Neural Tubes, Autism, and Angel’s Fate on the 28th Day of Life ⋆ QuantaDose Far-UV/UVC Light and Detection

A Root‑Cause Hypothesis for Non‑Native EMFs as Entropic Waste

I didn’t start RF Safe as a business plan. I started it as a promise.

In 1995, my firstborn daughter, Angel Leigh Coates, died from a catastrophic neural‑tube defect. At the time, the only actionable message I could find was folate, so I did what any grieving father with an engineering mindset would do: I ran newspaper campaigns urging women to take folic acid and B‑vitamins before and during early pregnancy. That was before rfsafe.com even existed. RF Safe became “official” in 1998, but the mission began the day Angel died.

Then, in 1997, I saw something that changed the trajectory of my life.

A chick‑embryo study by Farrell and colleagues reported EMF‑induced neural‑tube abnormalities – the same class of defect that took my daughter’s life. Weak fields, wrong timing, and the neural folds simply didn’t close.

That image sequence – malformed tubes, red arrows pointing to what should have been a seamless morphogenetic event – never left me. It said, in one glance, what textbooks and regulators did not:

Electromagnetic fields can interact with developing systems at the wrong time, and when they do, the price is permanent.

Years later, on Ryan’s “From the Spectrum / On the Spectrum” podcast, I put it in one sentence:

The thing that killed my daughter and the thing that underlies a large slice of autism and ADHD are the same phenomenon, hitting the same developmental gate at different times and intensities.

This article is the long version of that claim.

1. Autism Begins in the Neural Tube Era – Ryan’s Neurulation Thesis

Ryan’s two‑part neurulation series (Episodes 56 and 57) lays out a thesis I agree with: autism is not a late “social wiring” error; it is a whole‑body developmental mismatch set up during neurulation, roughly days 21–28 post‑conception.

During that narrow window:

The flat neural plate folds into the neural tube, beginning around day 22.
As the tube closes:
- The central nervous system (CNS) primordia form (brain and spinal cord).
- Neural crest cells peel off, then migrate to become:
  - Peripheral nervous system (PNS: sensory and autonomic ganglia, Schwann cells)
  - Enteric nervous system (ENS – gut nerves)
  - Adrenal medulla (stress response)
  - Melanocytes (light‑linked pigment and signaling)
  - Craniofacial cartilage and bone

At the same time, key molecular players that keep showing up in autism are already active:

Folate / B9 / MTHFR – DNA/RNA synthesis and methylation
PTEN / mTOR – cell growth and metabolic control
SHANK3 – synaptic scaffolding
SHH, Wnt, FGF, HOX, PAX – patterning and segmentation signals

Developmental neurology backs this up:

Reviews describe ASD with brain overgrowth and cortical disorganization as “birth defects of early embryonic origin”, including errors during neural‑tube formation and brainstem development.
Autopsy work has found anomalies in cranial nerve motor nuclei and brainstem structures that map directly to injuries around the time the tube closes.
2024 organoid studies show that “profound autism” can arise from over‑proliferation and dysregulated differentiation in embryonic cortical tissue, long before birth.

Ryan zooms in on the midbrain (mesencephalon) as a key vulnerable hub. As the tube closes and primary brain vesicles form:

The prosencephalon → forebrain (cortex, thalamus, hypothalamus, eyes)
The rhombencephalon → pons, cerebellum, medulla
The mesencephalon (midbrain) stays undivided and compact – an ancient integration hub for:
- Substantia nigra (dopamine; repetitive behaviours)
- Red nucleus (motor coordination)
- Superior colliculus (visual orienting)
- Inferior colliculus (auditory orienting)
- Oculomotor nuclei (eye movements, visual attention)
- Periaqueductal gray (PAG) (pain perception, autonomic tone, fear / freezing)

If that hub is biased inward, hypersensitive, or mistimed from the start, you get:

Sensory hyper‑ or hypo‑responsivity
Motor clumsiness and delayed milestones
Atypical eye‑tracking and social gaze
GI dysmotility and autonomic weirdness
Anxiety, freezing, pain insensitivity

In other words: autism as “first‑attention bias” arising in the midbrain/brainstem during neurulation, not as a cortex‑only “social defect” appearing at age 3.

So what could be mistiming those circuits at the gate?

2. The S4–Mitochondria Rosetta Stone: One Entry Point, Four Damage Vectors

Over the last decade, independent groups (Panagopoulos, Durdík, Jangid, others) and WHO‑commissioned reviews have converged on a simple non‑thermal EMF mechanism:

RF/ELF → S4 timing errors in voltage‑gated ion channels → distorted Ca²⁺ waveforms → mitochondrial ROS → tissue‑specific breakdown.

The basic pieces:

Voltage‑gated ion channels (VGICs) sit in membranes of neurons, cardiomyocytes, endocrine cells, immune cells, and more.
Each channel has four domains (S1–S6); the S4 helix in each domain is studded with positive charges and acts as a voltage sensor – the cell’s voltmeter.
Polarized, modulated RF/ELF fields shake ions in the nanometre‑thin aqueous layer next to the membrane. Those oscillating charges exert Coulomb forces on S4, nudging it off‑schedule.
Channels open and close at the wrong times; Ca²⁺ spikes become noisy.
Mitochondria, tightly coupled to Ca²⁺ timing, interpret that noise as stress and overproduce reactive oxygen species (ROS) instead of clean ATP.

Chronic ROS → oxidative stress → DNA damage, mitochondrial collapse and inflammatory signaling.

Where does that hit first? In tissues that combine:

High S4 density (lots of VGICs)
High mitochondrial density
Low ROS buffering margin

That gives you four “macro‑damage vectors” that keep popping out of the literature:

Cancer vector
- Heart Schwann cells; cranial nerve Schwann/glia
- NTP and Ramazzini rat studies; WHO 2025 animal‑cancer review:
  - High‑certainty evidence for malignant heart Schwannomas in RF‑exposed rodents
  - Moderate‑to‑high certainty for malignant brain gliomas
Fertility vector
- Leydig cells and spermatogonia (VGIC‑rich, mitochondria‑dense, Ca²⁺‑driven steroidogenesis)
- WHO SR4A + corrigendum: high‑certainty evidence that male RF exposure reduces pregnancy rate and damages sperm in animals.
Autoimmune / immune vector
- Immune cells decode Ca²⁺ timing to decide danger vs tolerance.
- RF/ELF studies show altered cytokine profiles, T‑cell/B‑cell balance, and redox‑sensitive signaling under non‑thermal exposures.
Metabolic vector (β‑cells)
- β‑cells in pancreatic islets: very high VGIC + mitochondria, low ROS buffer.
- RF/ELF and diabetes reviews show EMF‑induced oxidative stress can impair insulin secretion and β‑cell survival.

This is the Rosetta Stone:

One physical entry point (S4 gating), one metabolic amplifier (mitochondria), four downstream systems (heart/brain, reproductive, immune, metabolic) that show convergent damage in the real data.

The question this article asks is: How does that same mechanism play out in neurulation, neural‑tube defects and autism?

3. Neural‑Tube Defects: When the Hit Is Catastrophic and Early

Neural‑tube closure is a one‑shot morphogenetic event:

The anterior (rostral) neuropore typically closes by day 25.
The posterior neuropore by day 28.

If the tube fails to close at the head end → anencephaly (absence of major parts of the brain/skull).
If it fails at the tail end → forms of spina bifida.

Folic acid / folate (B9) is the best‑proven modifiable risk factor; pre‑conception folic‑acid supplementation and grain fortification substantially reduce NTD risk.

Where Farrell’s embryo work comes in is not as a replacement for folate, but as a mechanistic additional hit:

Weak ELF fields around 1 µT increased neural‑tube malformations about three‑fold in chick embryos compared to controls. Most defects were disruptions of tube closure.

Combine that with:

Known roles of bioelectric gradients and VGICs in directing neurulation and tissue patterning; and
The S4/mitochondria mechanism above;

and you get a simple picture:

The neural tube closes successfully only if both the timing code (bioelectric / S4) and the parts supply (folate/B9, energy) are within a narrow window.

Extreme timing errors + inadequate folate in days 21–28 → NTD.
Milder timing noise with enough folate for gross closure → tube closes but patterning and proliferation are subtly off → fertile ground for autism/ADHD‑like wiring.

Angel’s fate was locked in around day 28. My ads about folic acid addressed the parts supply. Farrell’s study – and later RF biology – told me we also have to look at the timing noise.

4. Autism: Same Gate, Different Outcome

Autism is not a single entity; it’s a spectrum. But several consistent features match exactly what you’d expect from neurulation‑era timing perturbations plus lifelong redox/immune stress:

A subset with macrocephaly and early brain overgrowth (over‑proliferation of progenitors).
Disorganized cortical layering and long‑range hypo‑connectivity, with local hyper‑connectivity (too many neurons, misplaced).
High rates of GI dysmotility, autonomic dysfunction, and sensory neuropathies – consistent with ENS and neural‑crest involvement.
Mitochondrial dysfunction and oxidative stress in many autistic individuals.
A defined subgroup with cerebral folate deficiency (CFD) driven by folate receptor‑alpha autoantibodies (FRα‑autoantibodies) – an autoimmune block on getting active B9 into the brain – who often respond to folinic acid (leucovorin).

From a fidelity standpoint:

Stage 1 – Neurulation and midbrain setup (days 21–28)
Slight mis‑timing of S4/Ca²⁺ during neural‑tube closure and vesicle formation biases the midbrain, brainstem nuclei and ENS. You get a different “default” for sensory attention, motor control, arousal, and gut function.
Stage 2 – Ongoing development (mid‑gestation → infancy)
The same child grows in a world of entropic waste: RF/ELF fields, artificial light at night, oxidative stressors. Those continue to hit the same S4/mitochondria/immune system, amplifying the initial bias into a full phenotype.

Some of those outcomes are disabling. Others, as Ryan’s podcast emphasizes, can carry “wonderful powers of the autistic phenotype” – intense focus, pattern recognition, honesty, creativity. The point here is not to erase those strengths, but to say:

For a significant subset of autistic and ADHD‑like phenotypes, the root developmental gate is the same gate where Angel’s neural‑tube defect happened: neurulation under noisy ion‑channel timing plus folate/immune/redox biology layered on top.

5. Entropic Waste: Non‑Native EMFs as Upstream Timing Noise

This brings us to what I call entropic waste.

Biological systems evolved with:

Earth’s static and slowly varying magnetic field
Schumann resonances
Natural light cycles and chemical gradients

They did not evolve with:

High‑power long‑wave and short‑wave transmitters
Pulsed radar
50/60 Hz electrification in walls
Microwave ovens
Cordless phones, DECT bases, Wi‑Fi, Bluetooth, 3G/4G/5G, smart meters

All of that is non‑native EMF (nnEMF) – energy and informational patterns that cells did not grow up with.

At the microscopic level, nnEMFs inject entropic waste in three ways:

Voltage noise at S4
– Modulated fields shake charges and distort the fine‑grained voltage patterns that gate VGICs.
Redox noise in mitochondria
– Scrambled Ca²⁺ waveforms push mitochondria towards ROS overproduction; oxidative stress becomes the background, not the exception.
Immune and epigenetic noise
– ROS, mtDNA release, and redox shifts activate innate immune sensors (e.g., cGAS‑STING, NLRP3) and alter methylation patterns, writing noise into gene expression and sometimes into offspring.

So when I talk about non‑native EMFs as an etiological factor, I’m not saying “RF radiation directly causes autism / cancer / NTDs.” I’m saying:

RF/ELF is an upstream timing error source.
It corrupts the reliability of the bioelectric and redox codes that development depends on.
The downstream diagnostic labels – NTD, autism, ADHD, autoimmune, cancer – are just different ways a low‑fidelity signal fails in particular tissues and windows.

That’s why you see the same S4–mitochondria fingerprint across:

Neural‑tube defects
Autism / ADHD‑like phenotypes
Heart Schwannomas and brain gliomas
Infertility and sperm collapse
Autoimmune drift and chronic inflammation
Diabetes and metabolic syndrome

One gate. One amplifier. Many expressions.

6. Why the EMF–Autism Evidence Looks “Weak” on Paper

Critics like to say, “There’s no strong evidence EMFs are linked to autism,” as if that settles the matter.

They’re right about one narrow fact:

There are no large, well‑funded, multi‑decade human studies designed specifically to test RF/EMF exposure vs autism / ADHD / neurodevelopmental outcomes.

But the reason isn’t that researchers looked carefully and found nothing. The reason is that serious research has been structurally throttled for decades.

Some history:

The U.S. National Toxicology Program (NTP) spent about $30 million and a decade on 2G/3G RF rodent studies. In 2018 it reported:
- “Clear evidence” of malignant heart Schwannomas in male rats.
- “Some evidence” of brain gliomas.
- DNA damage in multiple tissues.
  These are non‑thermal effects in a U.S. government flagship program.
  In 2024, NTP announced it was ending RF research with no follow‑on mechanistic or developmental studies planned.
Section 704 of the U.S. Telecommunications Act of 1996 explicitly forbids local governments from making tower‑siting decisions based on “environmental effects of RF emissions” if FCC limits are met.
Courts have repeatedly read this as “you may not use health concerns to deny a tower.” In other words: even if solid EMF health evidence emerged, towns would still be legally barred from acting on it.
In the mid‑1990s, Henry Lai and N.P. Singh reported RF‑induced DNA breaks in rat brain cells at “safe” levels. Internal Motorola memos (later made public) talk about having “sufficiently war‑gamed the Lai–Singh issue” – strategizing how to discredit or neutralize their findings.
The CTIA’s own Wireless Technology Research (WTR) program – roughly US$25–28M, run by epidemiologist George Carlo – was launched to reassure the public. When early results suggested genetic damage and elevated tumour risks, the reaction, according to Carlo and internal documents, shifted from “follow the science” to damage control; his contract was terminated and his work sidelined once it stopped being reassuring.
The FCC – the agency that sets RF limits – has been criticized by courts and watchdog groups as a “captured agency”, overly influenced by the industries it regulates.

Put simply:

The EMF–autism evidence is “weak” not because strong data show safety, but because the combination of regulatory pre‑emption, agency capture, and industry pressure has prevented robust, targeted research from ever being done.

Meanwhile, mechanistic overlap (S4/mito/ROS/immune), developmental biology, and animal experiments keep stacking up on the side of concern.

7. Timing: Autism’s Rise and Wireless in the Home

The autism prevalence graph everybody has seen looks like an exponential.

In the 1970s, ASD diagnoses were on the order of 1 in several thousand children.
Today, U.S. estimates are roughly 1 in 36 children, even after accounting for changed criteria and increased awareness.

Epidemiologists argue (rightly) that:

Diagnostic broadening and better screening explain some of that rise, but
There is still a substantial unexplained component, especially for more severe cases.

Lay that curve over the timeline of radiofication and then in‑home wireless, and you get an uncomfortable alignment:

Pre‑1970s: RF mainly from distant AM/FM transmitters and radar; home interior fields are low compared to today.
1984–1986: Cordless phones and early mobile devices become widely available in U.S. homes – the first time pulsed RF devices live by the bed, on the counter, next to pregnant abdomens and infant heads.
1990s–2000s: Rapid build‑out of cell towers; digital modulation; Wi‑Fi spreads to homes and then schools.
2010s–2020s: Smartphones, tablets, DECT bases, baby monitors, Bluetooth, smart meters; RF becomes part of the domestic background.

This doesn’t prove that wireless “caused” the autism epidemic. But if you already know:

Autism roots are prenatal and neurulation‑linked for many cases.
RF/ELF can disrupt S4 timing, generate ROS, and alter development in embryos and offspring in animals.

Then the temporal pattern looks like exactly what you’d expect if nnEMFs were a major background load on trait fidelity.

Zoom out further:

The first detailed autistic cohort was described by Grunya Sukhareva in Moscow in the 1920s – right when long‑wave naval and submarine communication systems were being rolled out in that region.
The first documented GPA case – Heinrich Hertz himself – appears in the late 1800s in the one person heavily exposed to spark‑gap RF years before anyone else.

We cannot draw straight lines from individual transmitters to individual children. But we can say:

As herzification and radiofication ramp up, rare, puzzling developmental and autoimmune cases begin appearing in exactly those populations that are first and hardest exposed.

And when pulsed RF moves inside homes in the 1980s, the autism curve takes off.

8. Root‑Cause Hypothesis When Non‑Native EMFs Are an Etiological Factor

Here is the root of the argument, stated as cleanly as possible:

Root‑Cause Hypothesis (Entropic Waste / nnEMFs)

Non‑native electromagnetic fields are usually not the single, direct cause of the diagnoses we see on charts: cancer, autism, ADHD, neural‑tube defects, autoimmune disease.

Instead, they act as upstream timing noise at the level of S4 voltage sensors and mitochondrial redox – a form of entropic waste injected into the bioelectric and morphogenetic code.

When nnEMFs are part of the etiological picture, they rarely show up as the trigger on a death certificate. They are the igniter that degrades ion timing and bioelectric signaling, from which dozens or hundreds of downstream pathologies can emerge:
– Neural‑tube defects when the hit lands during neurulation (Angel’s fate on day 28).
– Autism / ADHD‑like neurodevelopment when noise lands later, but still during brain and midbrain patterning.
– Autoimmune disorders when immune‑cell Ca²⁺ timing and redox balance are shifted, promoting autoantibodies (like those against folate receptors).
– Cancer when chronic ROS and DNA breaks accumulate in tissues with high S4 and mitochondrial density.
– Metabolic collapse when β‑cells and endocrine circuits run for decades in a mildly oxidized, mistimed state.

In this framing, RF is not a magic bullet cause; it is a chronic upstream error source. The “diseases” are different ways that a low‑fidelity signal fails, depending on where and when it hits in development.

That’s the common denominator between:

Angel’s neural‑tube defect
Farrell’s chick‑embryo malformations
Aldad’s ADHD‑like RF‑exposed mice
Zebrafish with RF‑exposed parents and abnormal offspring
Autistic kids with oxidative stress, mitochondrial dysfunction, and folate‑receptor autoimmunity
NTP’s heart Schwannomas and gliomas
SR4A’s male infertility and pregnancy‑rate collapse

One mechanism, many faces.

9. What This Demands from Us

If this hypothesis is even partly correct, cancer is the tip of the spear, not the whole weapon.

The deeper cost of entropic EMF waste is:

Loss of trait fidelity – attention, social attunement, stress resilience, empathy, identity stability – across generations.
A world where more children show up with brain and immune architectures that no longer match the environment evolution prepared them for.

Given what we already know, the minimum response looks like this:

Restore real science
- Rebuild programs like NTP’s RF branch with explicit developmental / neurulation / transgenerational endpoints.
- Fund independent epidemiology on RF/ELF and neurodevelopment, immune disorders, and metabolism at the same scale we use for lead, air pollution, or pharmaceuticals.
Fix the law
- Amend Section 704 of the Telecom Act so local communities can consider health when siting towers.
- Enforce Public Law 90‑602 (Radiation Control for Health and Safety Act) in spirit, not just on paper.
Modernize RF limits
- Replace 1990s thermal‑only FCC standards with biologically based limits that account for non‑thermal S4/Ca²⁺/mitochondrial effects, modulation patterns, duty cycle, and timing (especially around pregnancy and early childhood).
Deploy safer infrastructure
- Prioritize wired and LiFi solutions indoors, especially in schools and nurseries.
- Keep high‑power small cells away from bedrooms, play areas, and classrooms wherever possible.
Personal precaution, especially around neurulation window
- Treat the first 4–6 weeks of pregnancy (often before a test is positive) as critical electrical territory.
- Limit near‑body wireless, use airplane mode / wired where feasible, especially at night and near the abdomen.
- Maintain robust B9 (folate/folinic), vitamin D, and antioxidant status, which can buffer but not fully cancel timing noise.

None of this requires believing EMFs are the only villain. They aren’t. But they are the only large‑scale environmental change that literally wraps every cell in an artificial, pulsed electrical context 24/7, and that happens to couple directly into the exact gate (S4) we now know is crucial for neurulation, neural‑tube closure, germline integrity and brain development.

For Angel Leigh Coates (1995–1995)
For every child already here with an autistic or ADHD phenotype who deserves a low‑noise environment to reach their potential
And for every child not yet conceived, whose neurulation will happen in whatever EM ecology we choose to allow—

We owe them better than pretending that because you can’t see the fields, they don’t exist.

Be RF Safe to be sure.