My Research

How This Research Began

This research originated from my clinical work with clients suffering from a cluster of conditions: MCAS (Mast Cell Activation Syndrome), POTS, and EDS (Ehlers-Danlos Syndrome). I wanted to understand what had led to such a significant rise in cases.

The traditional explanation is that EDS is a genetic condition that leads to MCAS and POTS through weakened blood vessels and autonomic dysfunction. But I discovered that EDS was rising at rates that could not be explained by the hereditary nature of the disease.

Then I realized: I had likely had MCAS/POTS/EDS myself when I worked at a wireless networking company, surrounded by high-power WiFi routers daily — and I had cured myself. This led me to investigate environmental stressors, primarily EMF, as a root cause triggering mitochondrial dysfunction.

Pathway 1: Mitochondrial Disruption

The electron transport chain (ETC) in our mitochondria generates a weak endogenous electromagnetic field oscillating at 150-210 Hz. When a 60 Hz external field from a power substation occupies the same space, the superposition creates interference that disrupts electron transfer timing.

Complex IV (cytochrome c oxidase) normally produces up to 32 water molecules for every glucose molecule. This metabolic water is critical for collagen hydration. When production drops, collagen loses its elasticity.

Pathway 2: Cellular Dehydration & Acidosis

When mitochondria fail, cells fall back on glycolysis for energy. This shift has severe consequences:

Collagen is exquisitely sensitive to pH: even a small drop in alkalinity weakens the hydrogen bonds that hold the triple helix together. Combined with dehydration, tendons become brittle.

Pathway 3: Voltage-Gated Calcium Channels

Research by Martin Pall has shown that ELF magnetic fields activate voltage-gated calcium channels (VGCCs) on cell membranes. The voltage sensor is over seven million times more sensitive to electrical forces than the rest of the cell membrane.

This allows weak 60 Hz fields to keep calcium gates open, flooding cells with calcium ions. The downstream effects are devastating:

• Excess calcium in fibroblasts boosts nitric oxide production
• Nitric oxide + superoxide = peroxynitrite
• Peroxynitrite breaks proteins apart and degrades the extracellular matrix

Pathway 4: Collagen Piezoelectricity

Research by Robert Becker & Andrew Marino in the 1970s showed that collagen exhibits piezoelectric properties — it converts mechanical stress into electrical signals that govern tissue repair.

When external man-made fields override these natural signals, they disrupt the "crystalline lattice" of the collagen fibers, interfering with the body's ability to properly maintain and repair connective tissue.

The MCAS Connection

Beyond the direct cellular effects, EMF exposure triggers immune and inflammatory pathways that compound the damage to connective tissue.

Pathway 5: Mast Cell Activation

Research by Olle Johansson at the Karolinska Institute has shown that low-level ELF magnetic fields trigger mast cell degranulation in tendons and ligaments, releasing inflammatory mediators:

The result is chronic remodeling of connective tissue into mechanically compromised material — exactly what we see in the pattern of 49ers injuries.

Pathway 6: Chronic Immune Suppression

Andrew Marino's Neuroendocrine Theory (1993) explains how ELF fields function as persistent environmental stressors detected by the central nervous system, triggering HPA axis activation:

• Elevated cortisol (inherently catabolic to tissue)
• Reduced effectiveness of natural killer cells and T-lymphocytes
• Cytokine imbalance favoring inflammation over repair
• Elevated evening cortisol blocks nighttime repair initiation

Pathway 7: Circadian & Oxidative Disruption

Research by Joan Chang et al. (Nature Cell Biology, 2020) shows that disrupted circadian rhythms prevent proper collagen synthesis and cross-linking timing.

When melatonin is suppressed (via blue light exposure compounding EMF effects), the body loses endogenous antioxidant capacity. Oxidative stress accumulates, suppressing procollagen gene transcription while upregulating matrix metalloproteinases — a double hit of degradation.