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The following was published in the British paper "The Independent" 2 years ago. It's about a study funded by the NHS to determine the effectiveness of the MS drugs at delaying the progression of the disease. The conclusion was:
"It showed that the drugs failed to delay the onset of disability in patients – defined as walking with a stick or using a wheelchair – and may even have hastened it. On that basis, the drug companies would have had to pay the NHS to use them to make them cost effective."

The article also states:
"Multiple sclerosis is a chronic disease. It may take 40 years to run its course. In developing drugs to slow its progression, doctors have used brain scans to show lesions which the drugs appeared to prevent, and gave quicker results. Some experts thought the lesions were the disease but little effort was made to check. But preventing lesion formation does not prevent disability caused by the condition. The drugs deal with the lesions, not the disease."
http://www.independent.co.uk/life-style ... rnalSearch


This really makes me wonder about the autoimmune theory. They can stop the lesions by treating you with immune suppressants. But that doesn't stop the disease. So is the immune system the cause of the disease or a natural response to damage cause by something else, like CCSVI maybe

Sounds like Dr. Hubbard has a similar opinion.


And this one

Well, there are some indications that the immune system is a culprit, independent of what drugs work or why. My personal speculation is that autoimmunity is caused when cells that can be harmful get across the blood-brain-barrier, and that autoimmune damage is only one of the results.

I think the reasons they get across the barrier are, partly at least, treatable by venoplasty. Blood flow is critically important to the brain, and may be involved in a whole range of diseases. The lesions of "MS" are not all unique to "MS", and may not be directly related to BBB damage. What does correlate well, with disability or severity of symptoms? Loss of myelin, I would have thought, for one. Isn't that because of macrophages cleaning up dead oligo's, possibly killed by T-cells, but just as possibly killed by hypoxia or iron, or some virus? In any case, I think good neck circulation can only help, but why is ballooning so temporary so often? Is there anything that can be done to improve the odds?

the trouble with the autoimmune theory is that it neglects obvious feedback from the patient. My first attack came after a skiing accident where my immune system was at work bi time. Now a year after ccsvi the only l'hermitz I've felt was after a bout of food poisoning this winter. Once again my body was fighting hard to get rid of the poison but MS found a way... So it's when my body is immune active. not attacking itself that the ms sneaks in.

Isn't it possible to measure the strength of immune responses? I think the other systems react with vigour after at threat has gone, perhaps because of an overshoot type of reaction. My stress reactions seem to happen after the source of the stress has "left the building". I think my immune reactions are otherwise fine. Get maybe one minor cold over 2 or 3 years. Can't say much about my circulation, though. No use having immune cells if they can't get to the threat. In my brain's case (no pun) they are maybe having a hard time getting back out?

One example was right around the time I was diagnosed with MS. I was going to be down-sized. I heard this from insiders. I went around looking for a new job, and had it lined up before the axe fell. Very stressful time. The MS attack waited until I had the new job. Remember, my body was pumping out cortisol and adrenaline like there was no tomorrow. Maybe it just isn't easy enough to shut those systems off. A lot of people get sick with colds etc. after something stressful ends (exams, moving, etc.). I think maybe it's too unstable, or unable to turn off.

Having poor circulation, low through-put, and a leaky BBB doesn't help. Or maybe turning it off goes too far, and germs have a suddenly easy time attacking. I am assuming one of the reactions to stress is related to the immune system. Cortisol and solumedrol and cortisone being the same things. I also had a very rough time titrating myself off solumedrol, using cortisone pills, which were hospital-issue generics. If I ever take that again I will only use the brand name pills. I was prescribed the titration, but in two or three other encounters with high-dose steroids, I went cold-turkey just fine. Another possible link to the circulation: adrenaline helps stop bleeding, by constricting blood vessels.

1eye wrote: Blood flow is critically important to the brain, and may be involved in a whole range of diseases.

What if circulation issues are causing all autoimmune diseases?
What if CCSVI really is the cause of the immune reaction seen in pwMS?
What if poor circulation to people's joints is what gives them arthritis?
What if circulation problems to the pancreas leads to diabetes?

People have mentioned in the past brain circulation issues being behind ALS or Alzheimer's but I bet the big leap to come from accepting CCSVI as the cause of MS will be a whole new model to look again at the root cause of auto-immune diseases. It is quite a grab bag grouping if you ask me. And if you really look at the research being done they are sort of grasping at anything they can think of. Not a lot of fundamental science going into understanding the causes of these diseases. They are spending billion mapping the genes of people with autoimmune problems but what if it is just an epigenetic expression that happens over your life. It seems like the state of the art is for them to tell you to exercise and eat right. Pretty strange, two prescriptions that might actually help your body's circulation.

If you want to amaze yourself do a search on "diabetes and circulation". Or "arthritis and circulation". Or even "circulation" on this forum. Your hits will amaze you. We are what we circulate. Be it CSF, lymph, blood, hormones, etc.

Again the internet helping folks solve these "open" problems.

Rogan wrote:What if circulation issues are causing all autoimmune diseases?

Other autoimmune diseases have a known 'antigen' that the immune system is reacting against.
I would look further at any autoimmune disease that like MS has no identified antigen.

What if CCSVI really is the cause of the immune reaction seen in pwMS?

I suspect that the poor drainage and focal hypertension that is seen in CCSVI syndrome sets up an environment that is conducive to inflammation and to a weakened blood-brain barrier and unhealthy neurons and oligodendrocytes, which could in some people then contribute to the development of MS.
Which is to say, it is quite possible that CCSVI is the cause of the immune reaction seen in us.

What if poor circulation to people's joints is what gives them arthritis?
What if circulation problems to the pancreas leads to diabetes?

If the drainage of any organ has not been investigated, it should be. Venous drainage has been a neglected field of study.

Hi folks,

After reading through this thread i've always wondered if autoimmunity can explain, or if autoimmunity is responsible
for the breakdown of the BBB??? After doing a little research i came across these links.

Abstract
A sole pathological event leading to Alzheimer's disease (AD) remains undiscovered in spite of decades of costly research. In fact, it is more probable that the causes of AD are the result of a myriad of intertwining pathologies. However, hope remains that a single awry event could lead to the many pathological events observed in AD brain tissues thereby creating the presentation of simultaneous pathologies. Age-related vascular diseases, which include an impaired blood-brain barrier (BBB), are a common denominator associated with various degrees of dementia, including AD. Recently, a key finding not only demonstrated the anomalous presence of immunoglobulin (Ig) detection in the brain parenchyma of AD tissues but, most importantly, specific neurons that showed degenerative, apoptotic features contained these vascular-derived antibodies. In addition, subsequent studies detected classical complement components, C1q and C5b-9, in these Ig-positive neurons, which also were spatially more associated with reactive microglia over the Ig-negative neurons. Thus, it is possible that the mere presence of anti-neuronal autoantibodies in the serum, whose importance had been previously dismissed, may be without pathological consequence until there is a BBB dysfunction to allow the deleterious effects of these autoantibodies access on their targets. Hence, these observations suggest autoimmunity-induced cell death in AD.

http://www.ncbi.nlm.nih.gov/pubmed/15617848

And this:

http://mdc30.free.fr/pubblicazioni_sito ... own_MS.pdf

Last this:

Researchers have identified a novel mechanism by which immune cells wiggle their way across the blood-brain barrier in diseases such as multiple sclerosis (MS). A type of T-cell involved in autoimmune disease leads the way, entering the brain and perhaps priming the blood-brain barrier's membrane to attract other immune cells -- opening the door for those cells to do their inflammatory damage, according to a study published online yesterday (Mar 22) in Nature Immunology.


Read more: Breaching the blood-brain barrier - The Scientist - Magazine of the Life Sciences http://www.the-scientist.com/blog/displ ... z1y0vN06Rw

http://classic.the-scientist.com/blog/display/55517/

So my question is. Is autoimmunity the root cause of the breakdown of the BBB??


Bob

The alzheimer's research snippet is saying that the blood brain barrier breakdown is age-related, and that the pre-existing anti-neuron tcells in the blood couldn't hurt the brain until the age-related blood brain barrier breakdown occurred. So that does not support the idea that autoimmunity causes the blood brain barrier breakdown, only that aging does.

A type of T-cell involved in autoimmune disease leads the way, entering the brain and perhaps priming the blood-brain barrier's membrane to attract other immune cells -- opening the door for those cells to do their inflammatory damage, according to a study published online yesterday (Mar 22) in Nature Immunology.

We have a vascular explanation for how those t-cells get across: the abnormal shear stress due to reflux flow causes the endothelium of the capillaries of the brain to increase the number of adhesion molecules. Adhesion molecules are where the t-cells can cross over.

Inflammation itself weakens the blood-brain barrier, so once there is inflammation of the brain due to MS, it will self-perpetuate.