As many of you know I have been a RN for many years. And so when my daughter was diagnosed with MS last year I dove nose first into everything I could about MS and subsequently CCSVI.
Of course I am just tickled that she had a clear cut case of CCSVI and symptomatic relief of her MS symptoms. But being a mom I was plagued with worry about re-stenosis and all the unknown things about CCSVI/MS.
It concerned me that the physicians seemed to be focusing mostly on the "plumbing" and proving the very existence of the condition. There are some that seem to be trying to figure it all out. That is the physiology and etiology behind these 2 very connected conditions.
I was intrigued by some of the findings. It is believed that the blockages, that is these valvular and other vessel blocking anomalies are congenital.( studies by Dr Lee) yet the condition seems to get worse over time eventually causing changes that lead to myelin and axon damage and activation of the immune system.
I was trying to understand endothelial function and how NO (nitric oxide) and Endothelin1 control vascular tone and function. Much has been studied on these things mostly studying arteries and hypertensive drugs.
Of particular interest was this
Increased Endothelin 1 Plasma Levels in Patients <shortened url
Why would pwMS have levels of Endothelin1 hundreds times higher than normal people?
I truly think it fits.
My theory is that a baby is born. This baby is a person that will eventually be diagnosed with MS years later. But as a baby, a youngster and young person the persons vein anomaly(s)would cause some altered shear stress, some cerebral hypoxemia and some cerebral hypoglycemia. These things are all the triggers that increase Serum Endothelin1.
Endothelin1 is a very potent vasoconstrictor and it also can cause hypertrophy (thickening) and fibrosity (stiffening) of the blood vessels if in high levels. Over time this could cause the CCSVI to get worse. When the CCSVI gets worse the blood turbulence would get worse, causing more iron to be deposited, the altered shear stress would get worse, the cerebral hypoxemia would get worse, the hypoglycemia in the brain would get worse and the brain Cells- all types would be damaged by a slow incidious chronic starvation.
This supports the CCSVI causes MS.
Could Endothelin1 levels that are high be the reason that re-stenosis occurs?
Shouldn't we be looking for a way to lower the E1 levels to normal? now that sounds like a drug we could use.
Anyway this is food for thought. Maybe I should call our "friends" at Big Pharma and ask them to investigate this?