Two Stages, One Mechanism: How a 1997 embryo study turned a promise into RF Safe
I didn’t start RF Safe as a business plan. I started it as a promise.
In 1995, my firstborn, Angel Leigh Coates, died from a neural-tube defect. In the months that followed, the only actionable science pointed to folate. So I did the one thing a grieving dad with a technical bent could do: I spent thousands of dollars running newspaper ads in major cities urging expectant moms to take folic acid (B-vitamins) before and during early pregnancy. That was before I ever registered rfsafe.com. RF Safe became official in 1998, but the mission began the day I promised to fight whatever took Angel’s life—forever.
The study that changed my life
About a year later I saw an experimental paper (Farrell et al., 1997) reporting EMF-induced abnormalities in chicken embryos—the same class of defect that took Angel. Those images are etched in my mind: malformed neural folds, arrested closure, red arrows marking what should have been a seamless morphogenetic event. Replications have been scarce, but the signal to me was unmistakable: fields can hit developing systems at the wrong time—and the price is permanent.
Neural-tube closure is a one-shot job in week 3–4 after conception. There are no retakes.
Two different stories that meet at the same gate: ion channels
Over the years I’ve come to see a shared upstream vulnerability for both neural-tube defects (NTDs) and later neurodevelopmental divergence (including autism features): ion-channel timing and the bioelectric patterns it organizes.
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Bioelectric coherence. Cells talk in voltage. Voltage-gated ion channels—especially the S4 voltage-sensor domain—set the rhythms for proliferation, migration, and tissue patterning.
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Environmental “entropic waste.” When the environment injects noise—pulsed RF fields, certain drugs, inflammation, heat—you risk mistimed channel opening, Ca²⁺ spikes, oxidative stress, and transcriptional chaos.
Why timing dictates severity
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If the hit lands during neurulation (days ~22–28), you can derail tube closure—a structural failure with lifelong consequences.
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If it lands later (mid-gestation → infancy), you may perturb synaptogenesis, glial maturation, and myelination—changing function and circuitry more than gross anatomy.
You’ll hear similar language in the acetaminophen debate: its active metabolite can modulate sodium channels. Different input, same gate—ion-channel dysregulation—followed by the familiar cascade: ROS, immune signaling, epigenetic shifts.
Where folate fits (and why B9 keeps reappearing)
Ion-channel timing sits upstream; folate chemistry (vitamin B9) sits downstream and keeps the building line moving.
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Folic acid is the synthetic, oxidized B9 in fortification/prenatal vitamins. The body must activate it (DHFR → THF) before it can feed DNA/RNA synthesis and methylation. Taken before conception and very early in pregnancy, it reduces NTD risk because the parts bin is stocked before the one-shot event.
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Folinic acid (leucovorin) is already-active B9 (5-formyl-THF). It bypasses that activation step and can quickly top up the folate pools that support thymidine/purine synthesis (cell division/repair) and methylation (gene-programming and lipid chemistry important for myelin). Clinically, that’s why folinic is explored for cerebral folate deficiency phenotypes in a subset of autistic kids—not as a replacement for folic acid in NTD prevention, but as a targeted bypass when transport/processing is impaired.
Key point: B9 can buffer damage by keeping DNA synthesis and methylation on track, but no B-vitamin can re-time a missed morphogenetic cue. That’s why folic acid must be present before the tube closes—and why folinic later is about supporting function in vulnerable brains, not rewinding development.
How we got here with EMFs
In the late ’90s we were told the exposures were “safe.” Then came ubiquity: phones on bodies, Wi-Fi everywhere, complex pulsed signals. My engineering lens kept coming back to fields + moving charges = forces—what I’ve described as a reciprocating Lorentz force nudging ion-channel gates. Whether every detail of that model (including ceLLM) survives peer review, the biological plausibility is straightforward: voltage-gated channels are exquisitely sensitive timing devices. Add noise at the wrong window, pay for it in structure (NTDs) or function (wiring, myelination, behavior).
Two paths, one convergence
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Path 1 (1990s): Warn about folic acid because the best evidence said it prevents NTDs.
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Path 2 (1997 → today): Pursue EMF safety as literature and lab images point to field effects on developmental timing.
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Convergence: Both paths meet at ion-channel regulation and rely downstream on B9-powered DNA synthesis and methylation. Timing decides whether we face a structural catastrophe or a functional divergence.
What I’m asking readers to take away
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Don’t discount nnEMFs. They’re invisible, but like certain drugs, they can influence ion gates.
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Preconception folic acid (B9) remains a non-negotiable public-health win for NTD prevention.
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Folinic acid (leucovorin) is a different tool—pre-activated B9—for specific neuro cases with suspected transport/processing issues.
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Protect the cellular Goldilocks zone. Limit near-body, pulsed RF during pregnancy/infancy; treat timing as a safety parameter, not just “average power.”
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Mechanism matters. Whether the perturbation is a drug that modulates ion channels or an nnEMF that tweaks voltage sensors, the gate is the same; downstream support (B9 sufficiency, redox balance) helps, but timing still rules.
That’s why we must repeal Section 704 of the Telecommunications Act, enforce Public Law 90-602, and mandate LiFi where practical to reduce nnEMF load on children.
We do have solutions—if we stop pretending that because we can’t see it, it isn’t there.
John Coates
Be RF Safe to be sure!
#TrumpRepeal704
