating the literature on this question. His tallies show that roughly 90% of studies since the late 1990s find oxidative effects from electromagnetic field exposure — hundreds of studies, systematically counted. Rose told me she was already aware of his work. So when she asked for studies, I understood her to have the aggregate view already and that she would report anything within that context. Not reading those two carefully was still a mistake, but the larger mistake was assuming the episode would be based on a thorough review of the actual body of literature, rather than on whatever I happened to send that morning. The second email At 1:49 that same afternoon — three hours and twenty-nine minutes after the first — I sent them a second email that I had been preparing for a while. It was a structured document in six numbered sections, written in response to a request they had made two weeks earlier, laying out my entire argument with citations attached to every link in the chain. The episode aired on August 13th, five weeks later, and not a single item from the second email is in it. Here is how it opens: The full email is included at the bottom of this post in Appendix B. Nearly 1,500 words in total. It contains two named mechanisms with the physics behind them. Occupational studies in humans. The literature on oxidative stress and collagen. A section addressing the strongest counter-evidence against my own theory, which I raised myself. And a closing section stating plainly what the theory cannot yet show. My entire argument, in writing, with detailed citations for every claim, provided to them five weeks before broadcast, and none of it made it into the episode. That is the single largest omission, but it is not an isolated one. The whole episode is riddled with similar problems, and the conclusion they came to is not merely a difference of opinion about the scientific evidence. Through omission and through strategic editing, Science Vs misinformed its audience — about what the evidence shows, about what I argued, and about who they spoke to. That is a notable outcome for a show whose stated purpose is correcting misinformation. For the record I am not going to tell you that Science Vs set out to discredit me, or that they had come to their conclusion before they reported the story, or that they used misleading editing to make me look like a man retreating from his own theory. I cannot know what was in anyone’s head, and I am not going to pretend otherwise, either. What I can tell you is what is on the record. They asked me for evidence and aired the weakest thing I sent. They interviewed three scientists who supported my theory and aired none of them. They discussed childhood leukemia without ever saying the exposure level at which it appears. And they took an answer I gave weeks before Ken Karipidis, the one EMF scientist who was put on air, was interviewed, and placed it directly after his critique, where it comes off as a major concession. A friend of mine who has worked as a journalist for thirty years read that last one and called it sleazy. I agree with her. Those are just the four issues that are impossible to defend as pure editorial decision, but they are not the only issues. The most glaring issues stem from what they left out: The exposure level at which the childhood leukemia association actually appears — three to four milligauss, a number the episode never states despite it being much lower than what I measured. The mechanism itself: The episode gets as far as “oxidative stress could weaken collagen,” which leaves it sounding like speculation, rather than a known pathway. The second email, and all the studies in it. Dr. Paul Héroux at McGill, whose work my proposed mechanism rests on, whose contact details I supplied, and who was never called. Dr. Beatrice Golomb at UC San Diego, who runs a research group on oxidative stress and mitochondrial function and has specific expdertice in collagen, interviewed and not aired. Dr. David Carpenter at Albany, the most prominent academic voice on the harm from magnetic field exposure, interviewed and not aired. Dr. Joel Moskowitz at Berkeley, interviewed and not even credited. The specific, testable condition I put in writing that would make me abandon the theory. My own unprompted statement of the theory’s evidentiary gap. My caveats about my own measurements. My ranking of EMF as one factor among several rather than the only one. The new equipment installed at those facilities between 2010 and 2014, and the sharp rise in system load from 2013 onward. But that is not all. What they kept, they selectively edited to serve a narrative that was not served by the raw transcripts of the interviews. A description of thousands of commercial routers in a workplace, reduced to the Wi-Fi in your house. My own acknowledgment, multiple times, that "I'm not a scientist" clipped in an episode that spends considerable energy pointing out that I am not a scientist. And a qualification I volunteered about my own measurements, cut from my answer and delivered later by their EMF expert as a correction. Together their edit produce a portrait of a wellness guy with Wi-Fi phobia and two bad studies, backing away from his theory the moment a “real” scientist looked at it. A practice facility where nothing changed because no new substation was built. Injuries written off as random because the 49ers were not quite the single most injured team in the league over the period in question. That portrait is false even though almost no individual statement made in the episode is. Draw your own conclusions At the top of the episode, Pablo Torre says his show had been flooded with requests to investigate the substation — that it was the thing they were asked to look into over and over again. Neither show went hunting for this story. It arrived from their own audience, in volume, and it could not be waved off. A thread I posted on X reached twenty-two million people. A guy with a gaussmeter and a brand-new Substack obligated a Pultizer prize winning program to spend an hour on a question about player health, that is considered fringe enough that most media operations won’t touch it. Pablo Torre Finds Out could not ignore it. So Science Vs came in and ran a “debunking” operation instead of an investigation. Everything below is what had to be left on the cutting room floor to deliver the “debunking”. They could not ignore it. So they tried debunked it instead. The demand was strong enough to force an episode, and since the episodes release the 49ers have sustained more injuries, including season ending ones, and interest has only grown. Demand from fans and playets is strong enough to force a better investigation from someone else. An omission is not a lie until you find out what was omitted. What follows is the detailed record so you can see the full picture. Draw your own conclusions. I have drawn mine. I am going to keep publishing. A note about Pablo Torre Finds Out After the episode aired I posted publicly, calling out Pablo Torre Finds Out for concerns I had about the integrity of their investigation, and about an interview directly with Pablo Torre which had been offered but never happened. I have since spoken with a producer at PTFO. The offer had rested on a misunderstanding about where things stood between us, and it fell away as the Science Vs part of the production widened past the science. He apologized for the miscommunication and I accepted. The producer also confirmed to me that they did essentially hand off the entire investigation to Science Vs for narrative purposes — so Pablo would be genuinely curious or potentially surprised by their findings — while still taking responsibility for what went out under their name. I appreciated the candor and the accountability, and I am comfortable with where we left things. So this post is not about PTFO. My disagreement is with Science Vs. What they left out about childhood leukemia Childhood leukemia appears at three milligauss. They gave no number at all. 1. They built an EMF ruler, then discussed childhood cancer without it. The sequence on air went like this: First I measured almost 9 mG, then I measured up to 50 milligauss. Torre reacts with concern — “that sounds high.” Cut to Karipidis: the public limit is 2,000 milligauss. Torre reacts again — “What happens at 2,000?” Karipidis explains that nothing happens at 2,000, that safety factors are built in. Then: at more than 50,000 milligauss you get flickers of light in the retina, and higher still, nerve stimulation. The listener now has a ruler (their ruler) to measure these numbers with. Fifty is nothing by their ruler. Then the episode turns to childhood leukemia and states, accurately, that there is a real association — but tellingly, they never give the exposure level at which that association appears. Childhood leukemia appears at three milligauss. They conveniently left that out. The pooled analyses that produced the World Health Organization’s carcinogen classification found roughly a doubling of childhood leukemia risk above three to four milligauss. That is the number that belongs in that segment, and it is more than ten times below the reading that had just been dismissed as trivial. I gave them that number myself, on tape, in the interview. Describing my own threshold, I said my comfort level for long-term chronic exposure is three to four milligauss, but preferably one. 2. Six children in thirteen million. The episode reports that these fields might explain one to four percent of childhood leukemias, then reframes it as a German estimate of perhaps six cases among thirteen million children. Torre, to his credit, is uncomfortable. What never gets explained is why that number is small. Almost no children lives above three milligauss in Europe. Fewer than two children in a hundred, in the Italian data. So even if the risk to those children doubles, the number of additional cases across an entire country stays small — not because the hazard is small, but because hardly anyone is exposed to it. Count the whole population and the few who are exposed disappear. And the reason hardly anyone is exposed is that siting rules keep housing away from transmission lines. In Europe, at least. The Dutch government has a standing precautionary policy against building new homes in any zone where the annual average magnetic field exceeds 4 milligauss — the same number the episode never mentioned. Denmark and Norway treat 4 milligauss as the level that triggers a look at mitigation. That is five hundred times below the ICNIRP figure quoted on air. The United States has no federal equivalent. That is evidence of infrastructure siting policy working. It is not evidence that there is no hazard. It is evidence that we already act as though there is one. If you listen to the raw audio you will hear that my proposed solution is EMF exposure is to build better infrastructure. What they left out about the mechanism 3. They accused me of cherry-picking, and then cherry-picked themselves. On air, Zukerman tells Torre that people who worry about electromagnetic fields dismiss the studies showing null results and collect the ones showing harm, and that this is why you have to be careful not to cherry-pick. They had two papers I had rattled off in a hurry, and a second email containing a carefully chosen set. They ran the two weakest, graded them on air, and presented the result as the state of the evidence for not only my theory, but the whole question of oxidative stress from magnetic fields. That is cherry-picking from my emails. The bigger picture is what they did with the literature as a whole. Zukerman acknowledges it exists, dismisses it, and disposes of it in a single stroke. You can go online right now, she tells Torre, and find scores of studies showing these fields increase oxidative stress. The issue, she says, is that they are not studies in people. Many of them are in people. The occupational studies in my second email are in people. That email had been in her inbox for five weeks. She waved off the literature on a factual claim that the documents in her possession contradict. (I have written separately about the evidentiary standard at work here). The effect was that they essentially baited me: ask the subject to supply the evidence, take the weakest thing he sends, and let that stand as a proxy for the whole argument. Wendy has been doing this show for ten years and clearly knows how to extract what she needs for her desired narrative. 4. They presented the collagen-improvement research as a gotcha, but I had already addressed it. The episode treats the existence of studies showing that EMF can improve collagen as a surprise that undercuts me, but I had pre-emptively addressed that five weeks earlier in the email they ignored. Those studies use measured, high-intensity pulsed dosing. The mechanism by which they work is oxidative signalling. The cell reads a controlled rise in reactive oxygen species as a warning, upregulates its antioxidant defenses, mounts a repair response, and the therapy stops before the system is overwhelmed. The key point is that it induces an oxidative response, which means those studies are actually evidence for my proposed mechanism, not against it. A field that produces a therapeutic effect cannot be biologically inert (which is the implication when they say “Nothing happens at 2,000 milligauss). Chronic ambient exposure is the same pathway with no off switch, and it is most consequential during the evening and while sleeping, when the body is in repair mode and the exposure does not stop. Section 5 of my email is titled What about the study showing improved collagen synthesis. I raised the counter-evidence myself, explained why I did not think it refuted the theory, and wrote that I was disappointed the question had not come up in the interview. That is worth holding against the cherry-picking charge in the item above: the studies they presented as inconvenient for me were studies I had gone out of my way to put in front of them. 5. Section 1 of my email stated a critical argument that was never put to the expert directly responsible for it. My email says the exposure limits exist to prevent acute effects and do not address chronic exposure at all, and that my dispute is with the entire framework. Zukerman gestures at this once. After Karipidis gives the 2,000 milligauss figure, she tells Torre that I would object because those levels do not capture “more subtle effects.” That is not my argument, and “subtle” is doing a lot of work here. My argument is that the limits are built to prevent acute effects — nerves firing, muscles twitching, etc — and were not designed to address chronic exposure at all. In fact, ICNIRP’s own documents state as much themselves. Mine is a structural objection to what the standard measures, reduced as a concern about subtlety, it becomes a matter of degree, rather than a categorical difference. They interviewed Ken Karipidis, vice chair of ICNIRP — the body that writes those limits. He was asked what the limit is, but he was never asked how it applies to chronic exposure. The scientists Science Vs interviewed and did not air 6. They interviewed four officials of the standards body. The episode credits roughly a dozen researchers. Four of them are associated with ICNIRP. Ken Karipidis is the vice chair. Rodney Croft chaired ICNIRP from 2020 to 2024 and led the development of its current guidelines. Dan Baaken is ICNIRP’s scientific secretary. Frank de Vocht sits on the Main Commission. One of them speaks in the episode. Their institution’s position is more than adequately represented — the 2,000 milligauss figure, the safety factors, the assurance that nothing happens below the line. 7. The four who were left out. Dr. Beatrice Golomb is Professor of Medicine at UC San Diego — a physics undergraduate degree, a PhD in biology, an MD. She directs a research group whose stated focus is the relationship between oxidative stress, mitochondrial function and health. That is the mechanism the episode spent its first half dismissing. Her published work includes the fluoroquinolone case series behind the FDA’s black box warning on an antibiotic class that ruptures tendons, where the accepted mechanism is oxidative stress and mitochondrial toxicity — the back half of my chain, already on a drug label. She is in the credits. She is not in the episode. She has told me she finds my theory biologically plausible, and that she has a recording of her interview. Dr. David Carpenter directed the Institute for Health and the Environment at the University at Albany for decades and is the most prominent academic voice arguing these fields cause harm. Childhood leukemia is the reason these fields carry a WHO classification at all, and Carpenter is the person you call if you want that case made by someone who has spent a career on it. He is in the credits. He is not in the episode. He has told me that when he was interviewed they could not have been less interested in what he had to say. Dr. Joel Moskowitz directs the Center for Family and Community Health at UC Berkeley’s School of Public Health. He told me directly that they interviewed him and that he thought it went well. He does not appear in the episode, and unlike Golomb and Carpenter, he does not even appear in the credits. Dr. Paul Héroux at McGill is the researcher whose work provides the foundation for the oxidative stress mechanism my theory rests on. I gave Rose his email address and phone number. He was never interviewed. They never even called him. 8. “He’s not a scientist.” The episode leans hard on the fact that I am not a credentialed scientist. Zukerman says it. Torre repeats it. “At all.” Having built a segment on that, they then left out the physicist-biologist-physician, the professor of public health, the director of a university environmental health institute, and the McGill researcher whose work the primary mechanism comes from. They spent the episode telling their audience I am not a scientist, and then kept four actual scientists who support the theory off because their argument does not survive otherwise. How they misrepresented me and my case 9. They played my words as a response to an interview I had never heard. Near the end of the hour, Zukerman says she went to me and told me the evidence was lacking. Then she plays me saying I am not wedded to it being an EMF, that I have staked my reputation on it needing more study, and that I am not certain of anything. That segment was placed immediately after Karipidis had finished taking the cherry-picked papers apart. It plays as a man folding under expert scrutiny. Commenters have used it against me since, but it is incorrect. Here is the sequence as it happened. I was interviewed. Karipidis was interviewed weeks later. I was never told what he said, or even who he was. I was never asked to respond to it. I did not know his name until the episode aired. That is not a simple editing decision. That is a quote from one interview, moved to follow a critique from a different interview it was not a response to, so that it would land as a concession. A friend of mine who has spent thirty years as a journalist read that sequence and called it sleazy. She is right. The full passage is reproduced in Appendix A, and it is worth reading. What airs is the preamble. Four paragraphs later I say “to directly answer your question” — and that answer, about what would change my mind if the team relocated, is not in the episode. Neither is the sentence two paragraphs on, where I say the EMF might turn out to be ten percent of the problem. I will say the underlying point again, though, because I meant it and I still do. I am not wedded to my theory that magnetic fields from the substation are contributing to the 49ers injuries. I could be wrong. What I am wedded to is the process of scientific inquiry, and the fact that we should be cautious around these exposures and we need more independently funded studies. 10. Three telling edits. They cut “I’m not a scientist” mid-sentence. What I said: “...and I am not certain of anything. I’m not a scientist. To me, I find the mechanisms compelling. I will go back to the fact that I got into this not because of the 49ers, but because of clients I was working with who suffer from EDS...” What aired: “...and that I am not certain of anything. I’m not.” The clip ends on the first two words of the sentence in which I say I am not a scientist, in an episode that spends considerable energy establishing that I am not a scientist. The full sequence is in Appendix A. They cut my own description of my work. Asked what I do, I said I run a wellness business, that I am focused on writing software to help people navigate environmental stressors, that environmental health is my focus, and that I also do independent journalism and research. What aired is the wellness business and the environmental health, with the software and the journalism removed from my own answer. The software engineering does come up later — narrated by them, as a hacker who grew up to write firmware — but my current work, in my own words, arrives as “wellness guy.” Thousands of commercial routers became home Wi-Fi. What I described: working at a wireless networking company surrounded by thousands of Wi-Fi routers, and a stress-induced health collapse afterward that working in that environment contributed to. What aired: Wi-Fi, the kind you have at home — reinforced by a clip of Christian McCaffrey talking about turning his router off at night. Three cuts, and every one of them makes me seem less credible. That is not a coincidence. 11. I gave them my own caveats and the test that would disprove me. In the first email I wrote that a well-designed chronic, ambient-level exposure study in tendon showing no collagen degradation, run over many months, would undercut my confidence in the theory. That is a specific, testable condition, stated in advance and in writing. There was a second interview, weeks later, which was not used in the episode, but in that I asked again for the falsification criterion to be included. What the episode presents instead is a man saying “we need more study,” which reads as a hedge, an open-ended request for the benefit of the doubt. It is the opposite of a hedge. Section 6 of my second email says, unprompted, that as far as I am aware there is not a single study showing EMF-driven oxidative stress degrading collagen in a human in vivo or in human tendon in a lab. I wrote that because it is true and because it is the first thing anyone should check. Under their standard it becomes the hinge of the entire first half, framed as something they had to surface without my cooperation. I had handed it to them five weeks earlier. And in the interview I said that my 25 to 50 milligauss readings were taken at knee level, and that these fields attenuate quickly, so by the time it reaches your head it is not that high anymore. That did not air either. The qualification arrives later, from Karipidis, as a correction. How you would actually study the injuries 12. They measured the wrong thing. The episode spends its final act on whether the 49ers are the most injured team in the NFL, finds no clean ranking, and lands on “injuries are random”. That is the wrong test. You would define the exposure — measured field levels at the facility — and the outcome narrowly: soft-tissue injuries, not a single MSK injury count that a broken finger and a ruptured Achilles both land in. Then you would compare the 49ers to themselves before and after the exposure changed, and compare that change against every other team over the same window. That controls for league-wide shifts in rules, turf and training load. It is a difference-in-differences design, and it is standard. I sent them that argument on July 28th, in writing, along with the fact that in eleven of the past twelve seasons the 49ers had finished top ten in Adjusted Games Lost. And by the episode’s own reporting, the 49ers are second in games lost to injury over the past decade, with FTN’s Aaron Schatz confirming that once you adjust for starters they come out second worst in the league — after having been one of the healthiest teams for years before that. A finding like that is where an investigation starts, not where it stops. 13. I did a lot of substation research for the episode that was never aired. I had reported that the substation next to the facility was expanded in 2014. That was wrong, and Rose Rimler and I sorted it out together. They gave me credit on air, which I appreciated, but framed it as a concession on my part to something they had found. In fact I had been investigating it myself, was uncertain before they asked, but was waiting for clarification from Silicon Valley Power. The uncertainty centered around a substation named “Esparanca” that was proposed right behind the facilities as part of the stadium construction, but now appears to never have been built. I spent days in Silicon Valley Power’s records, and did eventually reach Silicon Valley Power for confirmation and indentified the mistake myself. I also gave them highly detailed documents on what we do know about those facilities: new equipment installed between 2010 and 2014, and load growth across the system with an inflection around 2013–2014, with the Northern Receiving Station carrying the highest capacity in the system and sitting closest to the data center corridor. None of that is in the episode. I have a separate piece about it coming out soon. *I cut 2 seconds from the raw audio to remove personal information that had no connection to anything in the episode. Appendix A: the passage the clip was taken from This is the sequence from my first interview, in full. The episode uses one fragment of it. It’s tricky because my understanding is that there’s something like a 15-year half-life on collagen remodeling issues. They’re going to get a new crop of players. What I really need, though, is for the injuries to be broken down so we can see the soft tissue injuries. Right now, they’re categorized as MSK injuries, but let’s say we can actually identify them more specifically. Is that right? He was able to do that? Oh, cool. I wasn’t able to find that information. Interesting — I didn’t know that data existed. I tried so hard to get it, and I didn’t know it was available. Maybe you could connect me with that person. That would be amazing. I’m not wedded to it being an EMF, honestly. I’m not. I would say that, to a certain extent, I’ve staked my reputation on the fact that it needs more study. It’s important to look into it, and I am not certain of anything. I’m not a scientist. To me, I find the mechanisms compelling. I will go back to the fact that I got into this not because of the 49ers, but because of clients I was working with who suffer from EDS, Ehlers-Danlos Syndrome, a tendon hypermobility issue. This condition is documented to be partially caused by oxidative stress. I’ve worked with them to mitigate their EMF exposure and have seen people improve. I think it’s a bigger story. In a way, the 49ers represent an occupational cluster with specific exposure risks. If someone would conduct a study on this, I believe we could learn a lot. Perhaps we would discover that it’s like, okay, maybe it’s 10% of the problem. I don’t know the exact number, but I think either way, conducting the study would provide valuable insights. To directly answer your question, it’s challenging for me because it’s part of a bigger story. If the 49ers move and stop having injuries, I might conclude that it was related to the substation. However, if they move and still experience injuries, I would want to analyze the nature of those injuries. Are they primarily soft tissue injuries? I don’t think it’s necessarily a case closed, but the story might lose traction at that point regardless. Three things are worth noting. The aired fragment stops immediately before the sentence in which I say I am not a scientist — the cut described in item 10. It also stops four paragraphs before the words “to directly answer your question.” What the episode plays is the throat-clearing. The actual answer, about what would change my mind, never airs. And two paragraphs in, I say the EMF might turn out to be ten percent of the problem. That is the ranking the episode says I never gave. Appendix B: the full email, July 6th, 1:39 PM Hi Rose, You asked me to send you some studies a couple of weeks ago. I apologize for the delay. I have been incredibly busy. I also wanted to give you a chance to dig in yourself, and get your own perspective before I influenced you too much with mine. That said, I do want to make sure that the actual argument is abundantly clear, so here it is! One note before I begin, there are really two separate questions here: Does the substation cause the soft-tissue injuries? That was my specific claim, and what the podcast is about. Is the theory biologically sound? Can 50/60 Hz fields at these levels do anything biological below the safety limits? Question two is why people have been calling me a conspiracy theorist. The regulatory and advisory bodies (ICNIRP, etc) maintain that anything below their exposure limits is biologically inert, and that position is broadly accepted within the mainstream, but the actual science paints a different picture. To defend my theory I’ve had to defend a much larger claim: that the advisory bodies have the biology wrong. I can’t honestly answer question 1 without first addressing that. Here’s is a simplified outline of my theory, with links to studies: 1. Advisory body thresholds for biological effects The ELF magnetic-field limits (ICNIRP’s ~2,000 mG public / 10,000 mG occupational) exist to prevent acute effects from exposure. If a magnetic field is strong enough, it makes nerves fire and muscles contract. Muscles twitch. You can see faint flashes of light in your vision. People can even feel tingling or even a shock. That happens due to Faraday’s law, which states that a time-varying magnetic field induces an electric field inside the body via the creation of Eddy currents.The standards assume that those currents do nothing below the twitch threshold. They do not consider chronic effects at all. My argument is that they are biologically active and do have chronic effects. 2. There are multipe ELF-EMF mechanisms for inducing oxidative stress. This is basic biophysics. Below are the two primary mechanisms. Simplest first. Dr. Paul Héroux of McGill has the most intuitive explanation, which rests on Maxwell’s principle of superposition: because Maxwell’s equations are linear, two sets of electromagnetic waves sharing the same space simply add together. In the interview I pictured a pebble dropped into a pond, sending out clean ripples. Then a boat motors past at distance, sending larger waves, and where they meet the ripples, the two add together and the original pattern gets distorted. In our cells, the mitochondria run on continuous currents of electrons and protons that carry their own faint electromagnetic fields. An external field from a substation, by the principle of superposition, adds to those internal currents and shifts the pattern. The electron transport chain in the mitochondria leaks a fraction of its electrons by design as reactive oxygen species (ROS), which act as signalling molecules in a healthy cell. Distorting that field increases that electron leakage, creating oxidative stress. A tiny electromagnetic interference results in a large downstream effect. https://www.sciencedirect.com/science/article/pii/S2405844025006474 The more complex pathway is Dimitris Panagopoulos’s Ion Forced-Oscillation / Voltage-Gated Ion Channel (IFO-VGIC) mechanism. Weak, polarized, low-frequency fields force the ions (calcium, potassium, sodium) next to an ion channel’s voltage sensor to oscillate; because that force scales with the inverse cube of the distance involved, fields far below the stimulation threshold can still force the channel open, disrupting the cell’s ion balance and driving ROS overproduction (Nitric oxide and superoxide interact and produce peroxynitrite, a highly unstable cytotoxin that breaks down into free radicals). https://www.researchgate.net/publication/366088934 https://www.spandidos-publications.com/ijo/59/5/92 https://www.mdpi.com/1422-0067/22/18/10041 https://www.frontiersin.org/journals/public-health/articles/10.3389/fpubh.2025.1585441/full https://pmc.ncbi.nlm.nih.gov/articles/PMC3772193/ 3. Evidence of oxidative stress, in vivo, in humans from ELF-EMF There are many studies, and the strongest are occupational, which applies to the 49ers situation. 115 power-plant workers vs. 145 office controls. Serum malondialdehyde (MDA, the standard lipid-peroxidation marker), superoxide dismutase, and catalase were all significantly higher in the exposed group, and the markers rose with increasing field exposure. https://journals.sagepub.com/doi/abs/10.3233/WOR-203244 A follow-up where they reversed the oxidative stress in power plant workers. A double-blind randomized controlled trial: 91 power-plant workers given vitamin E, vitamin C, both, or placebo for 90 days. The antioxidant groups showed reduced lipid peroxidation and raised antioxidant capacity versus controls. https://pubmed.ncbi.nlm.nih.gov/32191586/ A spot-welder study: 46 welders occupationally exposed at 50 Hz, showed significantly altered red-blood-cell antioxidant enzyme activity and concluded ELF-MF “might act as an oxidative stressor… even at the recommended levels of exposure.” https://pubmed.ncbi.nlm.nih.gov/18504600/ A substation-specific study found oxidative stress and DNA damage https://pubmed.ncbi.nlm.nih.gov/24460415/ 4. Oxidative stress degrades collagen This half isn’t controversial at all. Oxidative stress activates the matrix metalloproteinases (MMPs) that break collagen down and suppresses its synthesis. Here are three example studies: Siwik et al. 2001: Oxidative stress raises MMPs and lowers collagen synthesis in cardiac fibroblasts. https://pubmed.ncbi.nlm.nih.gov/11121376/ Fisher et al. 2009: Collagen fragmentation drives oxidative stress and elevates MMP-1 in aged human skin. https://pmc.ncbi.nlm.nih.gov/articles/PMC2631323/ Varani et al. 2006: Decreased collagen production in oxidatively aged skin. https://pubmed.ncbi.nlm.nih.gov/16723701/ 5. What about the study showing improved collagen synthesis I’m glad you asked this question, and I’m bummed we didn’t get to it in the interview because it is a great question, and very important to understand. Superficially it may appear to be a refutation of my theory, but I would argue that it actually supports the underlying argument. That study used a short, high-intensity pulsed dose: therapeutic-PEMF, the same type of field used clinically to stimulate bone and tissue healing. The reason this works is because it triggers the very same biological pathways that can lead to oxidative stress. The exposure still stimulates ROS production, but done at a controlled dosage, for a limited duration it has a different effect. The cell reads the ROS as a warning signal and it upregulates its antioxidant defenses, and mounts a repair/proliferation response. The therapy is then stopped before the cell gets overwhelmed. That is essentially a hormetic response: a small dose of a stressor producing a beneficial adaptation. Two things follow: At the very least, this means the field is biologically active, which by itself undercuts the regulatory claim that these fields are inert below their thresholds. There is a wealth of literature on PEMF (pulsed EMF) bone regeneration and calcium channel signalling (which is the second mechanims in section one). Here is one. https://www.nature.com/articles/srep13856 At best, it leads us straight to my actual concern, which is that under chronic, chaotic and unregulated exposure, the cell’s antioxidant capacity gets overwhelmed, resulting in oxidative stress. There are plentiful examples of things that are beneficial at controlled doses, but harmful at uncontrolled doses. Excecise is one obvious, uncontroversial example. Botox is perhaps a more interesting example. 6. What about a study that shows EMF causing collagen degradation in humans? As far as I am aware there is not a single study showing EMF-driven oxidative stress degrading collagen in a human, in vivo, or in human tendon in a lab. There are studies involving isolated fibroblasts though, which secrete collagen. The most relevant one showed that human fetal scleral fibroblasts exposed to 50 Hz ELF-EMF showed a significant decrease in collagen synthesis and that MMP-2 expression was upregulated, which is the exact mechanism I described in section 2. https://pmc.ncbi.nlm.nih.gov/articles/PMC3626379/ That’s it! Thanks again for the interview. Best, Peter Anthony Cowan Environmental Health · Wellness Tech · Researcher & Journalist Publisher & Editor, Living Energy Bio: petercowan.comSocial: X · Instagram · TikTokApp: sunlightis.lifePhone: [redacted]
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Good science requires much more than evidence
Empiricists believe that scientific theories are true only if they make correct empirical predictions: if we can't verify these predictions, then there is no reason to expect that they tell us anything about reality. However, Professor of Philosophy at King's College David Kyle Johnson argues that this is mistaken. In response to Bas van Fraassen, who has written on this subject for the IAI, he argues that we have many reasons for believing a theory to be true, such as it being parsimonious and having large scope — qualities which have been used throughout the history of science as criteria for judging theories. In 2024, Princeton philosopher Bas van Fraassen wrote a short article for IAI News entitled “Science Does not Describe Reality: The Limits and Benefits of Explanation.” At the time, I was working on two projects (a science book and a Great Course) that, when completed, would (among other things) defend science’s ability to describe reality. I wanted to write a response to van Fraassen, but the projects demanded too much of my attention. But now that those projects are complete, I am in a position to explain the objections to van Fraassen’s thesis. Summarizing van Fraassen’s argumentIn a nutshell, his argument is this: What scientists do is make predictions based on theories and then invite others to test to see whether those predictions are borne out. “If theory T is right, result R should happen in experimental condition C.” Many think that running an experiment that shows that R happens in condition C is proof that theory T is true (and should be believed). But, van Fraassen argues, that R happened in condition C is only a reason to think that R happens in condition C. That’s the only observable, or empirical, result we can actually see, so that is all that we are really justified in believing. (The underlying theory that made that prediction still may or may not be true.) That is why he calls those who accept his position “empiricists.”Before I explain what is wrong with this position, let me explain what it gets right. What van Fraassen Gets RightFirst, a theory correctly predicting the results of an experiment is not, strictly speaking, “proof” that the theory is correct. The basic line of reasoning is this:If the theory T is true, result R should happen. Result R did happen. Thus, theory T is true.In other words:“If T then R. R. Thus, T.”This is a deductively invalid, fallacious mode of reasoning, called “affirming the consequent.” Those premises do not guarantee that the conclusion follows. “If I am in Pennsylvania, then I am in the USA. I am in the USA. Thus, I am in Pennsylvania.” Clearly that argument doesn’t guarantee its conclusion; neither does the above argument.However, science is not a deductive method of reasoning; it is an inductive one. And inductive arguments merely try to raise the probability of their conclusion, not “prove” them for certain. Thus, the fact that an experimental result doesn’t prove a theory is true is irrelevant; it’s not supposed to. That is not what scientific reasoning is about.___If the hypothesis that something exists clearly provides the best explanation for what we can observe, then the belief that it exists is what is rational.___Second, it’s also true that a single experimental result doesn’t provide enough justification to believe that a theory is true. Scientists do not come to a consensus about whether a theory is true by looking at a single experiment; they look at all the evidence to determine where the preponderance of evidence points. The mere fact that I am in the USA raises the probability that I am in Pennsylvania, but not nearly enough to conclude that I am in Pennsylvania. However, if I am also regularly encountering people wearing Eagles and Phillies hats and seeing advertisements for Founding Father tours, I probably am. In the same way, a theory successfully predicting the outcome of one experiment is not enough to conclude that it is true; but if a theory makes a wide variety of predictions that are all vindicated by multiple experiments, performed by many different groups and people, all actively trying to prove the theory false (which is what good scientific experiments are designed to do)—that is a good reason to conclude that the theory is true. In other words, if you repeatedly try to prove something false but can’t, that is a very good indication that it isn’t. The problem of underdeterminationIn reply, those whom van Fraassen calls “empiricists” often point to the “problem of underdetermination.” For any given theory that makes successful predictions about what happens in experimental conditions, there are countless other possible theories that make exactly the same predictions—and since they do, the experimental evidence in question is just as much reason to accept any of those theories as it is to accept our original one. Thus, the argument goes, we have no way of knowing whether our original theory is true, or one of the other “predictively equivalent” theories is true. SUGGESTED VIEWING How Occam's Razor changed the world With Johnjoe McFadden As an example of underdetermination, philosophers often offer this example. The evidence of fossils seems to provide reason to conclude that the universe is quite old; ancient fossils are what the “ancient universe” hypothesis predicts. But it’s also possible that God created an ancient-looking universe 200 years ago, complete with a “fake” fossil record for us to find, to make it look old. The existence of fossils is what that theory predicts too. So, the argument goes, the fossil record can’t be used as evidence that the universe is ancient; the fossil record supports the “200-year-old ancient-looking universe” theory just as much. The problem of underdetermination points out that, for any theory with supporting evidence, we could invent another completely different theory that predicts exactly the same evidence, and thus undermine that evidence’s ability to support the original theory.But this “argument from underdetermination” betrays a fundamental misunderstanding of what scientific reasoning is and how it works. To explain, let me use another rather strange (but very real and commonly discussed) philosophical thought experiment called “The Grue Problem.” The “Grue” ProblemSuppose I want to know what color emeralds are, so I observe a few, see that they all appear green, and form the theory that “all emeralds are green.” I thus predict that the next 100 emeralds I find will also appear to be green. And let’s say that happens, and so I thus conclude that my theory that all emeralds are green is true. Now, one might rightly point out that I don’t know for sure that all emeralds are green—I have not seen them all. Maybe some I haven’t found yet are blue. Fair enough. After all, we used to think that all swans were white, until we found some black ones. But let’s say that I go on a quest and collect every emerald in the universe—and, for the sake of the argument, let’s say I can do this, and can even know that I have every one of them. So, I collect them all, look at them all, and verify that they all appear green. Can’t I now rightly conclude that all emeralds are green?Inspired by the problem of underdetermination, a friend might argue that I cannot.Sure, they all appear green now—but there could be another kind of color called “grue.” Something is grue if it is green up to a certain point in time, but then spontaneously turns blue. And there could be an infinite number of “shades” of grue. Something that is one shade of grue will turn blue at noon today, but something that is another shade of grue will turn blue at noon tomorrow, etc. So yes, the emeralds appear green now; and since they haven’t turned blue yet, they are not some “past” shade of grue. But they might be some “future” shade of grue (e.g., they may turn blue at noon tomorrow). And since all future shades of grue are consistent with “being green up to this point in time,” the evidence you have is completely consistent with the notion that all emeralds are some future shade of grue, rather than green. Indeed, that they would appear green until now is what the “some future shade of grue” hypothesis predicts. So, we have just as much reason to conclude that all emeralds are some shade of grue as we do to conclude that they are green.You’re probably thinking “It’s not equally possible that the emeralds are grue; they are obviously green.” You are right! But explaining why your instinctive reaction to my friend’s argument is correct will help inform why van Fraassen’s “empiricist” is wrong and science actually does describe reality.The main mistake my friend makes is in thinking that the “empirical evidence” (of all the emeralds appearing green) is (or even should be) all I am using to draw the conclusion that all emeralds are green. It is not. I am also considering known facts about how colors typically work; things don’t usually change color, and when they do, they don’t do so suddenly, without cause, and all at once. So, even though the simple evidence of the emeralds all appearing green up to this point is consistent with them being some future shade of grue—that is even what the grue hypothesis “predicts”—it is still exceedingly unlikely that they are. The hypothesis that they are green is much more likely. Understanding science refutes the problem of underdetermination The misunderstanding about science that the “empiricist” pointing to “the problem of underdetermination” makes is similar to the one that my friend made. Science is not just about considering experimental evidence; in fact, it’s not even just about considering empirical evidence. As Ernan McMullin and many other philosophers of science have pointed out, the inference that makes science is “inference to the best explanation” (sometimes called “abduction” or “retroduction” by McMullin). While, depending on the circumstances, scientists use many different kinds of reasoning, science as a whole is, simply put, the process of considering multiple competing explanations and comparing them to certain criteria—explanatory criteria (the kinds of things explanations must be and do, by definition, to be a good explanation)—to see which explanation is the best.And these criteria do not deal only with empirical results. Yes, successful predictions raise the probability of a hypothesis, but it’s also the case that the more new assumptions a theory makes, the less likely it is to be true; every new assumption presents an opportunity for the theory to be false. (The fewer assumptions a theory makes, the simpler or “more parsimonious” it is said to be.) Likewise, the more existing evidence a theory contradicts, the less likely it is, because in order for a theory to be true, every piece of evidence it contradicts has to be somehow faulty. (The fewer established theories a new theory contradicts, the more “conservative” it is said to be.) And, obviously, the more something explains, the better explanation it is. (This is called having “scope.”) If a theory raises unanswerable questions, it’s not expanding our understanding, and thus is not wide-scoping. Scientists consider all these things when deciding which theory to accept, because the theory that adheres best to these explanatory criteria is most likely to be true.___the mere fact that a theory’s predictive success is why it “sticks around” or “becomes accepted” in the scientific community is not a reason to be skeptical about its truth.___The reason the grue hypothesis is no good is because it invents an entirely new kind of color—not just a new shade, but an entirely different category of color (a different way colors work)—and thus is not parsimonious. It raises unanswerable questions about how and why emeralds would just spontaneously change from green to blue (and thus does not have wide scope). And it contradicts what is already well established about how color works (and thus is unconservative).The theories that the problem of underdetermination points to do the same thing. Yes, the theory that God created an “ancient-looking universe” (complete with an ancient-looking fossil record) two hundred years ago is also consistent with the empirical evidence (of a fossil record) that presently exists; but that theory is monumentally unparsimonious (it requires many extra assumptions about infinite entities) and not wide-scoping (it raises unanswerable questions about why God would do such a thing). So, I can rationally conclude that it is false.Indeed, the history of science includes many examples of theories that were rejected because they lacked parsimony and/or scope, even before their falsity (and the truth of their competing theory) was confirmed by observation. As I point out in my book, geocentrism was rejected by the scientific community because it lacked parsimony, almost 200 years before the observation of parallax confirmed that the Earth moves around the sun. And the continuum theory of matter was completely rejected by 1860, because it couldn’t explain chemical reactions or organize matter into a periodic table, even though the experiments that eventually confirmed atomic theory weren’t even proposed until the 1870s. Solving the best of a bad lot problemIn response, the “empiricists” are likely to object, this time pointing to the “best of a bad lot” problem. “We have no reason to conclude that an explanation that has been shown to be better than others is true because we have no guarantee that the true theory was among those that we were considering.” If you have a “lot” (a collection) of poor explanations, even the best one is not true.The responses to this problem, however, are numerous. Peter Lipton argues that the set of hypotheses that scientists consider are not just randomly selected and thus unlikely to contain a theory that is true; they use existing knowledge to home in on what is most likely to be true. A doctor trying to explain abdominal pain is not going to bother wondering whether demons are causing it; they are going to stick with things like appendicitis and kidney stones, because they are most likely. Further, despite its name, inference to the best explanation is not just the process of comparing hypotheses and accepting the best one; we also want one that is a good explanation in its own right. If it’s not, we are going to keep looking until we find an explanation that is. And while that process does not guarantee that we will come across the exact truth, it’s very likely that the theory that emerges as the best will be at least approximately true, and thus we will be justified in believing it. And lastly, as I point out in my book, although many theories not based in scientific evidence (like geocentrism and continuum theory) have been completely overturned, science almost always progresses by the refinement of scientifically established theories—not their replacement. (Although our sun is not the center of the universe, heliocentrism was our first step in understanding the Earth’s true place in the universe.) So even if a theory we accept today may not be completely right, accepting it is a step on the journey toward the complete truth. The example of atomic theoryNow, it’s worth pointing out that most empiricists are not skeptical of all scientific theories; they are only skeptical of the ones that hypothesize the existence of “unobservables.” It’s not like they think that round Earth, heliocentrism, and germ theory are just useful (but untrue) “instruments” for making predictions about how to most efficiently navigate the seas, predict planetary motion, and treat diseases. They admit that the Earth actually is round, that the planets revolve around the sun, and that germs exist and cause disease. These facts and entities can be observed; the theories that suggest they exist are true. It’s only when theories start hypothesizing the existence of unobservables—like electrons, or quantum fields—that can’t be observed directly, that we should start doubting the theories’ truth. And to be fair to van Fraassen, in this published work, he doesn’t really say that we should doubt the truth of such theories. Only that scientific reasoning does not rationally force us to accept them as true. Skepticism, or agnosticism, he argues, is warranted. SUGGESTED READING Science is based in metaphor By Andrew Reynolds But the history of atomic theory throws a monkey wrench into that argument. Atoms used to be unobservable; again, scientists first accepted the theory that they exist because it had such grandiose explanatory power. But then atoms were seen with electron microscopes. They thus moved into the category of the observable. But this didn’t substantially change anything about what scientists were justified in believing; it certainly didn’t change any “atomic skeptics’” minds. It just confirmed what everyone already knew! If the hypothesis that something exists clearly provides the best explanation for what we can observe, then the belief that it exists is what is rational. The fact that the thing itself is not technically observable does not make doubting its existence rational.What’s more, the atoms were seen with an electron microscope. But electrons are themselves unobservable. How can an electron microscope reveal an atom if electrons are not real? This leads us to what is famously known as Hilary Putnam’s “miracle argument.” It’s (not) a miraclePhilosopher Hilary Putnam’s miracle argument is somewhat famous. Basically, he argued that a scientific theory being able to repeatedly make successful predictions—even about unobservables—without being at least approximately true would require a “miracle.” In other words, it would be such an improbable occurrence that it could not rationally be believed—the better explanation for why scientific theories about unobservables make the right predictions is because the unobservable entities and structures they hypothesize exist.Van Fraassen has addressed this argument. Indeed, in his original article, where he references Alison Gopnik’s point about orgasms not being “necessary for procreation” even though the desire for orgasm “drives the creation of progeny,” he is pointing to his own argument about how organisms are not naturally selected by evolution to get true beliefs; to the extent that belief-forming processes are selected for, the ones that are selected are the ones that are useful for survival—not the ones that produce true beliefs. In the same way, van Fraassen argues, scientific theories are accepted, not because they are true, but because they aren’t falsified; they make successful predictions; that’s what makes them “stick around.” So, the fact that they make successful predictions (and thus became accepted) is not a reason to think they are true.This argument is similar to C. S. Lewis’s “argument from reason,” which he used to argue against evolution: “The truth of evolution undercuts our ability to know that it is true.” Lewis’ argument famously failed; Elizabeth Anscombe, by Lewis’s own admission, demolished Lewis in a debate on the topic, and I have explained elsewhere why modified versions of the argument fail as well. In short, it’s because it fails to recognize that a belief-forming process can make an organism more likely to survive because it reliably produces true beliefs. It is therefore not the case that beliefs generated by naturally selected belief-forming processes are automatically false or unjustified.In the same way, the reason a theory “sticks around” could be because it’s not falsified, because it “makes correct predictions.” But the reason it makes correct predictions is most likely because it is true. (In pointing this out, I am echoing the arguments of Musgrave, Lipton, Psillos, and Kitcher, who refuted van Fraassen’s argument and analogy long before his 2024 article.) It would be a huge coincidence that it could do so without being true. And that is the point of Putnam’s miracle argument. Thus, contrary to van Fraassen’s suggestion, the mere fact that a theory’s predictive success is why it “sticks around” or “becomes accepted” in the scientific community is not a reason to be skeptical about its truth. ConclusionLet me close by saying something about the fact that empiricists don’t doubt the truth of all scientific theories, just the ones that hypothesize unobservables. In today’s society, this theory is dangerous to espouse publicly. The nuance between being skeptical about all of science, and just the highly technical theories about unobservables, is guaranteed to be lost to the average reader. And there is so much unjustified skepticism and doubt about the findings of science and experts that a headline like “Science Does Not Describe Reality” could easily fuel the anti-science movement, worsen climate change denial and cause the next pandemic.This is why I believe it was important to still respond to van Fraassen’s article, a full two years after he wrote it. Not only, as I have argued, does it represent a philosophically inaccurate view of how scientific reasoning works and what scientific reasoning can do, but it is a dangerous view to boot. It should thus be rejected.
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