endoterin 1?

[Cece]

But why have so many of those treated later regressed? Dr Tomasz Ludyga, of the Euromedic Clinic in Katowice, who carried out the Scots’ procedures, offers an explanation.

“We can’t explain this entirely but we think when there is a blocked circulation some substances are secreted in the brain to protect it, which results in damage.”

He added: What we are looking at is a substance called Endoterin 1 and its levels before the procedure and after. After the procedure, the veinous obstructions are cleared and we think these substances disappear. And we can get some initial improvement in the body functions such as headaches going, feet warming, improved retina, balance improving.

“But if a patient, for example, had a disease for 20 years or more then you can’t expect them to be cured immediately. The damage to the neurons in the brain and the spinal cord means that the restoration could take several years. The feeling of the neurons has just started.”

http://www.heraldscotland.com/life-styl ... -1.1063560

[ErikaSlovakia]

Correct word is Endothelin 1.
You can find more info here: http://www.ncbi.nlm.nih.gov/pubmed/11315981
"RESULTS: The plasma ET-1 levels were, on average, 224% higher in the patients with MS than in the controls (p < 0.005). "

Erika

[cheerleader]

Thanks for the paper, Erika.

Endothelin- 1 is a strong vasoconstrictor created by the endothelium. It's a sure sign of endothelial dysfunction....a disturbance in the lining of the vessels walls, creating nitric oxide disruption. Check out the Endothelial Health Program paper if you haven't yet. Lots of ideas on how to avert this process. www.ccsvi.org
under "helping myself."

EGCG and all of the endothelial health program suggestions are shown to reduce Endothelin-1 and rebalance nitric oxide.
http://endo.endojournals.org/cgi/conten ... /151/1/103
HTH,
cheer

[MegansMom]

CCSVI itself increases Endothelin- as hypoxia and shear stress are both triggers for its increased production.

And Endothelin also increases fibrosis, hypertrophy, inflammation and vasoconstriction. which can make the stenosis get worse over time.......so its a circle that has to be broken with PTA and vascular hemodynamic correction.

Eliminate hypoxia and shear stress with successful PTA,

and I'll bet with a good endothelial health Endothelin levels will go back to a normal range.

[cheerleader]

CCSVI itself increases Endothelin- as hypoxia and shear stress are both triggers for its increased production.

And Endothelin also increases fibrosis, hypertrophy, inflammation and vasoconstriction. which can make the stenosis get worse over time.......so its a circle that has to be broken with PTA and vascular hemodynamic correction.

Eliminate hypoxia and shear stress with successful PTA,

and I'll bet with a good endothelial health Endothelin levels will go back to a normal range.

great points, MM...the process of CCSVI changes the vessel lining, and this would increase the levels of endothelin-1 in the serum. And endothelin-1 affects collagen in the vessel wall, making it stiffer---it's a vicious cycle.
link to paper on Endothelin-1 affects on collagen


here is the discussion in Bologna on how the jugular veins of pwCCSVI had changed. From my notes from Dr. Gabbiani's presentation:

Dr. Guilio Gabbiani from the Centre Medical Universitaire in Geneve, Switzerland speaking on jugular wall changes in MS. His laboratory was interested in the fibrotic changes. He was interested in learning the importance of venous morphology, and is surprised so little is known.

Comparing arteries to veins: Arteries are thicker and there is more resistance.

Dr. Gabbiani took 5 specimens from IJV tissue removed by Dr. Zamboni from some of the patients he treated endovascularly. The tissue was from the area NOT damaged by angioplasty.
He compared it to healthy tissue from autopsy controls.
He looked at eosin, hematoxylin, Miller’s elastic stain and massons trichrome.
He found smooth muscle cells were numerous and increased in MS compared to controls. He then used isoelectric focusing to measure contractions in the smooth muscle cells via actin heterogeneity to ID the smooth muscle cells in the veins.
There is an increased expression of smooth muscle actin in MS, much more than controls.

By red staining for collagen and using unpolarized and polarized light, he saw that there is less collagen 1 type fibers in the MS jugular vein tissue, and more collagen III fibers in MS. This is the exact opposite of the controls.

Connective tissue in MS switches from collagen I to collagen III and this takes place in the IJVs. THis switch also happens in fibromatosis, colloids and hypertrophied scars, and this remodeling may play a role in CCSVI disturbances.

Dr. Lee makes a comment...
This collagen conversion from I to III happens in the arteries had no idea it could happen in the veins as well!

answer: Collagen III is stiffer, and fibrosis takes place for some reason. There was no inflammation on the tissue samples, but inflammation might have occurred before the the intervention and the fibrotic changes happened. All is still speculation, we do not know.

Dr. Zivadinov asks, so the testing was in the normal, non-stenosed part of the IJV?

Answer: Yes, we are trying to examine the normal part of the vein not affected by stenosis.

cheer

[Cece]

If I'm understanding this right, it puts paid to the argument that MS causes CCSVI. Instead, CCSVI causes worsening CCSVI, through the endothelin effects.

[jimmylegs]

http://www.ncbi.nlm.nih.gov/pubmed/10916081
Kidney Int. 2000 Aug;58(2):575-86.
Zinc deficiency further increases the enhanced expression of endothelin-1 in glomeruli of the obstructed kidney.
...We therefore designed the present study to examine the effect of Zn deficiency on the expression of ET-1...
...the expression of prepro-ET-1 mRNA and ET-1 was substantially increased in the OK of the Zn-deficient diet group relative to the OK of the standard diet group...

http://ajplung.physiology.org/cgi/conte ... 80/5/L1040
Am J Physiol Lung Cell Mol Physiol 280: L1040-L1048, 2001;
Endothelin B receptor deficiency potentiates ET-1 and hypoxic pulmonary vasoconstriction

Endothelin (ET)-1 contributes to the regulation of pulmonary vascular tone by stimulation of the ETA and ETB receptors.
Although activation of the ETA receptor causes vasoconstriction, stimulation of the ETB receptors can elicit either vasodilation or vasoconstriction.
The actions of ET-1 are dependent on activation of at least two receptor subtypes, ETA and ETB.
ETA receptors are located on smooth muscle cells and mediate vasoconstriction and smooth muscle proliferation (17, 36).
In contrast, ETB receptors are present on both endothelial and smooth muscle cells in the rat pulmonary circulation...

i am still investigating potential causes of ETB receptor deficiency.

i have been trying to find out if the ETB receptor involves a zinc finger, which would make sense if correcting zinc deficiency lowers ET-1.

but, can't verify yet. have to switch tracks for the moment. will revisit later.

ciao!

[cheerleader]

If I'm understanding this right, it puts paid to the argument that MS causes CCSVI. Instead, CCSVI causes worsening CCSVI, through the endothelin effects.

that's what I think, Cece...but there's a lot more research involved to prove this. Makes sense, though, doesn't it? Note Dr. Lee's comment in my notes from Bologna...we know this process happens in the arteries in coronary arterial disease and arterial "hardening", but it hasn't been studied in the veins until now.
cheer

[Jasper9]

Just looked at the endothelial health page on CCSVI Alliance - there looks to be a real link between this theory and the ideas such as vit D, good fats etc that have been around for years. Seems this should definetly be a priority for further study.

Does anyone know if its possible to get tested for levels of Endothelin-1?

[ErikaSlovakia]

Just looked at the endothelial health page on CCSVI Alliance - there looks to be a real link between this theory and the ideas such as vit D, good fats etc that have been around for years. Seems this should definetly be a priority for further study.

Does anyone know if its possible to get tested for levels of Endothelin-1?

I only know it is a blood test.
I have not asked in my town this question as the doctors look at me as I was from Mars
Erika

[cheerleader]

Just looked at the endothelial health page on CCSVI Alliance - there looks to be a real link between this theory and the ideas such as vit D, good fats etc that have been around for years. Seems this should definetly be a priority for further study.

Does anyone know if its possible to get tested for levels of Endothelin-1?

Hi Jasper--
I wrote up that research back in 2008 to help my husband who has MS. I saw that all of the alternative treatments that helped pwMS (vitamin D, Swank Diet, prokarin, exercise, LDN) had some affect on the vascular system, and found a connection that made sense. That's when I contacted Dr. John Cooke at Stanford. He's the author of The Cardiovascular Cure, a book about the endothelium and vascular health. When we started discussing Dr. Zamboni's research on here later that year, I sent it to him. He thought it made sense, too. And that's how my husband was tested and treated for CCSVI at Stanford.

Dr. Zamboni, Dr. Zivadinov and others are now looking at how smoking, vitamin D, diet and lifestyle affect the endothelium and CCSVI.

I don't think a test for Endothelin-1 is really necessary. It's more important to know if you have CCSVI, a malformation in the veins draining your brain. Keep reading, and check out the rest of the CCSVI Alliance site. We've put together the most informative site on CCSVI--
take care,
cheer/Joan

[David1949]

Does this suggest that stenoses are not congenital, but develop over time?

[Cece]

Does this suggest that stenoses are not congenital, but develop over time?

There seems to be a lot of agreement (or should I say consensus) among the vascular docs that these malformations are congenital. So this would only suggest that the congenital malformations that already exist will worsen over time, which is something that has been suggested by the Buffalo research and perhaps the Beirut study...another of the studies, anyway.

[cheerleader]

Does this suggest that stenoses are not congenital, but develop over time?

no...they are most likely congenital, but they do worsen as they grow with the body, and as disturbed blood flow creates a vicious cycle of inflammation and endothelial dysfunction.
Here, Dr. BB Lee explains it best:
http://www.fondazionehilarescere.org/pd ... 8-ANGY.pdf

[Jasper9]

Cece - That's my interpretation too - a vicious circle. I can see David's point also. Perhaps there are multi-factors at work i.e. pre-existing CCSVI made worse by endothelial problems?

Cheer - thanks for your message and all you are doing. I have recently had a doppler that identified left jugular entirely blocked and right jugular mostly blocked plus poor valves. Am on waiting list for angioplasty hopefully to be done in new year. Meanwhile am trying to find out all I can about CCSVI and the bigger picture behind it. It feels that all these links (from vit D to bone structure to diet) are beginning to come together into a framework to understand MS. But there is much left to understand! That's why I was asking about testing for E-1 because it could provide another piece of the picture for me.