Is Multiple Sclerosis a Vascular Disease—Not an Autoimmune Mystery

For decades, multiple sclerosis (MS) has been treated as an autoimmune disease where the immune system attacks nerves for no clear reason. 

Groundbreaking research over the last several years is rewriting that story. Today, leading evidence points to MS as primarily a vascular disorder: a disease driven by chronic blood-vessel dysfunction, low oxygen, impaired venous drainage, which may in fact be caused by a parasitic infection. The immune system is involved, responding to vascular injury, not causing it.

 

Vascular Abnormalities: The Real Pathology in MS

Multiple studies, meta-analyses, and updated clinical criteria now describe a consistent vascular pattern in MS:

1. Endothelial Dysfunction

The innermost lining of blood vessels (the endothelium) shows early, persistent damage in MS. When the endothelium falters, oxygen and nutrient delivery fall, vessel tone is lost, and the blood–brain barrier (BBB) weakens.

 

2. Leaky Blood–Brain Barrier (BBB) – Early Vascular Damage Precedes Immune Attack in MS

Advanced MRI scans and tissue studies show that the blood–brain barrier (BBB) begins to leak in areas of the brain that still look normal on standard imaging—before visible MS lesions form. 

This means the disease process starts before immune cells arrive.

When the blood–brain barrier (BBB) becomes leaky, it sets off a chain reaction. The BBB’s job is to tightly control what can enter the brain from the bloodstream—keeping out toxins, microbes, and many other things found in the blood.

But when the BBB is damaged, it starts to leak small amounts of blood components into brain tissue. The immune system immediately senses that something is wrong. It recognizes that materials from the blood don’t belong inside the brain.

In response, the body signals immune cells to the area to clean up the mess and protect the brain. 

This protective process, however, creates inflammation—a battle between the immune system and the unwanted contents from the blood in the brain. The inflammation is not the cause of the damage; it’s the body’s attempt to protect the brain, repair the breach and restore normal physiology.

In short:

Leaky BBB → Immune activation → Inflammation → Lesion formation.

It all starts with vessel injury, not a mistaken immune attack.

 

3. Abnormal Venous Drainage (CCSVI)

Advanced imaging and autopsy studies reveal sluggish drainage and reflux in brain veins—a pattern described as chronic cerebrospinal venous insufficiency (CCSVI).

Outflow through the jugular and azygos systems can be obstructed or reversed.

Venous congestion raises pressure, stretches vessel walls, and weakens the BBB.

Nearly every MS lesion forms around a central vein, showing venous stress.

 

4. 2024 McDonald Criteria—Central Vein Sign (CVS)

Worldwide diagnostic guidelines were revised to include the central vein sign: a small vein running through the middle of lesions on advanced MRI.

If ≥6 white-matter lesions are CVS-positive, or if the majority are when total lesion number is <10, true MS is highly probable.

Experts feel this may help distinguish MS from lookalikes and formally places veins at the heart of MS lesion formation.

 

5. Microvascular Remodeling and Hypoperfusion

Chronic hypoxia (low oxygen from poor flow) turns on vascular “rescue” signals—VEGF, HIF-1α, and Notch—that grow fragile new vessels and worsen BBB leakiness.

SPECT and fMRI consistently show 20–30% less oxygen-rich blood in MS brains.

 

6. Iron Deposition and Microbleeds

With ongoing vessel breakdown, iron from damaged red blood cells leaks into tissue and forms ring-like deposits at lesion edges.

 

7. Fibrin and Collagen Deposition

When veins in the brain are injured, the cells lining their walls (endothelial cells) become activated, causing inflammation of the vessel wall (vasculitis) and sometimes partial blockage of blood flow (vascular occlusion).

Fibrin, a clotting protein that appears during vessel injury, then builds up along these damaged walls. Its presence is a clear marker of active MS lesions. Under the microscope, these vessels look swollen and thickened from inflammation and fluid buildup.

Laboratory staining for collagen type IV confirms that these lesions start within the blood vessels themselves, proving their vascular origin.

Fibrin leaks into the brain at vessel-injury sites as an initial repair molecule. Over time, collagen build-up and vessel fibrosis increase stiffness and risk of stroke.

 

8. Arterial Stiffness / Early Vascular Aging

Research shows that people with MS have stiffer arteries and signs of early blood-vessel aging compared to those without MS.

 

9. Homocysteine Elevation and Endothelial Microparticles

Research shows that people with multiple sclerosis often have higher levels of homocysteine in their blood even when vitamin B12 and folate levels are normal, meaning the rise isn’t caused by nutrient deficiency.

Elevated homocysteine in MS directly damages the lining of blood vessels, making them weaker and more prone to leaks and inflammation. 

Studies also find increased endothelial microparticles—tiny fragments released from injured blood-vessel cells—in the blood of people with MS. These microparticles are clear evidence of ongoing vascular stress and damage.

High homocysteine = blood-vessel injury and chronic vascular strain in MS.

 

Vascular Disorders Are Common in People with MS

Research shows that blood-vessel issues are much more common in people with multiple sclerosis than in the general population. These findings further support that MS is deeply connected to vascular dysfunction rather than being an autoimmune disease.

• Venous thromboembolism (VTE):
  Blood clots that form in deep veins—known as deep-vein thrombosis (DVT)—and clots that travel to the lungs (pulmonary embolism) occur two to three times more often in people with MS, especially soon after diagnosis.
• Ischemic heart disease and heart failure:
  Damage to the cells that line blood vessels (endothelial dysfunction) increases the risk of heart attacks and heart failure, showing that MS affects the cardiovascular system as a whole.
• Peripheral vascular disease:
  MS doesn’t just affect the brain and spinal cord. It also impacts arteries and veins throughout the body, reducing circulation to muscles and organs.
• High blood pressure and abnormal cholesterol (hypertension and dyslipidemia):
  Blood-pressure and cholesterol problems tend to appear earlier and more severely in people with MS.
• Stroke, especially ischemic:
  Recent meta-analyses show a 2 to 3 times higher risk of stroke, particularly ischemic stroke, likely caused by vessel injury and micro-clotting.
• Small-vessel (microvascular) disease:
  Damage to the smallest blood vessels in the brain closely tracks with MS symptoms and long-term disability, linking microvascular injury directly to disease progression.

 

Immunity, Inflammation, and Repair—A New Perspective

Fibrin: Not a Villain

Fibrin is often seen as a marker of inflammation in multiple sclerosis, but it’s not the real villain. In fact, fibrin is part of the body’s emergency repair system.

When a blood vessel is damaged, fibrin acts like a biological bandage—it helps seal leaks, trap microbes, and stabilize the injured area so healing can begin.

The problem arises when the underlying vessel injury isn’t repaired. In that case, fibrin keeps forming, and the ongoing cleanup response leads to chronic inflammation. Simply blocking fibrin without addressing the **root cause—blood-vessel damage—**can actually make things worse.

Fibrin is a sign of the body trying to heal, not the source of the problem.

 

Granulomas

In multiple sclerosis, scientists sometimes see granulomas—small, tight clusters of immune cells. These clusters form when the body tries to contain something it can’t easily remove, such as microbes, debris, or irritants.

What’s important is where they appear. These immune clusters are usually found around blood vessels, not scattered randomly through brain tissue. This perivascular pattern shows that the immune activity in MS begins at the site of blood-vessel injury, supporting the idea that MS starts as a vascular problem—not an autoimmune one.

 

Leptomeningitis

Leptomeningitis is inflammation of the thin layers that cover the brain—sometimes called brain-lining inflammation.

In multiple sclerosis, this inflammation often develops right next to damaged blood vessels or in areas where the blood–brain barrier (BBB) has started to leak. This is a reaction to vascular injury, not a random immune attack on healthy brain tissue.

 

Could chronic and cerebral malaria (or a similar protozoa) be the driver behind MS vascular abnormalities?

A growing body of research points to chronic and especially cerebral malaria or a similar protozoa—as the infectious disease that most closely mimics the vascular pathology seen in multiple sclerosis (MS). While many infections impact the nervous system, few reproduce the full spectrum of vascular damage, red blood cell changes, and tissue consequences observed in MS as thoroughly as malaria does.

How Cerebral Malaria Mirrors MS Vascular Injury

• Endothelial Dysfunction and BBB Breakdown: In chronic and cerebral malaria, parasite-infected red blood cells adhere to the lining of brain blood vessels, causing direct injury and triggering widespread blood–brain barrier (BBB) breakdown. This leakage lets plasma proteins, inflammatory cells, and toxins into the brain—exactly as found in early MS lesions.
• Impaired Venous Drainage and Central Vein Sign: Sticky, less-flexible red blood cells cause venous congestion and microvascular blockages. Pathologists describe “ring hemorrhages” and perivenous iron stains that resemble MS’s “central vein sign”—a diagnostic marker now officially required for MS by the 2024 McDonald Criteria.
• Microvascular Remodeling, Hypoxia, and Vessel Fibrosis: Both conditions feature microvessel remodeling, hypoxia-induced signaling (via VEGF and HIF-1α), excessive angiogenesis, and ultimately fibrosis from chronic inflammation. Iron leaks, ongoing fibrin deposition, collagen build-up, and stiffer vessels disrupt local blood flow, raising the risk for further brain injury and stroke.
• Red Blood Cell Abnormalities: Malaria and MS share “sticky” and poorly deformable red blood cells, resulting in reduced oxygen delivery, blockage of small vessels, and chronic or fluctuating anemia. Bloodwork often shows increased red cell distribution width (RDW), abnormal MCV/MCH/MCHC, and occasionally rouleaux (stacked RBCs), signifying impaired microcirculation and disease severity.
• Vascular Disorders: Both conditions show increased rates of venous thrombosis, hypertension, heart failure, and stroke—clear signals of chronic vascular stress.

Brain Lesions: Overlapping Geography and Structure

Strikingly, cerebral malaria and MS produce brain lesions that localize in the very same regions—periventricular white matter, subcortical regions, and along small veins. Both exhibit:

• Perivenous (central vein) lesions: Lesions consistently form around veins in both diseases, with bleeding or immune infiltration tracing the vessel’s path.
• Ring hemorrhages and iron deposits: Pathologists have found perivenous iron rings in both cerebral malaria and MS brains, a sign of microbleeds and vascular breakdown.
• Cortical, juxtacortical, and deep white matter involvement: The lesion map in advanced imaging is nearly identical.
• Small vessel infarcts and microinfarcts: Both show signs of microvascular occlusion, with subsequent hypoxia and tissue death.

The True Cause of MS

Recent reviews and comparative studies emphasize that not only the laboratory abnormalities (sticky RBCs, hypoxia, vessel wall fibrosis), but also the pattern of brain lesions and the underlying vascular pathophysiology are almost indistinguishable in chronic/cerebral malaria and MS.

Because the malaria parasite (Plasmodium falciparum and its close relatives) causes the same types of blood and vessel damage seen in multiple sclerosis, researchers believe it may be one of the most likely known pathogens capable of triggering the full range of vascular problems found in MS.

In other words, the effects of malaria on red blood cells and blood vessels provide an important clue to how similar infections could set off the chain of events that lead to MS.

This represents a major shift in how we understand multiple sclerosis—from viewing it as an autoimmune mystery to recognizing it as a disease rooted in chronic blood-vessel injury and infection. Seeing MS this way helps explain its wide range of symptoms and offers new hope for treatment and recovery.

Instead of suppressing the immune system, this approach focuses on healing the vascular system, addressing infection, and restoring proper blood flow—treating MS as a consequence of chronic neurovascular infection and its aftermath.

Conclusion

MS is not simply an autoimmune or nerve disease. It begins with chronic blood-vessel injury—reducing oxygen, triggering leaks, and inciting a defensive immune response. The 2024 McDonald Criteria now require radiologists to look for veins in the center of MS lesions, officially placing vascular pathogenesis at the center of diagnosis.

When we restore blood-vessel health by supporting the body, treating the infectious root cause and managing inflammation, genuine MS recovery and meaningful prevention is possible.

There are real solutions to recover from parasites today!

To restore health, we must focus on treating the cause of inflammation, which are parasites. First, identify the enemy (parasites), then support the body and treat the parasites while following a holistic approach. When parasitic infections are treated effectively, we can overcome inflammation or disease.

If you’re frustrated with the fact that our standard of care STILL doesn’t offer a real solution for treating MS and other diseases, then click on the link below to watch Pam Bartha’s free masterclass training and discover REAL solutions that have allowed Pam and many others to live free from MS and other diseases.

CLICK Here to watch Pam’s masterclass training

 

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