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I just wanted to add that as well as Celiac Disease I believe that many of us are gluten sensitive. I tested negative for Celiac and yet a gluten free diet changed my life. This was before I was treated for CCSVI.

My benefits included less fatigue, better mental processing, elimination of lifelong seasonal allergies and far less gas! I am only angry that I waited so long.

After reading Dr Tuckers piece on the effect of compression because of reflux of a solid (blood), my mind has gone to thinking about the endothelium layer that is compromised.
If the layer is cut, torn, stretched, ruptured and basically miss aligned by an assault then there is an opening, an area that is no longer 'secure'.
The body no doubt would heal that area as fast as possible and in a one off event the immune system would likely be able to clean up any issues the cross the BBB for instance.
If that area of breach was ongoing because of an expansion or flexible area of a vein that is not able to seal a breach, I believe we have an area that would 'leak'. I also believe that this would be a progressive leak or a leak that was an issue over time, years maybe until the immune system is unable to control the leakage and the scared area would be a large area for endothelium leakage that the body is unable to repair adequately.
When a scar or lesion is watched over months on MRI there is often examples where the area disappears and new areas form over time. This was shown in monthly MRI sequences and I would imagine that what we are seeing is the RRMS form in action. The endothelium layer weakened and healing to a level of almost complete healing and the leakage minimized or stopped and the lesion is reabsorbed.
Comparing this to lesions on the spinal cord of a person with SP or PP where the lesion is not absorbed because of incomplete healing and ongoing leakage and damage to the nervous system occurs.
Well that's morning thought from sleeping.
Regards Nigel

Hooch I 'think' the problem may be in your type of example that there 'may' not be gluten sensitivity or allergy, it may purely be that the endothelium layer is stressed by various reasons (reflux/stretching) and that the layer is weakened by a high gluten diet for the condition. Leaky gut or stretched CCSVI related veins for instance, or possibly veins in feet and legs.
Without the gluten the permeability of the veins is lessened because the zonulin is able to keep tight junctions in the endothelium layer.
This is all opinion by the way.
Regards Nigel

I would like to try a gluten free diet, but I have looked into it and don't really think I could do it. Is anyone here doing this diet and can you give some advice or recipes that work for you? Thanks!

Sounds complicated. I'm going to try cutting out all the bread/flour products and stick to meat, fruit & veggies. I'd rather just 'cut out' offending foods rather than substitute with foods/grains I've never heard of before. Maybe add them in after a while?

PN

So, zonulin may contribute by weakening tight junctures...and it's probably a great idea to cut back on gluten (for many reasons)

but I still believe the real culprit is endothelial dysfunction due to altered cerebral hemodynamics. The better the blood flow, the better the tight junctions...hypoperfusion and venous reflux may could be responsible for the breakdown of the BBB.

Dr. Simka wrote up a great paper on this thesis of loss of shear stress, and how this changes the BBB.

Yet, it was recently demonstrated that the blood-flow- associated forces, predominantly the level of shear stress, can profoundly affect the expression of tight junction proteins, thus regulating the strength of the endothelial barrier. It has been shown that increased shear stress, especially with pulsatile flow characteristics, upregulated pivotal tight junction proteins, such as occludin and ZO-1 in the cerebrovascular endothelium. Consequently, increased expression of these proteins was associated with reduced transendothelial permeability (Colgan et al., 2007). In parallel, loss of shear stress after flow cessation enhanced the blood-brain barrier permeability. (Krizanac-Bengez et al., 2006a; Krizanac-Bengez et al., 2006b)

Therefore, a reduced shear, for example due to the refluxing venous blood flow, could potentially result in the weakening of the blood-brain barrier. In addition, it has been found that steady shear stress upregulated the activity of the Na-K-Cl cotransporter in cerebral microvascular endothelium. Although it remains unclear whether this protein could control the integrity of the blood-brain barrier, it is suspected that it plays a role in the regulation of endothelial cell volume (Chang et al., 2008; Suvatne et al., 2001).

check out the full paper here:
http://www.ccsvi.co.uk/resources/Simka% ... S%2009.pdf
cheer

Joan I personally don't think it is chemical or cellular based problem I see it as physical and have now found Dr Trevor Tuckers addition to this knowledge.

This three part presentation gives meaning to the observations made so far in MS and Vascular problems found in CCSVI. It links all of the key theories in Vascular interplay seen in MS by the literature and from the the main Scientists and Doctors and Researchers, enjoy and tell others please,





Regards Nigel

http://stroke.ahajournals.org/content/e ... 7.abstract

Basic Science Advances for Clinicians

Blood–Brain Barrier Breakdown in Acute and Chronic Cerebrovascular Disease

Yi Yang, MD, PhD;
Gary A. Rosenberg, MD

+ Author Affiliations

From the Departments of Neurology (Y.Y., G.A.R.), Neurosciences (G.A.R.), and Cell Biology and Physiology (G.A.R.), University of New Mexico Health Sciences Center, Albuquerque, NM.

Abstract

Disruptions of the blood–brain barrier (BBB) and edema formation both play key roles in the development of neurological dysfunction in acute and chronic cerebral ischemia. Animal studies have revealed the molecular cascades that are initiated with hypoxia/ischemia in the cells forming the neurovascular unit and that contribute to cell death. Matrix metalloproteinases cause reversible degradation of tight junction proteins early after the onset of ischemia, and a delayed secondary opening during a neuroinflammatory response occurring from 24 to 72 hours after. Cyclooxygenases are important in the delayed opening as the neuroinflammatory response progresses. An early opening of the BBB within the 3-hour therapeutic window for tissue-type plasminogen activator can allow it to enter the brain and increase the risk of hemorrhage. Chronic hypoxic hypoperfusion opens the BBB, which contributes to the cognitive changes seen with lacunar strokes and white matter injury in subcortical ischemic vascular disease. This review will describe the molecular and cellular events associated with BBB disruption and potential therapies directed toward restoring the integrity of the neurovascular unit.

The authors are listed as being in the department of neurology. Neurologists! Is it common knowledge among neurologists that chronic hypoxic hypoperfusion opens the blood-brain barrier?

Thank you Cece, in the same vein I re-posted this on my FB site 'CCSVI in NZ' yesterday, (https://www.facebook.com/pages/CCSVI-in ... 1636357984)


* Question for Sal; I'm having a bout of low BP which I often do and or hypoxia at present and wonder if the attachment they use in the beginning of the clip would measure what we need to know about oxygen saturation/content of our blood? Clip it to an ear?

Edited, later today
just went and had my BP checked 136/79 sitting and 118/76 standing, pulse 74, Blood sugar 5.4
then had the oxy check 99% on my finger checked a couple of times and then checked on my ear 82%.
So what this means if anything is interesting, if the oxy test is accurate on an ear then there is something to look into?
My fatigue, low energy and strength, nystagmus and blurred vision, cog fog in particular are at a peak at the moment so naturally I am curious as to why this has changed over the last week.

Regards all, Nigel

GREAT paper find, Cece.

So, hypoxia and hypoperfusion allow the BBB to open and begin the cascade of events we recognize, all too well, in MS. MMPs, inflammation and an immune response.
Just from lowered oxygen and slowed blood flow through the brain.
going to bump the hypoperfusion thread and add this paper...it's a winner.
cheer

I thought it might be useful! Thanks, Cheer. It also refers to the 'neurovascular unit' which is a great way of looking at the interaction between the neurons and the blood-brain barrier, not separately but as one unit. What affects the endothelium will affect the neurons.

http://www.nature.com/nbt/journal/vaop/ ... .2247.html

Thought this was fascinating! Researchers in Madison WI have coaxed stem cells into taking on the characteristics of the blood-brain barrier. This means not just becoming endothelial cells but becoming endothelial cells that have junctions ten times as tight as the endothelial cells elsewhere in the body.

Here are the attributes of a blood-brain barrier endothelial cell:

The resulting endothelial cells have many BBB attributes, including well-organized tight junctions, appropriate expression of nutrient transporters and polarized efflux transporter activity. Notably, they respond to astrocytes, acquiring substantial barrier properties as measured by transendothelial electrical resistance (1,450 ± 140 Ω cm2), and they possess molecular permeability that correlates well with in vivo rodent blood-brain transfer coefficients.

http://www.sciencedaily.com/releases/20 ... 071052.htm

another bit of new research:

"We now know that the blood-brain barrier also plays a vital role in the process by 'vacuuming' -- so to speak -- the brain fluid for extraneous glutamate, which is then pumped into the blood where it does not have a damaging effect. This is new knowledge that can have enormous impact on future drug development. We have charted a biological mechanism that other scientists eventually can try to influence chemically, for example, in the form of medicine to limit cell death after a stroke. When the brain lacks oxygen, the glutamate level in the brain fluid increases dramatically, which kick starts a toxic chain reaction that kills cells," explains Associate Professor Birger Brodin.

The research results have just been published in the scientific journal GLIA.

In chronic CCSVI, we could expect both excessive glutamate to occur due to subnormal levels of oxygen in the brain, and we could also expect a weakened blood brain barrier to be less adept at clearing the glutamate?

These are questions for the neurologists, who don't seem to be taking questions at the moment. Or maybe it will be the phlebologists who will do this research.