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Which comes first? Candida, CCSVI or MS?

Posted: Mon Nov 09, 2009 2:18 pm
by Ruthless67
This will be a long post, but please bear with me and hear me out. I have NO medical background, I’m just another MS patient on a similar search for answers to the question, What causes MS.
My little uneducated brain keeps coming to the conclusion that we are what we eat and absorb through our skin and breath from our environment. I can’t wrap my head around the thought that our own bodies would turn on themselves without some trigger mechanism.
I’m actively attempting to have a MRV done at Stanford and if Dr Dake confirms I have stenosis in my arteries, then the stenting procedure is for me, I’m going to go for it! Why wouldn’t I fix something if it’s broke?
But I still want to get to the bottom of the question, which came first, the MS or the Stenosis?
I’m leaning toward believing that an overgrowth of Candida albicans is the culprit and that the micotoxins it produces become brain microvascular endothelial cells or (BMEC) that affect the BBB permeability and start the whole ball rolling.
The article about T-Cells crawling was interesting, especially when it stated that their movement is usually against the flow of the bloodstream. Could that mean that T-cells might enter our brains initially through the same veins that drain the spine and brain and later suffer from stenosis as the disease progresses?
If you read about candida, you find that it can start overgrowing when we are children and doesn’t really manifest itself until we are in our 20’s or so. (Sound familiar?) That candida is feed by our high fat & sugar laden diets and fueled even more by antibiotics. I don’t want to make this post any long than I have already, so I’m not going into candida any further at this time; with the exception of saying that supposedly most people diagnosed with MS also have candida overgrowth.
So could other MS’s with a medical background weigh in on this topic for me. Give me a yeah or nay. I mean it seems so simple to me; could it really be all that simple? Or am I just being simple minded? lol
:roll:
Real-Time Observation Sheds New Light On Multiple Sclerosis
Alexander Flügel, supervisor of the study and director of the Department of Experimental and Clinical Neuroimmunology at the University Medical Center Göttingen and Head of the MS Hertie-Institute.
"Things got really exciting when we observed that the cells can actually crawl, a behavior so far unheard of for T-cells", Ingo Bartholomäus relates his observations. Here, "crawling" describes an active cell movement, usually against the flow of the bloodstream.
Although the scientists already knew that T-cells must make contact with phagocytes in order to become immune-activated, they were now able to observe these interactions right where they happened, i.e. at the blood-brain-barrier. And indeed, the T-cells did not launch their attack on the nervous system by releasing their inflammatory neurotransmitters until they had bonded with the phagocytes. As a result of the T-cells' activation, more and more T-cells passed through the vascular walls. "The activation of T-cells at the border to the nerve tissue appears to be a decisive signal for the invasion of the immune cells".
Journal of Neuroimmunology
The adhesion molecule ICAM-1 and its regulation in relation with the blood–brain barrier
Abstract
The blood–brain barrier (BBB) is formed by high resistance tight junctions within the capillary endothelium perfusing the vertebrate brain. Normal BBB maintains a unique microenvironment within the central nervous system (CNS). In neurodegenerative disorders (for example multiple sclerosis, MS), the BBB becomes impaired. Perivascular cells (astrocytes, macrophages and microglial cells) and brain microvascular endothelial cells (BMEC) produce various inflammatory factors that affect the BBB permeability and the expression of adhesion molecules. Indeed, cytokines can stimulate the expression of several adhesion molecules on brain microvascular endothelial cells. Among these adhesion molecules, the intercellular adhesion molecule-1 (ICAM-1) binds to its leukocyte ligands and allows activated leukocytes entry into the CNS.
This review is dealing with the expression and regulation of ICAM-1 in relation with several properties of the BBB. Particularly, the role of ICAM-1 in the control of the leukocyte traffic into the CNS, as well as in cerebral malaria and in CNS infection by viruses, is discussed.

NLM Gateway
A service of the U.S. National Institutes of Health
University Medical Center Nijmegen, Nijmegen, Netherlands
The Harvard Mahoney Neuroscience Institute Letter
Multiple Sclerosis
The Immune System's Terrible Mistake
BY PETER RISKIND, M.D., PH.D.
Another explanation is the "molecular mimicry" theory, which suggests that normal immune responses to specific viruses may cross-react with particular body tissues, resulting in viral "triggering" of autoimmunity. Whether viruses actually trigger the onset of MS is not proved, but evidence supporting this hypothesis is accumulating.

Recent findings by Zamboni
Consequently, immune cells very infrequently adhere to endotheliocytes and transmigrate across the blood-brain barrier. It has not yet been studied before if the pathological venous flow could increase the expression of adhesion molecules by cerebral and spinal endotheliocytes.

CCSVI – A Huge Breakthrough in MS?
Ashton Embry
Perhaps the most important question that remains is “what is the ultimate
cause of the venous drainage problems?” Zamboni and colleagues did not offer
any explanations/speculations on this. Hopefully, this question will be the
subject of an intensive research effort.
This new understanding of the MS disease process makes the use of the
recommended nutritional strategies even more imperative. These strategies
enhance blood flow, strengthen the BBB, counteract autoimmune reactions and
quite possibly improve venous drainage from the brain. Overall, the Zamboni
work provides further insight into why nutritional strategies work so well
for many people.

Multiple Sclerosis - Best Bet Treatment
Ashton F. Embry
It appears that the activation of T-cells against the CNS by molecular mimicry initiated by food proteins and the constant irritation and weakening of the blood- brain barrier by immune reactions caused by food hypersensitivities eventually result in the onset and progression of MS. On this basis the best treatment for MS is to remove the foods which activate the T-cells and which damage the BBB and to add supplements which strengthen the CNS, the immune system, the BBB and the gut.

Healing Multiple SclerosisAnn Boroch
Diet, Detox & Nutritional Makeover for Total Recovery
Candida albicans overgrowth and it’s by-products (mycotoxins) are the primary cause of MS.
“Candida albicans is the most common human systemic pathogen, causing both mucosal and systemic infections, particularly in immune-compromised people.”

Posted: Mon Nov 09, 2009 2:38 pm
by cheerleader
Hi Ruth...
Thanks for posting. All interesting material to read. I'm familiar with Ann Boroch and her writings on candida. Dr. Zamboni's research has shown a linkage to congenital venous malformation. Some folks have cysts, carotid artery blockage, cramped necks, malformed valves, double jugs, etc...and those have been since birth, but there may also be people who have stenosis for other reasons, such as injury.

Dr. Zamboni spoke recently in Bologna about "endothelial disrupters" such as Cpn, Epstein Barr, low vitamin D, toxins, heavy metals and smoking...all outside influences which can worsen a stenosis and exacerbate reflux. Maybe candida could be added to that list. There will be many studies in the coming years. In my husband's case, he was born with crimped and mangled jugular veins. No candida, viruses, or bacteria....his MS exacerbations were from high altitude (low oxygen) and stress. But yours may be candida. It appears there are many variables in endothelial disrupters, but it looks like the stenosis comes first.

Also, there is no need for the autoimmunity and molecular mimicry theories in Dr. Zamboni's paradigm. He asserts that the immune system is merely going in to clean up axonal death from iron deposition and hypoxic injury to gray matter...a similar response to what we see in stroke, and also what happens in chronic venous insufficiency in the legs. Make sure to read Dr. Z's papers listed on the research sticky. So there is no need for "autoimmunity" in the CCSVI paradigm.

so...according to Dr. Zamboni's research, we see stenosis comes first, then reflux of blood into the brain (which can be exacerbated by endothelial disruption) which results in what we now call "MS."

Keep posting and welcome!
cheer

Posted: Mon Nov 09, 2009 4:52 pm
by Ruthless67
Thanks Cheer,
I'm glad to hear that CCSVI comes first because it is our 18 year Wedding Anniversary tonight, so if Candida is not the "cause" of MS, but CCSVI is, well then, I will have a glass of wine with my husband to toast our years together tonight at dinner.
So Cheers to us and you Cheer, lol.

Lora

I'll read Dr. Zamboni's research in the AM and hopefully, as a lay person, I'll be able to understand it. Thanks again for the quick response.

Posted: Mon Nov 09, 2009 7:27 pm
by jimmylegs
i used to have issues with candida and thought it was causative for some of my issues. mycotoxins/neuropathy thinking. now i have no issues with candida and it is because i identified a few problem areas with my nutrition. there are a few red flags with candida, including antibiotic intake, low stomach acid, and copper/zinc balance to name a few. i took probiotics, but they weren't enough. i have betaine HCL for my stomach acid, but i don't take it much. i did identify a serious zinc deficiency and corrected it. no more candida findings! this is just one of many benefits i have noticed since correcting my zinc level. (docs will tell you it's normal between say, 12 and 20... but the research says optimal is 18.2umol/L... just putting that out there...)

HTH,
JL

Posted: Sun Nov 15, 2009 4:48 pm
by Ruthless67
Thanks, JL, I checked my MV and it didn't include zinc, so I've added it to my supplements.

Cheer,
Here's another silly thought of mine,

In April of 2008 I watched Ann Boroch talk to Montel on his show about her own quest to find a cure for her MS. She had written a book called “Healing Multiple Sclerosis” Diet, Detox & Nutritional Makeover for Total Recovery.

So I sent her an e-mail at ann@annboroch.com on 10/29 and asked her to give me her opinion about CCSVI and I attached this link http://www.atlasorthogonality.com:80/Pa ... outAO.html She replied that it was interesting but was non-committal. Kind of like when your mom says, “That’s nice, dear”.

Since then, I got to thinking, wouldn't it be something if Ann would get an MRV of her jugular veins. If she truly had a diagnosis of MS (Even though she claims to have healed herself.) and Dr Z is correct, then she too should have stenosis. NOW THAT WOULD BE GREAT PROOF FOR CCSVI!!!!!!!
I sent her the info but I don't feel qualified to talk with her about CCSVI. I wonder if any of the researchers would be interested in contacting her? ann@annboroch.com or (818) 763-8282 I'm not aware of any others at this time who claim to have healed/cured their MS.

Posted: Sun Nov 15, 2009 5:17 pm
by radeck
Lora, good thought.

Furthermore, I believe some of those who had great success with using antibiotics against their MS now think that the stenosies were caused by Chlamydia Pneumoniae infection. What greater service to science and humanity could they provide than laying flat for two hours for an MRV and proving that they're the first previously diagnosed MS patients without blockage?

I mean this as nothing but encouragement, since I don't doubt their success, and personally find it quite possible that Cpn plays a role in MS.

Re: Which comes first? Candida, CCSVI, or MS?

Posted: Sun Nov 15, 2009 6:36 pm
by NHE
As many of us know, MS often presents itself clinically as a relapse remitting disease. For example, I had my first attack 8 years before I had my second attack which led to my diagnosis in 1999. During those 8 years, I was completely free of any MS like symptoms and was clueless about anything related to MS. Had I had an MRI at the time of my first attack and been diagnosed as a clinically isolated syndrome, by today's standards I might have been put on some medication. I'm certain that an 8 year free period of symptoms would have made me a poster child for the success of said medication even though it was just the natural course of my disease. Now this doesn't mean that I don't think that dietary changes and supplements cannot alter the course of MS. Indeed, one of my hypotheses is that by making changes to the diet which reduce inflammation and by taking anti-inflammatory supplements, such as omega-3 fish oil and others, that the time be the diagnosis of a clinically isolated syndrome and the eventual diagnosis of definite MS can be extended. Ann Boroch's book was published in 2007. While I haven't read it, it likely means that it's been a few years since she started making the changes she's promoting (and profiting from). However, due to the relapse remitting nature of MS, with an 8 year remission in my case, it would be difficult to say that such changes have cured her of MS. However, as I noted above, they may extend the time to a diagnosis of clinically definite MS. There are many people making claims similar to Ann Boroch, however, I would like to know if she's still doing all right, i.e., "cured", after 10 years or more.

Anyways, that's just my 2¢ for what it's worth.

NHE

Re: Which comes first? Candida, CCSVI, or MS?

Posted: Sun Nov 15, 2009 6:45 pm
by cheerleader
NHE wrote:However, due to the relapse remitting nature of MS, with an 8 year remission in my case, it would be difficult to say that such changes have cured her of MS. However, as I noted above, they may extend the time to a diagnosis of clinically definite MS. There are many people making claims similar to Ann Boroch, however, I would like to know if she's still doing all right, i.e., "cured", after 10 years or more.

Anyways, that's just my 2¢ for what it's worth.

NHE
Worth alot more than 2 cents, NHE. I think this is why we're seeing most of the folk heading to Stanford tend to be a bit older and have been 'round the MS meds bend already. They realize the disease is still progressing. As Marie has said many times, she was jogging for several years after her diagnosis, and was her neuro's postergirl for Copaxone efficacy. But time eventually catches up with most MSers....some much sooner than others. It was in coming here that I saw the writing on the wall for Jeff....even though he was seen as a 'Copaxone responder", I saw what the future held in store. And waiting around didn't seem like a viable option.
cheer

Posted: Sun Nov 15, 2009 7:00 pm
by ozarkcanoer
I was diagnosed in Jan 2008 at age 61 with RRMS, 40 some small lesions, and O-bands at 8. What did I do right for 61 years ???? I don't have relapses, only symptoms. Have I just suddenly started doing something wrong ?? I think not. I don't smoke. I am physically active. I eat a fairly good diet. I don't know if I have stenosis. I see Dr. Haacke December 7. I may or may not find if I have stenosis since he doesn't do the sonography. Maybe MSers for the first 61 years of their lives should eat just what I ate, LOL... and do just what I did. And take all the supplements that I took, which was nothing.

BTW, I DO have MS. Nothing below the neck. It's all in my head. And I DO SUFFER from this disease, believe me.

Posted: Sun Nov 15, 2009 9:28 pm
by Ruthless67
NHE,

At the end of Chapter 1 in Ann’s book see states, “For the last 9 years I’ve helped patients reclaim their health.” So I’m guessing your about right and it probably has been 10 years or so since she started making the changes she's promoting. So yeah, I’d love to see her get a MRV, no matter what they show, cause I’ just curious as heck either way.

And I wonder too if she’s had any symptoms, episodes or exacerbations?