Which comes first? Candida, CCSVI or MS?
Posted: Mon Nov 09, 2009 2:18 pm
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
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 barrierAbstract
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, NetherlandsThe 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.”
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
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 barrierAbstract
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, NetherlandsThe 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.”