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A Front Desk That Never Sleeps
One job where AI chatbots have proven their utility is 24-hour customer service for all manner of businesses.
Scientists Test an Unexpected Sleep Aid Made From Tree Roots
A pilot study suggests that oil from underused Hinoki roots could be used in scented products for relaxation. Falling asleep can be compared to easing down a dimmer switch, with brain activity gradually shifting as sleep deepens. Researchers studying Hinoki, or Japanese cypress, are exploring whether its scent could help smooth that transition for women
Health Tech Keeps Choosing Violence
Last week was an absolute dump of health tech litigation mayhem, with enough new filings to make my wife seriously question my bedtime reading. Here’s what’s inside: OpenEvidence v. Doximity: Doximity didn’t wait for the deadline. It wants OpenEvidence’s case thrown out entirely, and its motion adds some awkward details about vanished Slack data and borrowed NPIs. Plus, Epic v. Apple offers a look at what a normal discovery fight looks like. Texas v. Epic: Epic took another shot at the State’s antitrust pleadings, asking the court to make Texas spell out how its employment restrictions harm competition and why Texas law reaches a Wisconsin company’s noncompetes. Veeva v. Epic: The two Wisconsin law professors finally weighed in on whether a would-be employer can challenge someone else’s noncompete. Audacious Inquiry v. CRISP: Our sleepy patent case just evolved into a much more interesting form, with CRISP firing back with attempted monopolization and information blocking counterclaims. Cognizant v. Infosys: After weeks of emails and phone calls, I finally have Judge Starr’s sealed ruling on Infosys’s antitrust counterclaims. Some survived, offering clues about where the Epic (and other system of record) antitrust cases stand their best chance OpenEvidence v. Doximity
China's space diplomacy lifts Pakistani astronaut toward orbit
Two Pakistani pilots are memorising Mandarin, spinning in centrifuge drills and learning to eat, sleep and repair equipment while weightless as a decision nears on which one will become the first foreign astronaut aboard China's Tiangong space station.
Coffee Could Be Messing With Your Sleep—Even When You Drink It the ‘Right’ Way
A new study yields some surprising findings.
Why rheumatoid arthritis pain may persist even when inflammation is under control
Pain and fatigue in rheumatoid arthritis can persist even after inflammation improves, with depression, poor sleep, obesity, smoking, and chronic pain potentially helping sustain symptoms. Researchers say identifying these hidden drivers could prevent unnecessary medication changes and lead to more personalized treatment.
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.. [1] Intel, “Intel Tech Tour 2025 Panther Lake recap,” Doc. 866361, 2025. Accessed: Sep. 14, 2026. [Online]. Available: https://cdrdv2-public.intel.com/866361/ITT_2025_Panther_Lake_Recap1.pdf [2] Intel, “Core Ultra processors Series 3 datasheet, volume 1,” Doc. 872188-001, Jan. 2026. Accessed: Sep. 14, 2026. [Online]. Available: https://cdrdv2-public.intel.com/872188/872188-001.pdf [3] N. Horiguchi and E. Beyne, “Backside power delivery: How to power chips from the backside,” imec Reading Room, Nov. 25, 2022. Accessed: Sep. 14, 2026. [Online]. Available: https://www.imec-int.com/en/articles/how-power-chips-backside [4] W. Hafez et al., “Intel PowerVia technology: Backside power delivery for high density and high-performance computing,” in Proc. IEEE Symp. VLSI Technol. Circuits, Kyoto, Japan, Jun. 2023, pp. 1–2, doi: 10.23919/vlsitechnologyandcir57934.2023.10185208. [5] K. Fischer et al., “Intel 18A platform technology featuring RibbonFET (GAA) and PowerVia for advanced high-performance computing,” in Proc. Symp. VLSI Technol. Circuits, Kyoto, Japan, Jun. 2025, pp. 1–3, doi: 10.23919/vlsitechnologyandcir65189.2025.11075006. [6] K.-F. Cheng, C.-L. Teng, H.-Y. Huang, and H.-C. Chen, “Metal oxide composite as etch stop layer,” U.S. Patent 12 176 247 B2, Dec. 24, 2024. Accessed: Sep. 14, 2026. [Online]. Available: https://patents.google.com/patent/US12176247B2/en [7] S. W. King, “Dielectric barrier, etch stop, and metal capping materials for state of the art and beyond metal interconnects,” ECS J. Solid State Sci. Technol., vol. 4, no. 1, pp. N3029–N3047, 2015, doi: 10.1149/2.0051501jss. [8] A. V. Mule’, D. J. Towner, D. Seghete, C. R. Ryder, and A. A. Gonzalez, “Multi-layer etch stop layers for advanced integrated circuit structure fabrication,” U.S. Patent Appl. 20220102343 A1, Mar. 31, 2022. Accessed: Sep. 14, 2026. [Online]. Available: https://patents.google.com/patent/US20220102343A1/en [9] C.-C. Wang and J. H. Wang, “Interconnect structure with dielectric cap layer and etch stop layer stack,” U.S. Patent Appl. 20230253247 A1, Aug. 10, 2023. Accessed: Sep. 14, 2026. [Online]. Available: https://patents.google.com/patent/US20230253247A1/en [10] Y. J. Wu, K.-F. Cheng, C.-C. Lee, H.-K. Chang, and H.-Y. Huang, “Etch stop layer for interconnect structures,” U.S. Patent Appl. 20240332070 A1, Oct. 3, 2024. Accessed: Sep. 14, 2026. [Online]. Available: https://patents.google.com/patent/US20240332070A1/en [11] M. G. Rainville, N. Shankar, K. S. Reddy, and D. M. Hausmann, “Deposition of aluminum oxide etch stop layers,” U.S. Patent Appl. 20180197770 A1, Jul. 12, 2018. Accessed: Sep. 14, 2026. [Online]. Available: https://patents.justia.com/patent/20180197770 [12] J. S. Leib et al., “Conductive lines having molybdenum liner and tungsten fill for advanced integrated circuit structure fabrication,” U.S. Patent Appl. 20240429126 A1, Dec. 26, 2024. Accessed: Sep. 14, 2026. [Online]. Available: https://patents.justia.com/patent/20240429126 [13] M. Naik, “Cobalt enables power and performance scaling at single-digit logic nodes,” Applied Materials, Dec. 17, 2018. Accessed: Sep. 14, 2026. [Online]. Available: https://www.appliedmaterials.com/us/en/blog/blog-posts/cobalt-enables-power-and-performance-scaling-at-single-digit-logic-nodes.html [14] Lam Research, “Breaking through AI’s invisible barrier with molybdenum,” Lam Research Newsroom, May 6, 2025. Accessed: Sep. 14, 2026. [Online]. Available: https://newsroom.lamresearch.com/molybdenum-metallization-ai-revolution [15] P. Yashar, G. Malyavanatham, and H. Vijwani, “Integrated circuit interconnect structures with niobium barrier materials,” U.S. Patent Appl. 20240112951 A1, Apr. 4, 2024. Accessed: Sep. 14, 2026. [Online]. Available: https://patents.google.com/patent/US20240112951A1/en [16] Applied Materials, “Applied Materials unveils chip wiring innovations for more energy-efficient computing,” Applied Materials Investor Relations, Jul. 8, 2024. Accessed: Sep. 14, 2026. [Online]. Available: https://ir.appliedmaterials.com/news-releases/news-release-details/applied-materials-unveils-chip-wiring-innovations-more-energy [17] Samsung, “Samsung showcases AI-era vision and latest foundry technologies at SFF 2024,” Samsung Semiconductor, Jun. 13, 2024. Accessed: Sep. 14, 2026. [Online]. Available: https://semiconductor.samsung.com/news-events/news/samsung-showcases-ai-era-vision-and-latest-foundry-technologies-at-sff-2024/ [18] C. W. Yeung et al., “Channel geometry impact and narrow sheet effect of stacked nanosheet,” in Proc. IEEE Int. Electron Devices Meeting (IEDM), Dec. 2018, pp. 28.6.1–28.6.4, doi: 10.1109/iedm.2018.8614608. [19] S. Mochizuki et al., “Evaluation of (110) versus (001) channel orientation for improved nFET/pFET device performance trade-off in gate-all-around nanosheet technology,” in Proc. Int. Electron Devices Meeting (IEDM), Dec. 2023, pp. 1–4, doi: 10.1109/iedm45741.2023.10413854. [20] D. G. Ouellette et al., “Fabrication of gate-all-around integrated circuit structures having molybdenum nitride metal gates and gate dielectrics with a dipole layer,” U.S. Patent 12 051 698 B2, Jul. 30, 2024. Accessed: Sep. 14, 2026. [Online]. Available: https://patents.google.com/patent/US12051698B2/en [21] imec, “Advancing the CFET-based device roadmap with novel integration modules and standard-cell architectures,” imec, 2026. Accessed: Sep. 14, 2026. [Online]. Available: https://www.imec-int.com/en/articles/advancing-cfet-based-device-roadmap-novel-integration-modules-and-standard-cell [22] A. Reznicek, X. Miao, C. Lee, and J. Zhang, “Wrap around contact for nanosheet source drain epitaxy,” U.S. Patent 11 302 813 B2, Apr. 12, 2022. Accessed: Sep. 14, 2026. [Online]. Available: https://patents.google.com/patent/US11302813B2/en [23] J. A. Kittl, J. G. Hong, D. R. Palle, and M. S. Rodder, “Methods for varied strain on nano-scale field effect transistor devices,” U.S. Patent 9 978 833 B2, May 22, 2018. Accessed: Sep. 14, 2026. [Online]. Available: https://patents.google.com/patent/US9978833B2/en [24] S. Gandikota et al., “Method of reducing metal gate resistance for next generation NMOS device application,” Int. Patent Appl. WO 2024/137272 A1, Jun. 27, 2024. Accessed: Sep. 14, 2026. [Online]. Available: https://patents.google.com/patent/WO2024137272A1/en [25] J. Zhang et al., “Full bottom dielectric isolation to enable stacked nanosheet transistor for low power and high performance applications,” in Proc. IEEE Int. Electron Devices Meeting (IEDM), Dec. 2019, pp. 11.6.1–11.6.4, doi: 10.1109/iedm19573.2019.8993490. [26] C. Yoo, J. Chang, Y. Seon, H. Kim, and J. Jeon, “Analysis of self-heating effects in multi-nanosheet FET considering bottom isolation and package options,” IEEE Trans. Electron Devices, vol. 69, no. 3, pp. 1524–1531, Mar. 2022, doi: 10.1109/ted.2022.3141327. [27] S. S. Pradhan, D. B. Bergstrom, J.-S. Chun, and J. Chiu, “Tungsten gates for non-planar transistors,” European Patent Appl. EP 3 506 367 A1, Jul. 3, 2019. Accessed: Sep. 14, 2026. [Online]. Available: https://patents.google.com/patent/EP3506367A1/en [28] L. Schloss and X. Ba, “Tungsten films having low fluorine content,” U.S. Patent 9 754 824 B2, Sep. 5, 2017. Accessed: Sep. 14, 2026. [Online]. Available: https://patents.google.com/patent/US9754824B2/en [29] Intel Foundry, “Accelerating AI and HPC with advanced process and packaging technologies,” Doc. 367370-001US, Jun. 2026. Accessed: Sep. 14, 2026. [Online]. Available: https://www.intel.com/content/dam/www/central-libraries/us/en/documents/2025-11/intel-foundry-hpc-ai-brief.pdf [30] M. Lofrano, X. Chang, H. Oprins, and Z. Tokei, “Mitigating the thermal bottleneck in advanced interconnects,” imec, Sep. 28, 2023. Accessed: Sep. 14, 2026. [Online]. Available: https://www.imec-int.com/en/articles/mitigating-thermal-bottleneck-advanced-interconnects [31] S. Bair, “Intel at ISSCC 2025: Navid Shahriari invited talk, eight papers, forums, panelist & product details,” Intel Community, Feb. 19, 2025. Accessed: Sep. 14, 2026. [Online]. Available: https://community.intel.com/t5/Blogs/Tech-Innovation/Edge-5G/Intel-at-ISSCC-2025-Navid-Shahriari-Invited-Talk-Eight-Papers/post/1667592 [32] D. Chandra, E. Potladhurthi, D. R. S. Reddy, and K. S. Rengarajan, “Tunable negative bitline write assist and boost attenuation circuit,” U.S. Patent Appl. 20160203857 A1, Jul. 14, 2016. Accessed: Sep. 14, 2026. [Online]. Available: https://patents.google.com/patent/US20160203857A1/en [33] Synopsys, “Advantages of firmware-based training in high-speed DDR IP,” Synopsys IP Technical Bulletin. Accessed: Sep. 14, 2026. [Online]. Available: https://www.synopsys.com/articles/firmware-based-training-ddr-ip.html [34] N. Muralimanohar, R. Balasubramonian, and N. P. Jouppi, “CACTI 6.0: A tool to understand large caches,” Hewlett-Packard Laboratories, 2009. Accessed: Sep. 14, 2026. [Online]. Available: https://users.cs.utah.edu/~rajeev/cacti6/cacti6-tr.pdf [35] Intel, “Intel Tech Tour 2024 Lunar Lake AI hardware accelerators,” Doc. 824436, 2024. Accessed: Sep. 14, 2026. [Online]. Available: https://cdrdv2-public.intel.com/824436/2024_Intel_Tech%20Tour%20TW_Lunar%20Lake%20AI%20Hardware%20Accelerators.pdf [36] Y.-H. Chen, J. Emer, and V. Sze, “Eyeriss: A spatial architecture for energy-efficient dataflow for convolutional neural networks,” in Proc. 43rd ACM/IEEE Annu. Int. Symp. Comput. Archit. (ISCA), Jun. 2016, pp. 367–379, doi: 10.1109/isca.2016.40. [37] Intel, “Introduction to the Xe-HPG architecture,” Doc. 758306, Nov. 4, 2022. Accessed: Sep. 14, 2026. [Online]. Available: https://www.intel.com/content/www/us/en/developer/articles/technical/introduction-to-the-xe-hpg-architecture.html [38] Intel, “Core Ultra processors Series 3 for the edge,” Doc. 855291. Accessed: Sep. 14, 2026. [Online]. Available: https://cdrdv2-public.intel.com/855291/Intel%C2%AE%20Core%E2%84%A2%20Ultra%20Processors%20Series%203%20for%20Edge%20Overview_2.pdf [39] Intel Foundry, “Foveros technology brief,” Doc. 366411-001US, Feb. 2026. Accessed: Sep. 14, 2026. [Online]. Available: https://www.intel.com/content/dam/www/central-libraries/us/en/documents/2025-07/foveros-25d-product-brief.pdf [40] D. Das Sharma, “UCIe: Building an open chiplet ecosystem,” UCIe Consortium, 2022. Accessed: Sep. 14, 2026. [Online]. Available: https://www.uciexpress.org/_files/ugd/0c1418_c5970a68ab214ffc97fab16d11581449.pdf [41] Intel, “Intel launches Intel Core Series 3 processors,” Intel Newsroom, Apr. 16, 2026. Accessed: Sep. 14, 2026. [Online]. Available: https://www.intel.com/content/www/us/en/newsroom/news/client-computing/intel-launches-intel-core-series-3-processors-changing-the-game-for-everyday-computing.html [42] Intel, “Core Series 3 launch press deck,” Apr. 2026. Accessed: Sep. 14, 2026. [Online]. Available: https://download.intel.com/newsroom/2026/Intel-Core-Series-3/Intel-Core-Series-3-Launch-Press-Deck.pdf [43] Intel, “Intel outlines architectures for agentic AI at Hot Chips 2026,” Intel Newsroom, Aug. 24, 2026. Accessed: Sep. 14, 2026. [Online]. Available: https://www.intel.com/content/www/us/en/newsroom/news/client-computing/intel-outlines-architectures-for-agentic-ai-at-hot-chips-2026.html [44] Intel, “Intel accelerates process and packaging innovations,” Intel Investor Relations, Jul. 26, 2021. Accessed: Sep. 14, 2026. [Online]. Available: https://www.intc.com/filings-reports/all-sec-filings/content/0001193125-21-224438/d199788dex991.htm [45] Intel, “Intel reports third-quarter 2021 financial results,” Intel Investor Relations, Oct. 21, 2021. Accessed: Sep. 14, 2026. [Online]. Available: https://www.intc.com/news-events/press-releases/detail/1505/intel-reports-third-quarter-2021-financial-results [46] Intel, “3rd generation Intel Core processors bring exciting new experiences and fun to the PC,” Intel Investor Relations, Apr. 23, 2012. Accessed: Sep. 14, 2026. [Online]. Available: https://www.intc.com/news-events/press-releases/detail/577/3rd-generation-intel-core-processors-bring-exciting
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Teen suicide risk hit a 10-year low in 2025. Guns, sexual violence, and self-harm. Where are the 2025 data on transgender teens? Missing data changes public health policy. Teen suicide risk hit a 10-year low in 2025. CDC asked more than 10,000 high school students over 100 questions in spring 2025. Yesterday, it published a report covering a fraction of them. The report focsed on five areas: diet, physical activity, sleep, digital behaviors, and mental health, reflecting the priorities of the Make America Healthy Again movement. There was good news. Fewer teens seriously considered suicide in 2025 than in any survey year since 2015: 14%, down from 20% in 2023. Sadness fell. Underlying Conditions is a reader-supported publication. To receive new posts and support my work, consider becoming a free or paid subscriber. Subscribe Sports participation, which dipped to 49% in 2021, is back to its 2015 level of 58%. Daily PE fell from 27% to 20% in two years, while fewer students eat breakfast daily than a decade ago. Guns, sexual violence, and self-harm. The questionnaire is public, and it goes well beyond those five areas. Students answered questions about sexual violence, self-harm, and whether they got help when they felt sad or anxious. They said how quickly they could get a loaded gun. They reported whether food ran out at home and whether they felt close to people at school. There were questions about sexual identity, including whether they were transgender. The report did not publish any of the answers students gave to those questions. CDC posts the raw survey data online, so anyone can see what the report left out. The report doesn’t cover the health of sexual minority students. Among students who identified as gay, lesbian, bisexual, questioning, or another non-straight identity, persistent sadness fell from 66% to 57% between 2023 and 2025. Serious thoughts of suicide fell from 41% to 30%. Those drops were bigger than the ones among straight students, although the gap remains wide: 28% of straight students reported persistent sadness, about half the rate of LGBQ+ students. About 1 in 7 girls reported sexual violence in the past year. One in 6 students hurt themselves on purpose. Among students who needed help for sadness or anxiety, half rarely or never got it. And among students who had seriously considered suicide, 43% said they could get a loaded gun without an adult’s permission. One protective factor rose sharply. In 2023, 55% of students said they felt close to people at their school; in 2025, 63% did. CDC’s earlier research ties that kind of connection to better mental health. Where are the 2025 data on transgender teens? In 2023, CDC's national survey asked high school students, for the first time, whether they were transgender. Their answers are the only nationally representative data on transgender teens, and their mental health is by far the worst of any demographic. That year, 71% of transgender students reported persistent sadness, 54% seriously considered suicide, and 26% attempted it, compared with 38%, 18%, and 8% of cisgender students. But we don’t have 2025 data. The timing matters because students took the survey in spring 2025, as federal policy toward transgender youth shifted. On January 28th, an executive order directed agencies to end federal support for gender-affirming care for people under 19, and several hospitals paused that care within days. In February, the CDC said it would no longer process transgender identity data. Later in 2025, the Supreme Court upheld Tennessee’s ban on gender-affirming care for minors, and HHS ended the 988 Lifeline’s dedicated line for LGBTQ+ youth. Researchers disagree about how much state policy shapes trans teens’ mental health. A 2024 Trevor Project study estimated that anti-trans laws increased suicide attempts among trans and nonbinary youth. Critics dispute its methods and its estimates. The 2025 survey could have added national evidence to that fight. CDC collected the data but hasn’t publicly released it. Missing data changes public health policy. Surveillance works as a feedback loop. It can show officials whether their policies help or hurt. The CDC didn’t provide data on the students most exposed to transgender policy shifts. The report kept measures that frame health as personal choice, like fruit, breakfast, and sports. It left out measures that track policy, like gun access, mental healthcare, food at home, and school climate, all of which respond to what legislators and agencies decide. HHS did not respond to questions that I sent on September 21st.
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Culturally Relevant Cardiovascular Disease Prevention and Care Strategies
(Feature Impact) Driven by rising rates of obesity, diabetes, high blood pressure and other risk factors, cardiovascular disease has surpassed cancer as the leading cause of death among Hispanic adults in the United States. googletag.cmd.push(function() { googletag.display('fixed-big-ad-top-asset'); }); Hispanic people represent nearly 1 in 5 of the U.S. population and are the nation’s largest ethnic minority group, yet many continue to face barriers to achieving heart health and accessing high-quality healthcare. A new scientific statement published in the American Heart Association’s flagship journal, “Circulation,” revealed how social, economic, cultural and environmental factors contribute to persistent disparities in cardiovascular health, calling for culturally tailored prevention strategies, equitable access to care and greater representation of Hispanic populations in cardiovascular research.“Hispanic populations in the U.S. are incredibly diverse even within their own communities with differences in genetic ancestry, language, cultural traditions and social experiences that can significantly influence cardiovascular health,” said Johanna Contreras, M.D., M.Sc., FAHA, director of the Division of Heart Failure and medical director of the Hispanic Heart Center within the Mount Sinai Health System. “Yet Hispanic people remain underrepresented overall in the research that guides prevention and treatment strategies… Without better representation and more detailed data, we risk overlooking important differences that can help us improve care and save lives.”Hispanic Cardiovascular Health by the NumbersCardiovascular risk factors – obesity (nearly 46%), type 2 diabetes (15.5%) and high blood pressure (approximately 44%) – are prevalent among Hispanic adults and often emerge at younger ages and occur more frequently among Hispanic adults compared with white adults.According to the report, only about 1 in 5 Hispanic adults achieves ideal cardiovascular health as defined by the American Heart Association’s original Life’s Simple 7 metrics. Updated analyses using the Life’s Essential 8 framework demonstrated persistent disparities for heart and brain health, as well as suboptimal dietary quality, sleep patterns and levels of physical activity.Social and Economic Barriers MatterBiology alone does not explain cardiovascular health disparities. The environments where people live, work and age, along with social and economic challenges, impact heart health. In fact, approximately 17% of Hispanics live below the federal poverty threshold, compared with 8.2% of white adults. googletag.cmd.push(function() { googletag.display('fixed-big-ad-middle-asset'); }); “Many Hispanic adults face obstacles that extend far beyond the doctor’s office,” Contreras said. “Limited health insurance coverage, language differences, food insecurity, environmental exposures and concerns related to immigration status can make it more difficult to prevent disease, manage chronic conditions and receive timely treatment.”Contreras emphasized the cultural values and practices of Hispanic people also influence how they perceive their health and healthcare options.“Family plays a central role in many Hispanic communities and can be an extraordinary source of strength, support and resilience,” Contreras said. “At the same time, family members are often called upon to translate medical information, navigate health systems and help make healthcare decisions for loved ones. Those responsibilities can shape how health information is understood and acted upon.”An Action Plan for Improving Hispanic HealthThere are practical opportunities to achieve equitable cardiovascular health and reduce disparities through community engagement, culturally responsive care, inclusive research and policies that address the underlying drivers of health.“Reducing cardiovascular disease among Hispanic populations demands action at every level,” Contreras said, “from improving access to culturally responsive care and expanding research participation to addressing the social and environmental conditions that shape health.”By addressing both medical risk factors and the social conditions that shape health, experts believe there is an important opportunity to reduce disparities and help more people live longer, healthier lives. Learn more at Heart.org.Photo courtesy of Shutterstock googletag.cmd.push(function() { googletag.display('fixed-big-ad-bottom-asset'); });
Culturally Relevant Cardiovascular Disease Prevention and Care Strategies
(Feature Impact) Driven by rising rates of obesity, diabetes, high blood pressure and other risk factors, cardiovascular disease has surpassed cancer as the leading cause of death among Hispanic adults in the United States.Hispanic people represent nearly 1 in 5 of the U.S. population and are the nation’s largest ethnic minority group, yet many continue to face barriers to achieving heart health and accessing high-quality healthcare. A new scientific statement published in the American Heart Association’s flagship journal, “Circulation,” revealed how social, economic, cultural and environmental factors contribute to persistent disparities in cardiovascular health, calling for culturally tailored prevention strategies, equitable access to care and greater representation of Hispanic populations in cardiovascular research.“Hispanic populations in the U.S. are incredibly diverse even within their own communities with differences in genetic ancestry, language, cultural traditions and social experiences that can significantly influence cardiovascular health,” said Johanna Contreras, M.D., M.Sc., FAHA, director of the Division of Heart Failure and medical director of the Hispanic Heart Center within the Mount Sinai Health System. “Yet Hispanic people remain underrepresented overall in the research that guides prevention and treatment strategies… Without better representation and more detailed data, we risk overlooking important differences that can help us improve care and save lives.”Hispanic Cardiovascular Health by the NumbersCardiovascular risk factors – obesity (nearly 46%), type 2 diabetes (15.5%) and high blood pressure (approximately 44%) – are prevalent among Hispanic adults and often emerge at younger ages and occur more frequently among Hispanic adults compared with white adults.According to the report, only about 1 in 5 Hispanic adults achieves ideal cardiovascular health as defined by the American Heart Association’s original Life’s Simple 7 metrics. Updated analyses using the Life’s Essential 8 framework demonstrated persistent disparities for heart and brain health, as well as suboptimal dietary quality, sleep patterns and levels of physical activity.Social and Economic Barriers MatterBiology alone does not explain cardiovascular health disparities. The environments where people live, work and age, along with social and economic challenges, impact heart health. In fact, approximately 17% of Hispanics live below the federal poverty threshold, compared with 8.2% of white adults.#placement_976606_0_i{width:100%;max-width:550px;margin:0 auto;}var rnd = window.rnd || Math.floor(Math.random()*10e6);var pid976606 = window.pid976606 || rnd;var plc976606 = window.plc976606 || 0;var abkw = window.abkw || '';var absrc = 'https://ads.empowerlocal.co/adserve/;ID=181918;size=0x0;setID=976606;type=js;sw='+screen.width+';sh='+screen.height+';spr='+window.devicePixelRatio+';kw='+abkw+';pid='+pid976606+';place='+(plc976606++)+';rnd='+rnd+';click=CLICK_MACRO_PLACEHOLDER';var _absrc = absrc.split("type=js"); absrc = _absrc[0] + 'type=js;referrer=' + encodeURIComponent(document.location.href) + _absrc[1];document.write('');“Many Hispanic adults face obstacles that extend far beyond the doctor’s office,” Contreras said. “Limited health insurance coverage, language differences, food insecurity, environmental exposures and concerns related to immigration status can make it more difficult to prevent disease, manage chronic conditions and receive timely treatment.”Contreras emphasized the cultural values and practices of Hispanic people also influence how they perceive their health and healthcare options.“Family plays a central role in many Hispanic communities and can be an extraordinary source of strength, support and resilience,” Contreras said. “At the same time, family members are often called upon to translate medical information, navigate health systems and help make healthcare decisions for loved ones. Those responsibilities can shape how health information is understood and acted upon.”An Action Plan for Improving Hispanic HealthThere are practical opportunities to achieve equitable cardiovascular health and reduce disparities through community engagement, culturally responsive care, inclusive research and policies that address the underlying drivers of health.“Reducing cardiovascular disease among Hispanic populations demands action at every level,” Contreras said, “from improving access to culturally responsive care and expanding research participation to addressing the social and environmental conditions that shape health.”By addressing both medical risk factors and the social conditions that shape health, experts believe there is an important opportunity to reduce disparities and help more people live longer, healthier lives. Learn more at Heart.org.Photo courtesy of Shutterstock
Scientists want these 5 'maxxing' trends dead
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The Vivid Dreams Stage of REM Sleep Is Linked With a Lower Risk of 83 Diseases
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A Girlhood Museum: Look into ‘Warm, Cozy and Whimsy’ Bedroom
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Video GMA Health Alert: Sleep quality may help prevent disease
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Sometimes all you can do is laugh. That might actually be good for you
Sleep, diet and exercise are important for good health — but what about the benefits of a really good laugh? It turns out it’s contagious (in a good way).
Sometimes all you can do is laugh. That might actually be good for you
Sleep, diet and exercise are important for good health — but what about the benefits of a really good laugh? It turns out it’s contagious (in a good way).
Steam Frame Gets First SteamOS Update With Substantially Faster Charging
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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!
Your Health Apps Don’t Talk to Each Other. QBod Uses AI to Connect the Dots
The health and fitness coaching app uses artificial intelligence to consider a person’s nutrition, workouts, sleep, recovery and goals together, then translate that information into practical guidance.
Science Vs on the 49ers Substation: Anatomy of a Hatchet Job
In August, Pablo Torre Finds Out and Science Vs released an episode about my theory that electromagnetic fields from the electrical substation beside the 49ers facility may be contributing to the team’s run of soft-tissue injuries. As the originator of the theory, I was also a subject of the episode. I sat was interviewed by Wendy Zukerman and Rose Rimler of Sciene Vs. I sent them research, connected them with scientists, and spent hours digging through the City of Santa Clara’s and Silicon Valley Power’s records to help clarify critical details. Both Wendy and Rose came off as affable and professional, showing curiosity during the interviews, with Wendy going out of her way to question the “conspiracy theory” framing itself. Then they titled the episode We Solve the 49ers Viral Conspiracy Theory. I was familiar enough with their catalog that I never expected them to agree with my theory, but I did expect them to give it a fair hearing and to deliver their findings honestly. On both counts they came up short. They were not directly dishonest in anything they said, but rather in what they left out, in how what remained was cut, and in the picture painted by those two things in combination. They asked me to recorded the interview on my phone for better audio quality, and I held on to my copy for reference later. That turned out to be a fortuitous decision. Here is the raw audio of my first interview, unedited*. Only my side was recorded, so their questions aren’t on it, but you can generally infer them from the answers, and every claim I make below about what I said can be checked against my statements in this clip. (Note: Wendy had connection trouble at the beginning of the interview and was cutting in and out, which accounts for the false starts.) 0:00 -1:19:13 Audio playback is not supported on your browser. Please upgrade. Science Vs is a fun show. It is pitched at roughly a high-school understanding of science, for an audience that is skeptical, Snopes-oriented, and worried about misinformation. Take a claim circulating online, interview a supporter of the claim, interview consensus scientists, and then tell people which side of the line it lands on. I have listened to their episodes on raw milk, seed oils, 5G and other contested issues in the wellness space. I have problems with all of them, but each at least made an honest attempt to represent the actual range of scientific opinion by talking to credentialed scientists with differing perspectives. Dissenting researchers were heard from, answered, and often given a chance to respond. This episode did not do that. This article is not a relitigation of the science. I have written extensively about that already. This post is for the record. It is simply an accounting of what was wrong with their episode. Contents Is there a power plant next to the 49ers practice facility? — the clearest single example of getting something objectively wrong For the record — a high-level overview of all of the problems with their investigation Draw your own conclusions — why they had to make this episode at all What they left out about childhood leukemia — the exposure threshold, and playing games with statistics to minimize sick children What they left out about the mechanism — the body of literature they refused to cover, and evidence for the mechanism used against it The scientists Science Vs interviewed and did not air — four credential scientists who support myhe theory, recorded and cut, or not even called How they misrepresented me and my case — an answer severed from its question, and three telling edits How you would actually study the injuries — it doesn’t actually matter which team is the most injured, overall The theory: magnetic fields, oxidative stress, and collagen Since the episode never states my theory, here it is below. Those who are familiar with my work can skip this section. Electrical equipment produces magnetic fields, and those fields induce faint electrical currents in anything that passes through them, including people. My argument goes further than induced current. Mitochondria — the structures that generate a cell’s energy — run on continuous flows of electrons and protons, and those flows carry faint electromagnetic fields of their own. Maxwell’s principle of superposition shows that when two fields share the same space, they add together. An external field does not need to be strong to alter an internal field, it only needs to be present. The electron transport chain inside the mitochondria leaks a small fraction of its electrons by design, and those become reactive oxygen species — free radicals, which healthy cells use as signals. External magnetic fields cause the rate of leakage to change, increasing free radicals. When free radicals accumulate faster than the cell’s antioxidant systems can clear them, the result is oxidative stress. Oxidative stress is a recognized driver of chronic illness, including cardiovascular disease, neurodegeneration, diabetes and cancer, and it is in every medical school curriculum. One of its ordinary effects in connective tissue is that it switches on matrix metalloproteinases — MMPs, the enzymes that break collagen apart — while suppressing new collagen synthesis. Tendons are made of collagen. An athlete loading his soft tissue heavily six days a week is already creating oxidative stress in the tendons, so the addition of magnetic field exposure compounds the damage and inhibits repair, making him more susceptible to injury when enormous force lands on a tendon in a fraction of a second. That is the theory. We know that EMF causes oxidative stress, and we know that oxidative stress degrades collagen. The only thing missing is a study showing that direct connection. I have never claimed certainty that the substation is contributing to the elevated injury rate. I do believe it is likely, and I believe it warrants caution, and that a revenue machine like a major NFL team can easily afford to remove the exposure out of precaution. Is there a power plant next to the 49ers practice facility? Here is the clearest single instance of the problem with this episode. It requires no knowledge of electromagnetic fields at all. This story first came to me through Jon Feliciano, a former 49er, in an interview on Willard & Dibs on 95.7 The Game. Asked about why the 49ers are always injured, he said players used to joke that it was the power plant behind the practice fields. Wendy Zukerman corrects him on air. “It’s important to say that it’s not a power plant near the 49ers site.” Torre then asks her to explain the difference between a substation and a power plant. Her answer: a power plant generates electricity and transmits it to a substation, which converts the voltage into something your house can use and sends it on to your home or your business. There are two problems with that. The first is that there is a power plant on that site. The Gianera Generating Station is a natural-gas-fired peaker plant owned by Silicon Valley Power, and it has been there since 1986. I have published aerial photographs of the location from 1987 in which the gas plant is the only thing standing, before the practice facility was even there. I even mentioned the gas plant in my first interview. (Feliciano has since gone on record about this issue, and it is clear he had the substation in mind rather than the gas plant.) The second is that her definition describes a distribution substation, and the facility beside the 49ers is not that. It is the Northern Receiving Station, which takes in bulk power from outside the city’s grid and delivers it to distribution substations. Silicon Valley Power’s own map distinguishes receiving stations from substations, and Rose Rimler even reads the label out loud in the episode when she walks through that map on air. A few minutes before the map segment, Zukerman tells Torre: “like I said, we fact check everything.” Well, maybe not everything. I made a mistake On the morning of July 6th, at 10:20, I sent Rose and Wendy two studies. During the interview I had been asked which human studies show oxidative stress from electromagnetic fields, and I had not been able to name one on the spot. Rose emailed asking for the studies, I quickly searched for a couple, and I wrote that I thought these were the most relevant from that search. Unfortunately, I was busy and did not read either one closely at first. I picked them because they were topically relevant — one on substation workers, one on power plant workers. Neither were great studies, and their problems go past the ones raised in the episode. That was careless on my part. There is context that did not make the episode, though. Before that email I had been on a Zoom call with Rose talking about EMF and oxidative stress, and I pointed her to Dr. Henry Lai at the University of Washington, who has spent years aggregating the literature on this question. His tallies show that roughly 90% of studies since the late 1990s find oxidative effects from electromagnetic field exposure — hundreds of studies, systematically counted. Rose told me she was already aware of his work. So when she asked for studies, I understood her to have the aggregate view already and that she would report anything within that context. Not reading those two carefully was still a mistake, but the larger mistake was assuming the episode would be based on a thorough review of the actual body of literature, rather than on whatever I happened to send that morning. The second email At 1:49 that same afternoon — three hours and twenty-nine minutes after the first — I sent them a second email that I had been preparing for a while. It was a structured document in six numbered sections, written in response to a request they had made two weeks earlier, laying out my entire argument with citations attached to every link in the chain. The episode aired on August 13th, five weeks later, and not a single item from the second email is in it. Here is how it opens: The full email is included at the bottom of this post in Appendix B. Nearly 1,500 words in total. It contains two named mechanisms with the physics behind them. Occupational studies in humans. The literature on oxidative stress and collagen. A section addressing the strongest counter-evidence against my own theory, which I raised myself. And a closing section stating plainly what the theory cannot yet show. My entire argument, in writing, with detailed citations for every claim, provided to them five weeks before broadcast, and none of it made it into the episode. That is the single largest omission, but it is not an isolated one. The whole episode is riddled with similar problems, and the conclusion they came to is not merely a difference of opinion about the scientific evidence. Through omission and through strategic editing, Science Vs misinformed its audience — about what the evidence shows, about what I argued, and about who they spoke to. That is a notable outcome for a show whose stated purpose is correcting misinformation. For the record I am not going to tell you that Science Vs set out to discredit me, or that they had come to their conclusion before they reported the story, or that they used misleading editing to make me look like a man retreating from his own theory. I cannot know what was in anyone’s head, and I am not going to pretend otherwise, either. What I can tell you is what is on the record. They asked me for evidence and aired the weakest thing I sent. They interviewed three scientists who supported my theory and aired none of them. They discussed childhood leukemia without ever saying the exposure level at which it appears. And they took an answer I gave weeks before Ken Karipidis, the one EMF scientist who was put on air, was interviewed, and placed it directly after his critique, where it comes off as a major concession. A friend of mine who has worked as a journalist for thirty years read that last one and called it sleazy. I agree with her. Those are just the four issues that are impossible to defend as pure editorial decision, but they are not the only issues. The most glaring issues stem from what they left out: The exposure level at which the childhood leukemia association actually appears — three to four milligauss, a number the episode never states despite it being much lower than what I measured. The mechanism itself: The episode gets as far as “oxidative stress could weaken collagen,” which leaves it sounding like speculation, rather than a known pathway. The second email, and all the studies in it. Dr. Paul Héroux at McGill, whose work my proposed mechanism rests on, whose contact details I supplied, and who was never called. Dr. Beatrice Golomb at UC San Diego, who runs a research group on oxidative stress and mitochondrial function and has specific expdertice in collagen, interviewed and not aired. Dr. David Carpenter at Albany, the most prominent academic voice on the harm from magnetic field exposure, interviewed and not aired. Dr. Joel Moskowitz at Berkeley, interviewed and not even credited. The specific, testable condition I put in writing that would make me abandon the theory. My own unprompted statement of the theory’s evidentiary gap. My caveats about my own measurements. My ranking of EMF as one factor among several rather than the only one. The new equipment installed at those facilities between 2010 and 2014, and the sharp rise in system load from 2013 onward. But that is not all. What they kept, they selectively edited to serve a narrative that was not served by the raw transcripts of the interviews. A description of thousands of commercial routers in a workplace, reduced to the Wi-Fi in your house. My own acknowledgment, multiple times, that "I'm not a scientist" clipped in an episode that spends considerable energy pointing out that I am not a scientist. And a qualification I volunteered about my own measurements, cut from my answer and delivered later by their EMF expert as a correction. Together their edit produce a portrait of a wellness guy with Wi-Fi phobia and two bad studies, backing away from his theory the moment a “real” scientist looked at it. A practice facility where nothing changed because no new substation was built. Injuries written off as random because the 49ers were not quite the single most injured team in the league over the period in question. That portrait is false even though almost no individual statement made in the episode is. Draw your own conclusions At the top of the episode, Pablo Torre says his show had been flooded with requests to investigate the substation — that it was the thing they were asked to look into over and over again. Neither show went hunting for this story. It arrived from their own audience, in volume, and it could not be waved off. A thread I posted on X reached twenty-two million people. A guy with a gaussmeter and a brand-new Substack obligated a Pultizer prize winning program to spend an hour on a question about player health, that is considered fringe enough that most media operations won’t touch it. Pablo Torre Finds Out could not ignore it. So Science Vs came in and ran a “debunking” operation instead of an investigation. Everything below is what had to be left on the cutting room floor to deliver the “debunking”. They could not ignore it. So they tried debunked it instead. The demand was strong enough to force an episode, and since the episodes release the 49ers have sustained more injuries, including season ending ones, and interest has only grown. Demand from fans and playets is strong enough to force a better investigation from someone else. An omission is not a lie until you find out what was omitted. What follows is the detailed record so you can see the full picture. Draw your own conclusions. I have drawn mine. I am going to keep publishing. A note about Pablo Torre Finds Out After the episode aired I posted publicly, calling out Pablo Torre Finds Out for concerns I had about the integrity of their investigation, and about an interview directly with Pablo Torre which had been offered but never happened. I have since spoken with a producer at PTFO. The offer had rested on a misunderstanding about where things stood between us, and it fell away as the Science Vs part of the production widened past the science. He apologized for the miscommunication and I accepted. The producer also confirmed to me that they did essentially hand off the entire investigation to Science Vs for narrative purposes — so Pablo would be genuinely curious or potentially surprised by their findings — while still taking responsibility for what went out under their name. I appreciated the candor and the accountability, and I am comfortable with where we left things. So this post is not about PTFO. My disagreement is with Science Vs. What they left out about childhood leukemia Childhood leukemia appears at three milligauss. They gave no number at all. 1. They built an EMF ruler, then discussed childhood cancer without it. The sequence on air went like this: First I measured almost 9 mG, then I measured up to 50 milligauss. Torre reacts with concern — “that sounds high.” Cut to Karipidis: the public limit is 2,000 milligauss. Torre reacts again — “What happens at 2,000?” Karipidis explains that nothing happens at 2,000, that safety factors are built in. Then: at more than 50,000 milligauss you get flickers of light in the retina, and higher still, nerve stimulation. The listener now has a ruler (their ruler) to measure these numbers with. Fifty is nothing by their ruler. Then the episode turns to childhood leukemia and states, accurately, that there is a real association — but tellingly, they never give the exposure level at which that association appears. Childhood leukemia appears at three milligauss. They conveniently left that out. The pooled analyses that produced the World Health Organization’s carcinogen classification found roughly a doubling of childhood leukemia risk above three to four milligauss. That is the number that belongs in that segment, and it is more than ten times below the reading that had just been dismissed as trivial. I gave them that number myself, on tape, in the interview. Describing my own threshold, I said my comfort level for long-term chronic exposure is three to four milligauss, but preferably one. 2. Six children in thirteen million. The episode reports that these fields might explain one to four percent of childhood leukemias, then reframes it as a German estimate of perhaps six cases among thirteen million children. Torre, to his credit, is uncomfortable. What never gets explained is why that number is small. Almost no children lives above three milligauss in Europe. Fewer than two children in a hundred, in the Italian data. So even if the risk to those children doubles, the number of additional cases across an entire country stays small — not because the hazard is small, but because hardly anyone is exposed to it. Count the whole population and the few who are exposed disappear. And the reason hardly anyone is exposed is that siting rules keep housing away from transmission lines. In Europe, at least. The Dutch government has a standing precautionary policy against building new homes in any zone where the annual average magnetic field exceeds 4 milligauss — the same number the episode never mentioned. Denmark and Norway treat 4 milligauss as the level that triggers a look at mitigation. That is five hundred times below the ICNIRP figure quoted on air. The United States has no federal equivalent. That is evidence of infrastructure siting policy working. It is not evidence that there is no hazard. It is evidence that we already act as though there is one. If you listen to the raw audio you will hear that my proposed solution is EMF exposure is to build better infrastructure. What they left out about the mechanism 3. They accused me of cherry-picking, and then cherry-picked themselves. On air, Zukerman tells Torre that people who worry about electromagnetic fields dismiss the studies showing null results and collect the ones showing harm, and that this is why you have to be careful not to cherry-pick. They had two papers I had rattled off in a hurry, and a second email containing a carefully chosen set. They ran the two weakest, graded them on air, and presented the result as the state of the evidence for not only my theory, but the whole question of oxidative stress from magnetic fields. That is cherry-picking from my emails. The bigger picture is what they did with the literature as a whole. Zukerman acknowledges it exists, dismisses it, and disposes of it in a single stroke. You can go online right now, she tells Torre, and find scores of studies showing these fields increase oxidative stress. The issue, she says, is that they are not studies in people. Many of them are in people. The occupational studies in my second email are in people. That email had been in her inbox for five weeks. She waved off the literature on a factual claim that the documents in her possession contradict. (I have written separately about the evidentiary standard at work here). The effect was that they essentially baited me: ask the subject to supply the evidence, take the weakest thing he sends, and let that stand as a proxy for the whole argument. Wendy has been doing this show for ten years and clearly knows how to extract what she needs for her desired narrative. 4. They presented the collagen-improvement research as a gotcha, but I had already addressed it. The episode treats the existence of studies showing that EMF can improve collagen as a surprise that undercuts me, but I had pre-emptively addressed that five weeks earlier in the email they ignored. Those studies use measured, high-intensity pulsed dosing. The mechanism by which they work is oxidative signalling. The cell reads a controlled rise in reactive oxygen species as a warning, upregulates its antioxidant defenses, mounts a repair response, and the therapy stops before the system is overwhelmed. The key point is that it induces an oxidative response, which means those studies are actually evidence for my proposed mechanism, not against it. A field that produces a therapeutic effect cannot be biologically inert (which is the implication when they say “Nothing happens at 2,000 milligauss). Chronic ambient exposure is the same pathway with no off switch, and it is most consequential during the evening and while sleeping, when the body is in repair mode and the exposure does not stop. Section 5 of my email is titled What about the study showing improved collagen synthesis. I raised the counter-evidence myself, explained why I did not think it refuted the theory, and wrote that I was disappointed the question had not come up in the interview. That is worth holding against the cherry-picking charge in the item above: the studies they presented as inconvenient for me were studies I had gone out of my way to put in front of them. 5. Section 1 of my email stated a critical argument that was never put to the expert directly responsible for it. My email says the exposure limits exist to prevent acute effects and do not address chronic exposure at all, and that my dispute is with the entire framework. Zukerman gestures at this once. After Karipidis gives the 2,000 milligauss figure, she tells Torre that I would object because those levels do not capture “more subtle effects.” That is not my argument, and “subtle” is doing a lot of work here. My argument is that the limits are built to prevent acute effects — nerves firing, muscles twitching, etc — and were not designed to address chronic exposure at all. In fact, ICNIRP’s own documents state as much themselves. Mine is a structural objection to what the standard measures, reduced as a concern about subtlety, it becomes a matter of degree, rather than a categorical difference. They interviewed Ken Karipidis, vice chair of ICNIRP — the body that writes those limits. He was asked what the limit is, but he was never asked how it applies to chronic exposure. The scientists Science Vs interviewed and did not air 6. They interviewed four officials of the standards body. The episode credits roughly a dozen researchers. Four of them are associated with ICNIRP. Ken Karipidis is the vice chair. Rodney Croft chaired ICNIRP from 2020 to 2024 and led the development of its current guidelines. Dan Baaken is ICNIRP’s scientific secretary. Frank de Vocht sits on the Main Commission. One of them speaks in the episode. Their institution’s position is more than adequately represented — the 2,000 milligauss figure, the safety factors, the assurance that nothing happens below the line. 7. The four who were left out. Dr. Beatrice Golomb is Professor of Medicine at UC San Diego — a physics undergraduate degree, a PhD in biology, an MD. She directs a research group whose stated focus is the relationship between oxidative stress, mitochondrial function and health. That is the mechanism the episode spent its first half dismissing. Her published work includes the fluoroquinolone case series behind the FDA’s black box warning on an antibiotic class that ruptures tendons, where the accepted mechanism is oxidative stress and mitochondrial toxicity — the back half of my chain, already on a drug label. She is in the credits. She is not in the episode. She has told me she finds my theory biologically plausible, and that she has a recording of her interview. Dr. David Carpenter directed the Institute for Health and the Environment at the University at Albany for decades and is the most prominent academic voice arguing these fields cause harm. Childhood leukemia is the reason these fields carry a WHO classification at all, and Carpenter is the person you call if you want that case made by someone who has spent a career on it. He is in the credits. He is not in the episode. He has told me that when he was interviewed they could not have been less interested in what he had to say. Dr. Joel Moskowitz directs the Center for Family and Community Health at UC Berkeley’s School of Public Health. He told me directly that they interviewed him and that he thought it went well. He does not appear in the episode, and unlike Golomb and Carpenter, he does not even appear in the credits. Dr. Paul Héroux at McGill is the researcher whose work provides the foundation for the oxidative stress mechanism my theory rests on. I gave Rose his email address and phone number. He was never interviewed. They never even called him. 8. “He’s not a scientist.” The episode leans hard on the fact that I am not a credentialed scientist. Zukerman says it. Torre repeats it. “At all.” Having built a segment on that, they then left out the physicist-biologist-physician, the professor of public health, the director of a university environmental health institute, and the McGill researcher whose work the primary mechanism comes from. They spent the episode telling their audience I am not a scientist, and then kept four actual scientists who support the theory off because their argument does not survive otherwise. How they misrepresented me and my case 9. They played my words as a response to an interview I had never heard. Near the end of the hour, Zukerman says she went to me and told me the evidence was lacking. Then she plays me saying I am not wedded to it being an EMF, that I have staked my reputation on it needing more study, and that I am not certain of anything. That segment was placed immediately after Karipidis had finished taking the cherry-picked papers apart. It plays as a man folding under expert scrutiny. Commenters have used it against me since, but it is incorrect. Here is the sequence as it happened. I was interviewed. Karipidis was interviewed weeks later. I was never told what he said, or even who he was. I was never asked to respond to it. I did not know his name until the episode aired. That is not a simple editing decision. That is a quote from one interview, moved to follow a critique from a different interview it was not a response to, so that it would land as a concession. A friend of mine who has spent thirty years as a journalist read that sequence and called it sleazy. She is right. The full passage is reproduced in Appendix A, and it is worth reading. What airs is the preamble. Four paragraphs later I say “to directly answer your question” — and that answer, about what would change my mind if the team relocated, is not in the episode. Neither is the sentence two paragraphs on, where I say the EMF might turn out to be ten percent of the problem. I will say the underlying point again, though, because I meant it and I still do. I am not wedded to my theory that magnetic fields from the substation are contributing to the 49ers injuries. I could be wrong. What I am wedded to is the process of scientific inquiry, and the fact that we should be cautious around these exposures and we need more independently funded studies. 10. Three telling edits. They cut “I’m not a scientist” mid-sentence. What I said: “...and I am not certain of anything. I’m not a scientist. To me, I find the mechanisms compelling. I will go back to the fact that I got into this not because of the 49ers, but because of clients I was working with who suffer from EDS...” What aired: “...and that I am not certain of anything. I’m not.” The clip ends on the first two words of the sentence in which I say I am not a scientist, in an episode that spends considerable energy establishing that I am not a scientist. The full sequence is in Appendix A. They cut my own description of my work. Asked what I do, I said I run a wellness business, that I am focused on writing software to help people navigate environmental stressors, that environmental health is my focus, and that I also do independent journalism and research. What aired is the wellness business and the environmental health, with the software and the journalism removed from my own answer. The software engineering does come up later — narrated by them, as a hacker who grew up to write firmware — but my current work, in my own words, arrives as “wellness guy.” Thousands of commercial routers became home Wi-Fi. What I described: working at a wireless networking company surrounded by thousands of Wi-Fi routers, and a stress-induced health collapse afterward that working in that environment contributed to. What aired: Wi-Fi, the kind you have at home — reinforced by a clip of Christian McCaffrey talking about turning his router off at night. Three cuts, and every one of them makes me seem less credible. That is not a coincidence. 11. I gave them my own caveats and the test that would disprove me. In the first email I wrote that a well-designed chronic, ambient-level exposure study in tendon showing no collagen degradation, run over many months, would undercut my confidence in the theory. That is a specific, testable condition, stated in advance and in writing. There was a second interview, weeks later, which was not used in the episode, but in that I asked again for the falsification criterion to be included. What the episode presents instead is a man saying “we need more study,” which reads as a hedge, an open-ended request for the benefit of the doubt. It is the opposite of a hedge. Section 6 of my second email says, unprompted, that as far as I am aware there is not a single study showing EMF-driven oxidative stress degrading collagen in a human in vivo or in human tendon in a lab. I wrote that because it is true and because it is the first thing anyone should check. Under their standard it becomes the hinge of the entire first half, framed as something they had to surface without my cooperation. I had handed it to them five weeks earlier. And in the interview I said that my 25 to 50 milligauss readings were taken at knee level, and that these fields attenuate quickly, so by the time it reaches your head it is not that high anymore. That did not air either. The qualification arrives later, from Karipidis, as a correction. How you would actually study the injuries 12. They measured the wrong thing. The episode spends its final act on whether the 49ers are the most injured team in the NFL, finds no clean ranking, and lands on “injuries are random”. That is the wrong test. You would define the exposure — measured field levels at the facility — and the outcome narrowly: soft-tissue injuries, not a single MSK injury count that a broken finger and a ruptured Achilles both land in. Then you would compare the 49ers to themselves before and after the exposure changed, and compare that change against every other team over the same window. That controls for league-wide shifts in rules, turf and training load. It is a difference-in-differences design, and it is standard. I sent them that argument on July 28th, in writing, along with the fact that in eleven of the past twelve seasons the 49ers had finished top ten in Adjusted Games Lost. And by the episode’s own reporting, the 49ers are second in games lost to injury over the past decade, with FTN’s Aaron Schatz confirming that once you adjust for starters they come out second worst in the league — after having been one of the healthiest teams for years before that. A finding like that is where an investigation starts, not where it stops. 13. I did a lot of substation research for the episode that was never aired. I had reported that the substation next to the facility was expanded in 2014. That was wrong, and Rose Rimler and I sorted it out together. They gave me credit on air, which I appreciated, but framed it as a concession on my part to something they had found. In fact I had been investigating it myself, was uncertain before they asked, but was waiting for clarification from Silicon Valley Power. The uncertainty centered around a substation named “Esparanca” that was proposed right behind the facilities as part of the stadium construction, but now appears to never have been built. I spent days in Silicon Valley Power’s records, and did eventually reach Silicon Valley Power for confirmation and indentified the mistake myself. I also gave them highly detailed documents on what we do know about those facilities: new equipment installed between 2010 and 2014, and load growth across the system with an inflection around 2013–2014, with the Northern Receiving Station carrying the highest capacity in the system and sitting closest to the data center corridor. None of that is in the episode. I have a separate piece about it coming out soon. *I cut 2 seconds from the raw audio to remove personal information that had no connection to anything in the episode. Appendix A: the passage the clip was taken from This is the sequence from my first interview, in full. The episode uses one fragment of it. It’s tricky because my understanding is that there’s something like a 15-year half-life on collagen remodeling issues. They’re going to get a new crop of players. What I really need, though, is for the injuries to be broken down so we can see the soft tissue injuries. Right now, they’re categorized as MSK injuries, but let’s say we can actually identify them more specifically. Is that right? He was able to do that? Oh, cool. I wasn’t able to find that information. Interesting — I didn’t know that data existed. I tried so hard to get it, and I didn’t know it was available. Maybe you could connect me with that person. That would be amazing. I’m not wedded to it being an EMF, honestly. I’m not. I would say that, to a certain extent, I’ve staked my reputation on the fact that it needs more study. It’s important to look into it, and I am not certain of anything. I’m not a scientist. To me, I find the mechanisms compelling. I will go back to the fact that I got into this not because of the 49ers, but because of clients I was working with who suffer from EDS, Ehlers-Danlos Syndrome, a tendon hypermobility issue. This condition is documented to be partially caused by oxidative stress. I’ve worked with them to mitigate their EMF exposure and have seen people improve. I think it’s a bigger story. In a way, the 49ers represent an occupational cluster with specific exposure risks. If someone would conduct a study on this, I believe we could learn a lot. Perhaps we would discover that it’s like, okay, maybe it’s 10% of the problem. I don’t know the exact number, but I think either way, conducting the study would provide valuable insights. To directly answer your question, it’s challenging for me because it’s part of a bigger story. If the 49ers move and stop having injuries, I might conclude that it was related to the substation. However, if they move and still experience injuries, I would want to analyze the nature of those injuries. Are they primarily soft tissue injuries? I don’t think it’s necessarily a case closed, but the story might lose traction at that point regardless. Three things are worth noting. The aired fragment stops immediately before the sentence in which I say I am not a scientist — the cut described in item 10. It also stops four paragraphs before the words “to directly answer your question.” What the episode plays is the throat-clearing. The actual answer, about what would change my mind, never airs. And two paragraphs in, I say the EMF might turn out to be ten percent of the problem. That is the ranking the episode says I never gave. Appendix B: the full email, July 6th, 1:39 PM Hi Rose, You asked me to send you some studies a couple of weeks ago. I apologize for the delay. I have been incredibly busy. I also wanted to give you a chance to dig in yourself, and get your own perspective before I influenced you too much with mine. That said, I do want to make sure that the actual argument is abundantly clear, so here it is! One note before I begin, there are really two separate questions here: Does the substation cause the soft-tissue injuries? That was my specific claim, and what the podcast is about. Is the theory biologically sound? Can 50/60 Hz fields at these levels do anything biological below the safety limits? Question two is why people have been calling me a conspiracy theorist. The regulatory and advisory bodies (ICNIRP, etc) maintain that anything below their exposure limits is biologically inert, and that position is broadly accepted within the mainstream, but the actual science paints a different picture. To defend my theory I’ve had to defend a much larger claim: that the advisory bodies have the biology wrong. I can’t honestly answer question 1 without first addressing that. Here’s is a simplified outline of my theory, with links to studies: 1. Advisory body thresholds for biological effects The ELF magnetic-field limits (ICNIRP’s ~2,000 mG public / 10,000 mG occupational) exist to prevent acute effects from exposure. If a magnetic field is strong enough, it makes nerves fire and muscles contract. Muscles twitch. You can see faint flashes of light in your vision. People can even feel tingling or even a shock. That happens due to Faraday’s law, which states that a time-varying magnetic field induces an electric field inside the body via the creation of Eddy currents.The standards assume that those currents do nothing below the twitch threshold. They do not consider chronic effects at all. My argument is that they are biologically active and do have chronic effects. 2. There are multipe ELF-EMF mechanisms for inducing oxidative stress. This is basic biophysics. Below are the two primary mechanisms. Simplest first. Dr. Paul Héroux of McGill has the most intuitive explanation, which rests on Maxwell’s principle of superposition: because Maxwell’s equations are linear, two sets of electromagnetic waves sharing the same space simply add together. In the interview I pictured a pebble dropped into a pond, sending out clean ripples. Then a boat motors past at distance, sending larger waves, and where they meet the ripples, the two add together and the original pattern gets distorted. In our cells, the mitochondria run on continuous currents of electrons and protons that carry their own faint electromagnetic fields. An external field from a substation, by the principle of superposition, adds to those internal currents and shifts the pattern. The electron transport chain in the mitochondria leaks a fraction of its electrons by design as reactive oxygen species (ROS), which act as signalling molecules in a healthy cell. Distorting that field increases that electron leakage, creating oxidative stress. A tiny electromagnetic interference results in a large downstream effect. https://www.sciencedirect.com/science/article/pii/S2405844025006474 The more complex pathway is Dimitris Panagopoulos’s Ion Forced-Oscillation / Voltage-Gated Ion Channel (IFO-VGIC) mechanism. Weak, polarized, low-frequency fields force the ions (calcium, potassium, sodium) next to an ion channel’s voltage sensor to oscillate; because that force scales with the inverse cube of the distance involved, fields far below the stimulation threshold can still force the channel open, disrupting the cell’s ion balance and driving ROS overproduction (Nitric oxide and superoxide interact and produce peroxynitrite, a highly unstable cytotoxin that breaks down into free radicals). https://www.researchgate.net/publication/366088934 https://www.spandidos-publications.com/ijo/59/5/92 https://www.mdpi.com/1422-0067/22/18/10041 https://www.frontiersin.org/journals/public-health/articles/10.3389/fpubh.2025.1585441/full https://pmc.ncbi.nlm.nih.gov/articles/PMC3772193/ 3. Evidence of oxidative stress, in vivo, in humans from ELF-EMF There are many studies, and the strongest are occupational, which applies to the 49ers situation. 115 power-plant workers vs. 145 office controls. Serum malondialdehyde (MDA, the standard lipid-peroxidation marker), superoxide dismutase, and catalase were all significantly higher in the exposed group, and the markers rose with increasing field exposure. https://journals.sagepub.com/doi/abs/10.3233/WOR-203244 A follow-up where they reversed the oxidative stress in power plant workers. A double-blind randomized controlled trial: 91 power-plant workers given vitamin E, vitamin C, both, or placebo for 90 days. The antioxidant groups showed reduced lipid peroxidation and raised antioxidant capacity versus controls. https://pubmed.ncbi.nlm.nih.gov/32191586/ A spot-welder study: 46 welders occupationally exposed at 50 Hz, showed significantly altered red-blood-cell antioxidant enzyme activity and concluded ELF-MF “might act as an oxidative stressor… even at the recommended levels of exposure.” https://pubmed.ncbi.nlm.nih.gov/18504600/ A substation-specific study found oxidative stress and DNA damage https://pubmed.ncbi.nlm.nih.gov/24460415/ 4. Oxidative stress degrades collagen This half isn’t controversial at all. Oxidative stress activates the matrix metalloproteinases (MMPs) that break collagen down and suppresses its synthesis. Here are three example studies: Siwik et al. 2001: Oxidative stress raises MMPs and lowers collagen synthesis in cardiac fibroblasts. https://pubmed.ncbi.nlm.nih.gov/11121376/ Fisher et al. 2009: Collagen fragmentation drives oxidative stress and elevates MMP-1 in aged human skin. https://pmc.ncbi.nlm.nih.gov/articles/PMC2631323/ Varani et al. 2006: Decreased collagen production in oxidatively aged skin. https://pubmed.ncbi.nlm.nih.gov/16723701/ 5. What about the study showing improved collagen synthesis I’m glad you asked this question, and I’m bummed we didn’t get to it in the interview because it is a great question, and very important to understand. Superficially it may appear to be a refutation of my theory, but I would argue that it actually supports the underlying argument. That study used a short, high-intensity pulsed dose: therapeutic-PEMF, the same type of field used clinically to stimulate bone and tissue healing. The reason this works is because it triggers the very same biological pathways that can lead to oxidative stress. The exposure still stimulates ROS production, but done at a controlled dosage, for a limited duration it has a different effect. The cell reads the ROS as a warning signal and it upregulates its antioxidant defenses, and mounts a repair/proliferation response. The therapy is then stopped before the cell gets overwhelmed. That is essentially a hormetic response: a small dose of a stressor producing a beneficial adaptation. Two things follow: At the very least, this means the field is biologically active, which by itself undercuts the regulatory claim that these fields are inert below their thresholds. There is a wealth of literature on PEMF (pulsed EMF) bone regeneration and calcium channel signalling (which is the second mechanims in section one). Here is one. https://www.nature.com/articles/srep13856 At best, it leads us straight to my actual concern, which is that under chronic, chaotic and unregulated exposure, the cell’s antioxidant capacity gets overwhelmed, resulting in oxidative stress. There are plentiful examples of things that are beneficial at controlled doses, but harmful at uncontrolled doses. Excecise is one obvious, uncontroversial example. Botox is perhaps a more interesting example. 6. What about a study that shows EMF causing collagen degradation in humans? As far as I am aware there is not a single study showing EMF-driven oxidative stress degrading collagen in a human, in vivo, or in human tendon in a lab. There are studies involving isolated fibroblasts though, which secrete collagen. The most relevant one showed that human fetal scleral fibroblasts exposed to 50 Hz ELF-EMF showed a significant decrease in collagen synthesis and that MMP-2 expression was upregulated, which is the exact mechanism I described in section 2. https://pmc.ncbi.nlm.nih.gov/articles/PMC3626379/ That’s it! Thanks again for the interview. Best, Peter Anthony Cowan Environmental Health · Wellness Tech · Researcher & Journalist Publisher & Editor, Living Energy Bio: petercowan.comSocial: X · Instagram · TikTokApp: sunlightis.lifePhone: [redacted]
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The politics and possibilities of ‘AI could kill us all’
I found myself fielding a lot of questions from folks who don’t usually talk much about AI this week. They were mostly along the lines of “do you think AI is going to kill us all?” or “how worried should I be about this human extinction stuff?” Motivating this wave of existential anxiety was the highly dramatic resignation of now-former Anthropic employee Jacob Coxon, who quit his job while publicly sharing his concerns about safety practices at the leading AI companies. More specifically, he declared that almost everyone at OpenAI and Anthropic, the leading AI labs, believes that there’s a decent chance the AI systems they’re producing could “kill us all” by the end of the decade, and the companies aren’t “acting responsibly.” Other AI safety researchers, including those still employed at Anthropic and OpenAI, all confirmed that yes, Coxon is correct, they’re all worried that their company’s products might prove fatal for the entire human race as well. Two more AI employees quit and joined the chorus. Now, the warning shot has been covered everywhere from the Wall Street Journal to Fox News to WIRED to the Guardian. I understand why all this sounds scary, but my response to those who have asked, has generally been: No, you don’t need to worry that AI will kill go rogue and kill us all. But that does not mean we shouldn’t worry, period. Far from it. The companies building AI products are now among the wealthiest and most powerful entities in the world. And they very much are building enormous engines of mass surveillance, extraction, and automation. They can and have allowed their AI systems to carry out felony hacks of other companies, provided the government with autonomously generated kill lists, and sold enterprise technology to firms around the world that is explicitly intended to replace jobs. But “AI” has done these things not because they have all-powerful minds of their own but, ultimately, because people have programmed, calibrated, and directed them to. In other words, it’s not AI we need to worry the most about. It’s the people and corporations working to profit from and gain power by deploying it. The technology is sophisticated, sure, and, especially in cybersecurity contexts, potentially disruptive to plenty of existing systems. But if we want to stop this predatory, profiteering, and extractive form of AI—and it’s worth noting that at this point, most people do—we absolutely can. A quick note/plea: I can only do all of this with the support of readers like you, so if you find value in independent, critical tech journalism and analysis, please consider becoming a paid subscriber. I want to keep as much of this un-paywalled as absolutely possible, and I need your support to do so. Many thanks to all who continue to chip in, it’s very much appreciated. Onward. Subscribe First, some context: AI industry folks like Coxon have been discussing the prospect that AI will destroy humanity for years. Even before the beginning of the AI boom, many working in the industry, from the executive staff to the rank and file researchers, have obsessed over ‘x-risk’, or the possibility that AI will become sentient or semi-sentient and move one way or another to exterminate humanity. This is ostensibly why Elon Musk bankrolled OpenAI in the first place, and is the grounds for his lawsuit alleging OpenAI betrayed its charter by abandoning its nonprofit status to become a commercial enterprise. Many AI engineers and startup founders have calculated their own personal p(doom), or the probability that the tech product they are working on will initiate an actual humanity-extinguishing apocalypse. 10-25% p(doom)s are pretty common. (I wrote about a long weekend I spent among these folks at one of their top conferences here, to give you an idea of their ideas and belief systems.) Sam Altman himself drove the narrative of the imminent rise of a super-powerful AI, or artificial general intelligence, to prominence by declaring that the technology he was building posed an existential risk to humanity. This idea is in other words baked into the DNA of modern AI companies and into the products they engineer. It’s also why the industry is routinely accused, by myself and others, of “doom marketing,” ie, using such proclamations and framings to impart the sheer power of the technology behind your product onto investors, partners, consumers, and the state. Some ambient understanding of this tendency may have helped prevent the press from repeating the claim every time one of the x-risk folks made it over the years, including when they quit their jobs at AI companies while doing so. Yet Coxon’s AI x-risk alarm has broken containment, as they say, and has exposed the idea to the mainstream media once again. This has happened, I think, for a number of reasons. First, when AI CEOs were going around saying AI might kill everyone in 2023, their companies were well-capitalized, but not nearly to the extent they are today. They were more easily dismissed as eccentric geeks of the sort that Silicon Valley is supposed to produce. Now, not only do their products have much greater market saturation, but people are more aware of a) the often unethical ways the executives and companies comport themselves b) the other adverse impacts of AI that have already arrived, and c) the physical cost of building these systems, particularly when it comes to data centers. Finally, toss in the constant stream of headlines in 2026 about AI models going rogue or potentially upending the world’s infrastructure. [ ](https://www.bloodinthemachine.com/p/with-the-backlash-to-data-centers) [ With the backlash to data centers, Flock and AI glasses, a mass opposition to big tech is underway. Silicon Valley is in denial. ](https://www.bloodinthemachine.com/p/with-the-backlash-to-data-centers) Brian Merchant · Aug 27 [ Read full story ](https://www.bloodinthemachine.com/p/with-the-backlash-to-data-centers) As a result, general sentiment was already overwhelmingly skeptical of AI and its overlords, so the table was pretty well set for someone to come along and say ‘just a reminder, the companies that are building the product that promises to take your job and leave a data center in your neighborhood also think that it might exterminate the human race’ and get a strong reaction from the media and the public. The question is: Should we understand this stuff as hype, strategically fanned to feed already swelling valuations? Is it doom marketing? Genuine cause for alarm that the infrastructure that undergirds modern life is facing a novel threat vector? Or reason to be sincerely worried that AI companies are amassing too much power, and that their products are genuinely dangerous? The answer, I’m afraid, is “yes.” Let me try to untangle all of this a bit, because arguments over how to navigate this moment are extremely heated right now, as they are essentially arguments over how to approach the politics of AI at a moment where there may be a unique opening for action. Those sympathetic to AI alignment concerns and x risk arguments—which increasingly includes a faction on the left who want to shut down AI over safety concerns—argue that people who dismiss AI as all hype have their heads in the sand. Meanwhile, critics of the x-risk narrative—which I might note includes a cadre of investors and tech folks on the right, too—argue that it is hype and can be used to further inflate valuations or for pursuing regulatory capture. The challenge is that many feel that dismissing AI as just hype or purely marketing also diminishes the urgency of taking on the AI industry as the novel and threat to labor, civil society, and the public sphere it is; others that by accepting the industry’s own terms, we imbue it with undue power and enable it. But let’s be clear: Declarations that AI is so powerful it might end the world are a kind of marketing, and anyone who says otherwise is just as off base as those who say that’s all that it is. If you don’t think that these sub-trillion dollar companies have higher-ups who noticed that when their founders talked about super-powerful dangerous AI they got spikes in media interest and phone calls from investors, or that those founders didn’t notice that themselves, and lean into certain narratives to advantage their products, then I don’t know what to tell you. Not all marketing is a Pepsi ad campaign with a celebrity spokesperson. Yet confronting the AI industry should certainly be considered an urgent project. Do I share the x-riskers’ fear that out-of-control, super-intelligent AI agents might end the world? I do not. I’ve read a good deal of AI extinction literature over the last couple of years and I have not come across a credible, step-by-step documentation of how exactly AI might move from self-recursively improving AI to killing every single human on the planet. Most of what I’ve read seems predicated on a sort of reverse Ian Malcolmian logic: Eventually, it becomes smart enough and AI, uh, finds a way (to exterminate humanity). Are the AI companies also overstating and dramatizing what their products can do? Yes, pretty much all the time. They’re in a knife fight for market share and are trying to win customers and government contracts before their investors come knocking. And yet. They have concentrated enormous amounts of compute, have extensive data collection and surveillance capacities, have inserted themselves into the state in numerous capacities, including military kill chains, and they are being run by egomaniacal billionaires who are rushing to monopolize an entire new market. The way I think about their most recent frightening-seeming exploits is not as a “swarm of rogue AI agents building a new civilization” or whatever, but as corporations with a hitherto-unimaginable amount of compute at their disposal recklessly experimenting with automation programs, completely unafraid of any repercussions because we have been unwilling or unable to impose any on them. So I think we should welcome any newfound imperative to hold them accountable. I also think that ultimately, the AI critics, Pause AI folks, leftists, doomers, effective altruists, and, honestly, most of the public, want a lot of the same things: legitimate checks and limits on AI companies’ power, actual transparency into what the companies are doing, and for more of AI to be under public control. (Ultimately, a lot of what animates the x-risk fears are rooted in just that: a fear of losing control.) How we move towards all this, exactly, is the question of the day, and while there’s much to be argued over in terms of building a viable political platform to challenge the AI industry’s power, I do want to cast a vote against one particular approach. Not to pick on Chris here, as there are a lot of folks out there proposing stuff like this, and the policy ideas actually stem from AI safety groups. But not only would this be challenging to land politically (I can already hear the ‘China will beat us to AGI’ calls) and all but unworkable in practice, this approach is a) far too limiting, b) fails to address the current harms caused by AI and c) would likely only wind up serving Anthropic and OpenAI; it’s what regulatory capture looks like in action. Full model transparency is the floor for what should be on offer here. If these companies believe their products will kill us, the very least we deserve is to know how. It’s in the public interest. I would also argue we might get a lot of the way to stopping any currently envisioned robot apocalypse simply by forcing AI companies to assume liability, and to submit to the full brunt of the law. If Sam Altman were liable to be charged with a felony for approving the hack on Hugging Face1, if Google was forced to pay defamation fines each time it published a false and injurious AI Overviews, these companies might suddenly find cause to restrain their models’ output, and we might hear less about rogue AI. We would need to introduce new frameworks and available tools for tracking automated lawbreaking, to be sure, but I’d wager that little would frighten the AI companies more than actually being held accountable for what their products enable. To that end, Illinois has passed an AI liability law, which the industry fought tooth and nail, and Florida is considering one. The next steps would be towards moving AI under public control; again, it’s only reasonable, since everyone, not just AI insiders, should get a say over how a technology whose developers say might kill us is developed and deployed. Dismantling the whole industrial project as currently structured should be on the table, too, pending democratic input. But that’s for another post. For now, suffice to say that while I won’t be losing any sleep about an AI-enabled extinction event, Mr. Coxon and co. have given us an opportunity to underscore the urgency of the clear and present damage AI companies are doing, the extreme power they wield and the extent to which they hold themselves unaccountable, and the abundance of political capital there is out there for taking them on. Subscribe 1 Purely speculative! I do not know if he did or not.
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