One of the key moves in the S4–mitochondria framework was to stop treating all tissues as equally vulnerable to non‑thermal EMF. Instead, vulnerability was treated as a function of structure and density:
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How many voltage‑gated channels with S4 helices are present?
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How much mitochondrial (and NOX) ROS capacity is packed into the cytoplasm?
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How tightly is Ca²⁺ timing wired into that cell’s fate decisions?
That logic cleanly explains why the “macro‑damage” endpoints cluster where they do: heart conduction fibres, cranial nerve/glial tissues, Leydig and germ cells, immune cells. Those are high‑S4, high‑mitochondria, high‑NOX environments.
The recent red blood cell (RBC) rouleaux data and the 5G skin‑cell null together point to an analogous idea on the spin side:
spin‑engine density – roughly, how much heme/flavin radical‑pair substrate is concentrated in a given cell type – gates how visible spin‑state EMF effects become.
RBCs as heme‑saturated spin engines
Mature RBCs are almost absurdly specialised: they expel their nucleus and mitochondria and turn into bags of hemoglobin plus a minimal support apparatus. By mass, the overwhelming majority of RBC protein is hemoglobin; each hemoglobin carries four heme groups. In practice, that means:
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a single RBC is packed with heme iron centres,
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redox and spin states of those hemes shift constantly as O₂ binds, is released, and as hemoglobin cycles through oxidized forms,
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a relatively small set of flavin enzymes (e.g., cytochrome b₅ reductase, glutathione reductase) and NADPH oxidase (NOX) handle the redox housekeeping.
In spin‑chemistry language, an RBC is a heavily loaded radical‑pair substrate:
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huge heme density,
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a defined set of flavin‑dependent reactions,
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redox and spin changes that directly impinge on the membrane (via oxidative modification of proteins and lipids).
When a smartphone’s near field nudges the spin dynamics of those heme/flavin systems, the consequences are immediately visible at the mechanical level: a small shift in redox balance can lower the zeta potential just enough that RBCs lose their mutual repulsion and start stacking into rouleaux. The Brown & Biebrich ultrasound study shows exactly that in vivo within five minutes.
The point is not that RBCs are uniquely “weak”; it is that they are uniquely dense in one particular kind of EMF‑sensitive machinery: heme‑based spin engines directly coupled to a zeta‑sensitive membrane.
Skin cells in 5G studies: moderate spin‑engine density, strong buffers
Now compare that to the fibroblasts and keratinocytes used in the well‑publicised 5G skin‑cell studies (3.5 GHz, mmWave FR2), which reported essentially no effects on:
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global gene expression,
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DNA methylation,
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standard oxidative stress markers,
under carefully controlled, non‑thermal conditions.
Those cells are not “deficient” in heme or flavin. They are normal nucleated cells with:
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mitochondrial heme proteins (cytochromes in the respiratory chain),
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flavoproteins in energy metabolism and antioxidant systems,
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NADPH oxidases (NOX/DUOX) as ROS engines.
What they do not have is either of the extremes:
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They are not high‑S4/high‑mitochondria nodes like heart or certain neurons.
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They are not heme‑saturated bags like RBCs.
In the language of the framework, their spin‑engine density (heme+flavin in configurations where radical pairs matter) is moderate, and it is embedded in a relatively well‑buffered metabolic context:
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monolayer culture, rich medium, strong antioxidant capacity,
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no rheology (no low‑shear venous flow for rouleaux to reveal small zeta shifts),
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endpoints read out at the level of whole‑transcriptome and methylome, not fine‑grained zeta or micro‑rheology.
Given that profile, the extended model does not need to see a big signal there. A modest, spin‑mediated tweak in heme/flavin chemistry under those 5G conditions could easily:
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stay below the detection threshold of gene‑wide expression and methylation assays, and
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be absorbed by buffers without producing a sharp oxidative burst.
Same density logic, different pillar
Conceptually, this is the same logic that already underpins the S4–mitochondria pillar:
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S4/mitochondria pillar
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High S4 density + high mitochondrial/NOX capacity → large, amplifiable Ca²⁺ timing errors → big ROS excursions → cancer, infertility, immune dysregulation.
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Low S4 + modest mitochondria → weak coupling → often null or subtle results.
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Spin‑state pillar (heme/flavin/NOX)
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High spin‑engine density (e.g., RBCs loaded with heme; certain liver, heart, or immune cells with dense heme/NOX) → small EMF‑driven biases in radical‑pair dynamics can produce visible redox and membrane effects (like rouleaux and zeta collapse).
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Moderate spin‑engine density (e.g., fibroblasts, keratinocytes in vitro) → the same class of spin‑state effects may be present but muted, often below the level of transcriptome‑wide or methylome‑wide significance in short‑term assays.
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Seen that way, the 5G skin‑cell null is not a contradiction; it is a sanity check on the density argument:
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A system with moderate S4 density and moderate spin‑engine density, under high‑frequency 5G exposure and strong buffering, does not show large oxidative bursts or global gene changes.
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A system with extreme heme density (RBCs) exposed to a near‑field RF/ELF mix does show acute, mechanically visible consequences via spin‑mediated redox and zeta changes.
Frequency windows still matter
On top of density, the frequency window is important:
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Radical‑pair systems are most obviously sensitive to static and ELF/low‑MHz magnetic components, where Zeeman splitting matches internal hyperfine couplings.
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A real smartphone in the pocket emits a complex waveform: RF carriers plus bursts and low‑frequency modulation, including ELF components that can, in principle, couple to spin dynamics.
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A highly controlled FR2 5G exposure at tens of GHz, with tight thermal control and relatively simple modulation, may simply be poorly matched to the spin‑system’s “window”, especially in cells with only moderate spin‑engine density.
So the density story and the frequency story are additive:
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High spin‑engine density + “right” ELF/B‑field window → RBC rouleaux and similar acute phenomena.
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Moderate density + high‑GHz, carefully smoothed exposure → often null at the endpoints usually measured.
Take‑home framing
For your readers, the punchline can be framed simply:
The 5G skin‑cell null does not falsify the spin‑state extension of the S4–mitochondria framework. It quietly confirms that, just as S4 + mitochondrial load gates vulnerability for Ca²⁺‑driven ROS bursts, heme/flavin “spin‑engine density” gates vulnerability for spin‑mediated redox effects. Red blood cells, with their extraordinary heme load, sit at one extreme of that spectrum and therefore act as a natural in vivo sensor for these spin‑state effects, while ordinary skin cells in 5G in vitro assays sit closer to the middle and are correspondingly less responsive under those specific conditions.