Welcome! This blog contains research & information on lifestyle, nutrition and health for those with MS, as well as continuing information on the understanding of the endothelium and heart-brain connection. This blog is informative only--all medical decisions should be discussed with your own physicians.

The posts are searchable---simply type in your topic of interest in the search box at the top left.

Almost all of MS research is initiated and funded by pharmaceutical companies. This maintains the EAE mouse model and the auto-immune paradigm of MS, and continues the 20 billion dollar a year MS treatment industry. But as we learn more about slowed blood flow, gray matter atrophy, and environmental links to MS progression and disability--all things the current drugs do not address--we're discovering more about how to help those with MS.

To learn how this journey began, read my first post from August, 2009. Be well! Joan

Tuesday, December 7, 2010


December 7, 2010 at 12:01pm

Myelin, the insulating sheath around all of our nerves,  is damaged by an auto-immune reaction in stroke, spinal cord injury, neurovascular disease, dementia, and carbon monoxide poisoning.  
This is a fact.
MS is not unique.  The immune system has the same reaction in situations where there is oxidative stress.
Here's some of the research: 

Long term immunologic consequences of experimental stroke and mucosal tolerance
An inflammatory insult following middle cerebral artery occlusion (MCAO) is associated with a predisposition to develop a deleterious autoimmune response to the brain antigen myelin basic protein (MBP)

The "autoimmune" reaction of t-cells in spinal cord injury ( SCI) 
Previously, we demonstrated that CNS-reactive T cells are activated in SCI [29,30]. Other groups have shown activation of myelin basic protein (MBP)-reactive T cells after experimental and clinical nerve trauma [31,32]. Clinical studies that show increased frequencies of MBP-reactive T cells in SCI and stroke patients provide further evidence of an association between CNS trauma and the activation of CNS-autoreactive T cells.

Myelin basic protein antigens in carbon monoxide poisoning 
We hypothesized that acute CO-mediated oxidative stress causes alterations in MBP and that immune responses to the modified protein precipitate delayed neurological dysfunction.

These findings provide insight into the pathophysiology of brain injury due to CO poisoning. Biochemical and immunological studies indicate that MBP undergoes charge and antigenic alterations. A causal relationship between lipid peroxidation and MBP modifications is supported by colocalization of MDA-adducts.


In every single one of these instances, antigens (attackers) to myelin basic protein (MBP reactive t-cells) go after the myelin and destroy it. This is considered an "auto-immune" response.
But in stroke, vascular disease, spinal injury, dementia and CO poisoning, the real culprit, ischemia (injury due to low oxygen) and a break in the blood brain barrier is known.  

-No one calls a stroke an "auto immune disease."

What is the culprit in MS?  Why doesn't the myelin repair in MS?    What activates this auto immune response? The answer has been that it's just a faulty immune system.

EAE, the current mouse model for MS, doesn't look like MS.  It doesn't relapse and remit, like MS in people.
But Dr. Zamboni has found a reason for the antigenic response to MBP.  It's called CCSVI.  
A chronic vascular disorder that waxes and wanes.  Just like all the other reasons why MBP reactive t-cells form in all the other instances---blood flow, inflammation and oxygenation.

It's time to look at MS as a potential chronic disease of ongoing diffuse cerebral hypoxia and inflammation, with breaks in the blood brain barrier as separate injurious "events." 
It's time to measure perfusion before and after angioplasty (like the wonderful Haacke protocol)
It's time to look at brain oxygenation in MS--the same way we look at stroke, arterial occlusion, hypoxia. 

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