"This is Marie-

Joan's excellent post can be found here:

http://www.facebook.com/note.php?note_id=10150278627447211

Joan writes so well it is really fun to read what she writes. Her points are really important.  The second to last paper she mentions is one on sickle cell disease where the patients get different kinds of vascular strokes based on their HLA type.  This is really worth exploring further.

Sickle cell disease is a genetic disease in which there is an altered gene related to hemoglobin.  Because of this the red blood cells take on an elongated shape.  These elongated red blood cells get stuck in the blood vessels and cause a kind of blood "stickiness" and vascular disease/strokes.  What is so interesting about the paper Joan cited is that people with SCD have different kinds of strokes or vascular issues based on the kind of HLA they have.

It's not their gene related to the sickle cell that dictates what kind of stroke they have-- It is the kind of genetic HLA that makes the difference.  You have one type and small vessels get blocked up, with another type it's the large ones.

Reverting now to MS/CCSVI, it is possible that the kind of immune system we have makes a difference to how the body responds to CCSVI.  Does HLA DRB1-1501 cause MS-type lesions when CCSVI is present?  All the lesions are on venules (vessels that are smaller) does the HLA type cause vulnerability in these vessels that just isn't present in others? Is it possible that the healthy people with CCSVi in Zivanidov's study had HLA other than HLA DRB1, therefore no lesions?

Conversely is it possible that CCSVI stenoses (webs and altered valves etc.) caused by the HLA type?  The Ferlini paper suggests all kinds of t-cell responses interact with the blood vessels in a complex dance that is greatly influenced by the HLA which could mean this line of thinking is worth investigating

In my book I said repeatedly, and Joan and I have proclaimed from the very beginning of this debate, that no one knows how much of MS is caused by venous issues and how much is caused by immune system differences.  At this point anyone claiming to know is speaking on opinion and not science--the jury is still out.  It could be 80% one and 20% of the other.   That doesn't mean that one aspect can or should be ignored, notice the sickle cell disease mentioned above; addressing and treating vascular problems as they come up is part of good disease management.

All we are asking is that the vascular aspect of MS which has long been ignored should be fully investigated and the role of these venous issues should be clarified.  It doesn't help to pretend there isn't a vascular aspect to MS--there is.  Better to figure out how these vascular changes relate to the disease process than to simply pretend this aspect of MS is unimportant.  

Thankfully there are dedicated people all over the world devoting their energy to investigating this for us.  Often these people suffer the slings and arrows of the status quo.  We owe all our researchers a big debt of gratitude for taking this on in the face of such strong bias against the idea, and I owe a debt of gratitude to everyone who contributes their energy to the grassroots side of CCSVI too.  Together we are bringing this foward.

Thanks!

~Marie

http://ccsvibook.com