Multiple Sclerosis: A Ferroptosis-Driven Disease

For decades, Multiple Sclerosis (MS) has been treated as an autoimmune condition. But emerging research reveals something far deeper: MS is a metabolic and redox disorder driven by ferroptosis — an iron-induced form of cell death that destroys myelin and neurons from the inside out.

Ferroptosis is iron-dependent oxidative cell death. It happens when:

• Iron escapes its storage proteins and becomes “free” (labile).
• Glutathione — the cell’s master antioxidant — becomes depleted.
• GPX4, the enzyme that protects cell membranes, shuts down.

Without defense, iron and oxygen react to form toxic radicals that attack fats in cell membranes — especially in the brain’s myelin. The result is cell rupture, demyelination, and neurological decline.

Modern imaging and pathology now show unmistakable signs of ferroptosis inside MS lesions:

• Iron buildup in brain tissue and spinal lesions
• Lipid peroxidation markers like 4-HNE in demyelinated areas
• Low glutathione in cerebrospinal fluid and neurons
• Reduced GPX4 in oligodendrocytes
• Inflammatory cytokines (IL-6, TNF-α) that trap iron and sustain the damage

MS isn’t just inflammation — it’s iron toxicity, redox collapse, and lipid destruction occurring in slow motion.

1️⃣ Inflammation raises hepcidin, trapping iron inside cells.
2️⃣ Iron fuels the Fenton reaction, generating hydroxyl radicals.
3️⃣ Myelin lipids undergo oxidative damage.
4️⃣ Glutathione depletion disables GPX4, halting repair.
5️⃣ Oligodendrocytes die → myelin is lost → neurons degenerate.

This cycle drives the relentless progression of MS — unless the iron-glutathione imbalance is corrected.

Glucoferrin® tackles the root drivers of ferroptosis in a comprehensive, metabolically precise way. First, it binds and neutralizes excess iron, preventing the toxic reactions that damage cell membranes. At the same time, it supplies sulfur-rich amino acids, such as cysteine and methionine, to restore glutathione levels — the cell’s master antioxidant. By replenishing glutathione, Glucoferrin® reactivates GPX4, the key enzyme that protects lipids from oxidative damage.

It also prevents further lipid peroxidation by neutralizing reactive oxygen species before they attack cell membranes. At the systemic level, Glucoferrin® helps normalize hepcidin and liver signaling, ensuring proper iron export and preventing accumulation in tissues. Finally, by stabilizing redox balance, it protects mitochondrial function and supports energy production, giving cells the metabolic environment they need to survive and repair.

In short, Glucoferrin® doesn’t just treat symptoms — it restores the entire ferroptosis pathway, addressing iron, glutathione, lipid protection, and mitochondrial health all at once.

Most conventional treatments for MS focus on suppressing symptoms rather than addressing the underlying metabolic causes. Immunosuppressants may reduce inflammation, but they do nothing to correct iron overload or restore redox balance. Traditional iron chelators, like EDTA or DFO, are non-specific and can strip essential minerals while increasing oxidative stress. Standard antioxidants, such as vitamin C or NAC, are limited because they cannot stop lipid peroxidation once GPX4 has been inactivated. Even natural products like lactoferrin or colostrum are too weak systemically and lack the sulfur-based redox support needed to repair the ferroptotic damage.

The bottom line: these treatments manage symptoms temporarily but do not address the ferroptosis at the root of MS.