Thanks for bumping this thread, Cece, and linking Arlene Hubbard's notes from Dr. Cooke's presentation. It was great to speak to Dr. Cooke again, now three years past Jeff's treatment. We discussed how weight loss, cardiovascular exercise and a heart healthy diet has continued Jeff's recovery, and my better health, too. Dr. Cooke commented that I looked younger than he remembered...(I've also lost weight and am in better health since we changed our family's diet and exercise.) Increased bloodflow, vasodilation and increased shear stress "de-age" and heal the endothelium. The endothelium benefits from a moving body and flowing blood. Epigenetic changes due to lifestyle can make a tremendous difference.
And, yes....the proposal to make an animal model of CCSVI is the first time Dr. Cooke has ever had a research proposal rejected by the NIH. This confuses and angers him.
Here are my notes from Dr. Cooke's presentation:
Dr. Cooke and Dr. Dake’s research was just published as a retrospective. This included the first patients treated at Stanford in 2009. There were large collateral channels in most of the pwMS seen at Stanford. The average patient had an 80% stenosis, which was reduced to 0% after stenting. The paper was delayed a year, due to political factors, but it is published now.
The endothelium is a single layer of cells, and it exerts control over circulating blood elements. Changes in venous flow and pressure can set up cerebral inflammation. increased strain increases endothelial cell (EC) adhesion molecules, EC chemokines, EC permeability, vein wall thickening, perivenular cuffing, oxidative stress, local hypoxia and plaque formation.
Dr. Cooke likes to say, “One is as old as one’s endothelium”---
The endothelial cells regulate vessel tone and the force of blood flow causes sheer stress, EC cells like blood flow. Blood vessels adjust to flow, changing diameter size. Flow mediated vasodilation is completely mediated by the endothelium. Structural changes of blood vessels long term. Endothelial cells line up in response with flow and hemodynamics.
There is disturbed blood flow in bends and arches of blood vessels--like an eddy in a river. Plaque forms in these areas where EC are exposed to abnormal flow. Platelets adhere to EC cells at bends, branches and bifurcations. Disturbed venous pressure--creates more adhesion, more inflammation is responding.
Zamboni’s evidence looked at how venous disease in the legs is like MS---venules in skin of venous insufficiency. Low shear stress starts epigenetic activation, which is causing thickening of vessel wall.
Smooth muscle cells are increased. CCSVI changes venous flow patterns, and creates hemodynamic alterations. White blood cells are attracted to endothelial adhesiveness.
Dr. Cooke would like his lab to study the endothelial cells in CCSVI. He would also like to create animal models of CCSVI beyond the mouse model. He has applied to all his previous sources to fund his research (like the NIH) He also applied to the MS Society, but this is the first time in his career he has been turned down. Controversy is keeping money away from this. We need funding to investigate this hypothesis.
Husband dx RRMS 3/07
dx dual jugular vein stenosis (CCSVI) 4/09
dual stents placed 5/09
CCSVI in MS