Bioelectric and Redox Terrain Failure as a Precursor to Immune Collapse: A Diagnostic Model for ME/CFS, POTS, MCAS, and Neurodevelopmental Syndromes

Why D-dimer, Fibrinogen, and “Normal Labs” Are Not Reassuring. They're the Smoke Signals of Systemic Terrain Collapse

Jul 07, 2025

This clinical IP is offered openly for patient and provider empowerment, under active copyright. Attribution is expected.

Three weeks ago, I published a diagnostic framework showing how ferroptosis (a redox-triggered, iron-dependent form of cellular death) acts less like a cell death program and more like a terrain alarm.

Now, I’ve released the second axis of that framework.
This one makes it clinical.

In plain terms: we can begin diagnosing chronic illness earlier, by recognizing the cellular signaling breakdown that happens before symptoms appear, and long before cells actually die.

What This Paper Shows

Across conditions like ME/CFS, POTS, MCAS, and other chronic syndromes, patients often present with:

Elevated D-dimer
High fibrinogen
Increased VEGF

Traditionally, these are dismissed unless there's obvious clotting, infection, or cancer.

But what if they’re not random?

What if they’re the biochemical footprints of terrain failure, a shift in cellular signaling that reflects a body trying to hold its structure under stress, but beginning to misfire?

This paper proposes exactly that:

These aren’t diseases of one cell type. They’re breakdowns in how cells coordinate under metabolic and redox pressure.

The Core Idea: Pattern Collapse Happens First

Cells don’t just die.
They first lose pattern: electrical, metabolic, and structural coherence. That mis-patterning:

Triggers ATP leakage
Activates danger receptors (like P2X7)
Amplifies immune signaling, even in the absence of infection

This sets off a cascade that feels like inflammation, fatigue, brain fog, pain, or autonomic instability, but doesn’t match classic pathology. That’s because it’s not damage-driven.
It’s coordination-driven.

What Makes This Paper Different?

Terrain as Diagnostic:
Most papers chase “what’s broken.” This one shows how collapse begins, from redox stress to pattern failure to immune bifurcation.
Sublethal Signaling as Clue:
Cells don’t need to die to trigger chaos. The moment they leak ATP or mismanage calcium, your system interprets it as a threat, and responds.
Clinically Actionable Markers:
- D-dimer
- Fibrinogen
- VEGF
- Ferroptic Markers
- Micronutrient Status
- Redox/Methylation Markers
These aren't “confusing labs.” They’re early diagnostics, if you know what terrain to look for.
Liability Logic
This isn’t a thought exercise. It’s a diagnostic system. Misusing or fragmenting it without understanding how the pieces work together could mis-stage patients and cause harm. The framework is non-transferable without fidelity.

For Clinicians: What You Can Start Doing Now

When patients have “inexplicable” fatigue, POTS, or MCAS symptoms, check:
- D-dimer
- Fibrinogen
- VEGF
- Ferroptic Markers
- Micronutrient Status
- Redox/Methylation Markers
Don’t just interpret them as thrombotic risk. Interpret them as terrain collapse markers.
Start looking at P2X7, calcium signaling, and glutathione depletion not just as consequences, but as diagnostic entry points.

This lets you stratify disease stages, and maybe even intervene before irreversible damage occurs.

For Patients: What This Means for You

If you've been told:

“Your labs are normal”
“It’s probably stress”
“We don’t know what causes this”

…you’re not alone.
What you’re likely experiencing isn’t invisible, it’s just upstream of what medicine usually tracks.

This paper begins the map.
It shows that what feels like energy failure, inflammation, or brain fog may be your cells trying to hold the system together under too much stress. Not broken, just overwhelmed, misfiring, or out of sync.

And yes, this gives us a way to start making it visible.