Dr. Gayatri Devi is a neurologist at Lenox Hill Hospital in NYC. She has recently published a book called "The Spectrum of Hope: An Optomistic and New Approach to Alzheimer's Disease and other Dementias."
Dr. Devi is redefining Alzheimer's as a spectrum disorder, meaning that this diagnosis is not the same for every patient, that each patient will have a unique experience, and that there is much which can be done to empower the individual patient to reclaim their health. A diagnosis of Alzheimer's is not "one size fits all." And she attacks the biggest myth---that all people with an Alzheimer's diagnosis will end up incompetent in a nursing home. She says this simply isn't true.
In this new book, Dr. Devi outlines ways to treat and arrest Alzheimer's progression through nutrition, exercise, lifestyle and medication. She asserts that 60% of all Alzheimer's cases are preventable, and that science has shown that less than 5% of Alzheimer's cases are genetic. link
I like Dr. Devi. A lot. She is positive, informed and uses real data and science to back up her claims. She has worked with Alzheimer's patients for 23 years, and she wants to dispel the myths about the disease.
Dr. Stuart Zola of Emory University has been making the same case. He has been advocating for a spectrum disorder classification for Alzheimer's Disease and has specific recommendations for treatment.
link
His most important lifestyle interventions are the exact same as Dr. Devi's.
1. Heart Healthy Diet
2. Stress Reduction
3. Exercise
4. Sleep
5. Cognitive training--use it, or lose it.
Does this list look familiar to anyone else?
I would submit that the exact same case could be made for Multiple Sclerosis.
MS is a neurodegenerative disease which is not genetic. MS is a vastly different disease in individuals. MS also occurs more commonly in women. MS progression can be halted. MS is a spectrum disorder.
Then why aren't MS neurologists using this same language in discussing treatment and lifestyle intervention with their patients?
The difference is that MS has a $20 billion dollar a year drug industry attached to the diagnosis. And it is important for MS specialists to maintain the narrative that MS is a destructive, incurable autoimmune disease which must be attacked at the very beginning with immune modulating drugs. No matter the disease presentation, the age of the patient, the level of neurologic damage---the narrative has been that ONLY drug intervention can arrest the MS disease process. And this narrative has been pushed and publicized by MS Societies, MS advocacy groups, MS blogs, MS groups (which are sponsored by pharma) and in the press. There's a lot of money wrapped up in telling this story.
Watch this Canadian news story from 1989, almost 30 years ago. It will take you 18 minutes, but I believe it is important. The first half is about chemo treatment for MS, the second half is about nutrition.
Link to 5th Estate MS Story
Notice how the neurologists speak to the MS patient about his wheelchair prognosis "in two years" if he does nothing to treat his MS aggressively. Jeff had a very similar prognosis. He was having trouble walking, was spending the day on the couch, exhausted. Just like Ron, he was told to "do everything he could" to fight his MS. But that "everything" only included drug therapy. Listen to how Ron accepts the risks of cyclophosphamide (Cytoxan), a cancer treatment with very serious side effects, which would eventually be shown to be ineffective as a monotherapy for MS. link
At 10 minutes in we meet another person with MS. She has been part of Dr. Roy Swank's 35 year observational study of a low fat diet. Dr. Swank's patients are still walking, working, living, remaining stable. Dr. Swank gave his patients hope of disease reversal, of remaining mobile. His program is simple. Avoid fats from meat and dairy, eat mostly plants. What we would call a "heart healthy diet."
The MS neurologist speaks for the medical profession, saying diet has "little to no role" in the care of MS patients. And this is the position of the MS Society today---even though the science shows that the diet has made a difference. Again, this was 30 years ago. And it is still true---as the MS Society threatens to sue Matt Embry for speaking out about true MS Hope, and a program based on the Swank Diet. link
We need to reframe the dialogue. MS is a spectrum disorder. It can be treated with lifestyle, nutrition, and exercise. A healthy heart and vasculature can protect the brain. Yes, MS will be different for every individual, medications may help some--and not all will recover. But that does not negate the very real improvements made for many.
Push back against the pharma narrative.
Write your own story,
Joan
From Rindfliesch's discovery of the central vessel in the MS lesion in 1863, to CCSVI and the CNS lymphatic discovery. 160 years of research on blood flow, CSF, lymph and perfusion of the central nervous system. Because the heart and the brain are connected.
Welcome! This blog contains research & information on lifestyle, nutrition and health for those with MS, as well as continuing information on the understanding of the endothelium and heart-brain connection. This blog is informative only--all medical decisions should be discussed with your own physicians.The posts are searchable---simply type in your topic of interest in the search box at the top left.Almost all of MS research is initiated and funded by pharmaceutical companies. This maintains the EAE mouse model and the auto-immune paradigm of MS, and continues the 20 billion dollar a year MS treatment industry. But as we learn more about slowed blood flow, gray matter atrophy, and environmental links to MS progression and disability--all things the current drugs do not address--we're discovering more about how to help those with MS.To learn how this journey began, read my first post from August, 2009. Be well! Joan
Showing posts with label MS. Show all posts
Showing posts with label MS. Show all posts
Friday, December 22, 2017
Wednesday, October 25, 2017
Setting the record straight
I want to simply state some facts for my readers. Because if I don't, journalists and bloggers will continue to create a narrative of the kooky singing wife, who found some crazy researcher online and led the world on a goose chase. And that's not true. And it's really hurtful.
Some factual, documented history:
1. I believed there was a vascular connection to my husband's MS diagnosis from day one. That would be March 23, 2007, the day we got his serum results from the doctor and I saw so many numbers that were way out of normal range. Coincidently, my birthday.
2. Using Jeff's serum results as a point of reference, I went to the library and took out every single book they had on MS, including McAlpine's history of Multiple Sclerosis--which had a section on the long history of the vascular connection. This is where I first read about Dr. Tracy Putnam. link The pile of textbooks also included Dr. Swank's research. Dr. Swank wrote about the connection of MS to the blood. He published over 100 research papers on MS. He wrote about capillary fragility, petechiae and hypercoagulation in his MS patients--all of this research rang a lot of bells for me. link
3. I was on a forum called "This is MS" in September 2007. I wrote about Jeff's serum results, hypercoagulation, and postulated on a bunch of research with other people with MS and caretakers. It was a great community, and we shared papers, programs and MS research.
4. Using pubmed and my local library, I eventually came to the intersection between the vascular and immune system I had been searching for---the endothelium. Using published and peer-reviewed science, I created The Endothelial Health Program for Jeff and shared it on This is MS in the summer of 2008. I saw a connection between many of his vascular issues (petechiae, high Crp levels, hypercoagulation, high liver enzymes), endothelial dysfunction, and his MS diagnosis. We found that by changing his diet to a Swank program, increasing his Vitamin D levels, including cardiovascular exercise, thinning his blood with proleolytic enzymes, getting him out in sunshine, reducing work stress, improving his sleep---he was doing much better, he did not have a relapse and his serum results normalized. http://ccsvi.org/index.php/helping-myself/endothelial-health
5. I wrote to endothelial researchers at USC and Stanford, asking if they had any knowledge of studies or published research on the function of the endothelium in MS. Both of them e-mailed me back. I began a correspondence with the researcher at Stanford, because he was the most interested in this connection. Here is part of his reply. I have all of the e-mails, if anyone aside from me ever truly wants to get this story correct.
"I enjoyed reading your treatise.
I quite like the hypothesis that MS is secondary to a derangement of the endothelium of the cerebrovasculature, that results in inflammation and local damage.
I am also in agreement with your contention that a functioning endothelium is a major key to health.
Furthermore, I agree that diet and exercise are critical for endothelial health."
6. It would be three months later I would send more research to this doctor. One of the papers was Dr. Zamboni's new publication on CCSVI, which had been shared with me, the "vascular hypothesis gal" on This Is MS. He was fascinated by the research, and suggested further testing for Jeff. Here's part of that e-mail.
"You could get more evidence for cerebral venous abnormalities (I would be particularly concerned about venous stenoses) by MR imaging, with attention to the cerebral veins. "
7. We would eventually bring Jeff up to Stanford for TESTING to see if he had any venous abnormalities. It took a few months to schedule, as he was busy composing and we needed to travel from LA to the Bay Area. He was tested in April, 2009. My mistake was that I wrote about all of this online, on the This is MS forum. I should not have done this. It is my one, deep regret. But it is also why I continue to blog and write. Because I feel hugely responsible for what would later happen.
8. Jeff had serious venous abnormalities, documented on MRV. link He had a 99% stenosis in his left jugular vein and an 80% closure of his right. The doctor we were consulting with felt this was a serious issue for his brain perfusion, and suggested we think about potential treatment. We went home.
9. After consulting with other physicians, Jeff scheduled his venoplasty treatment for May 2009. He went back up to Stanford and was treated for his venous abnormalities. He had a profound response on the table---he felt as though the "lights came on" after a stent was opened on his left side. He came home and slept soundly, without spasms, for the first time in over a year. He was dreaming again. He also had a terrible headache the first day, and would develop severe shoulder pain from having his accessory nerve pinched by stents. These side effects from the treatment would pass, but it was scary. Again, I wrote about it online.
10. People read what I wrote, called Stanford, were treated there or tried to get treated elsewhere. The press picked it up, and the rest is pretty well documented. What is never reported correctly is that I didn't force an IR to treat Jeff. We asked him to TEST Jeff for venous abnormalities. When we saw how bad they were, the IR suggested treatment, and we eventually agreed.
I never called venoplasty a cure for MS. I also never meant for people to get hurt, or travel for medical tourism, spend thousands of dollars (as Jeff was covered by our insurance) or most terribly, to die from complications. I certainly didn't want to be labeled the crazed wife who forced an IR to treat her husband. I always said this was only part of living a vascularly healthy life, to encourage healing and strengthen the heart-brain connection. I never used the word cure. I started the Facebook group because I was really concerned with how this research was being discussed as a cure. link I was also shocked with how vehemently the MS specialists were denying any link to the vasculature. I wanted people to know this was only a treatment, and it might not be right for them. Which is partially why I stayed online. That, and a huge amount of pride, I'm sure. Ego is never a good thing, and I know it complicated this issue.
But in all honesty, all I wanted were answers for the love of my life. And we hung around because we had hoped this could be helpful to others. But to be continually portrayed as cure seekers, zealots and wingnuts by the NY Times, the Wall Street Journal, and other publications (which will live online ad infinitum) and to have our names linked to false and incomplete reporting is simply too much.
So, there it is.
Going for a walk with my love, and our 17 yr. old dog, Angel (another medical anomaly)
Have a nice day,
Joan

Some factual, documented history:
1. I believed there was a vascular connection to my husband's MS diagnosis from day one. That would be March 23, 2007, the day we got his serum results from the doctor and I saw so many numbers that were way out of normal range. Coincidently, my birthday.
2. Using Jeff's serum results as a point of reference, I went to the library and took out every single book they had on MS, including McAlpine's history of Multiple Sclerosis--which had a section on the long history of the vascular connection. This is where I first read about Dr. Tracy Putnam. link The pile of textbooks also included Dr. Swank's research. Dr. Swank wrote about the connection of MS to the blood. He published over 100 research papers on MS. He wrote about capillary fragility, petechiae and hypercoagulation in his MS patients--all of this research rang a lot of bells for me. link
3. I was on a forum called "This is MS" in September 2007. I wrote about Jeff's serum results, hypercoagulation, and postulated on a bunch of research with other people with MS and caretakers. It was a great community, and we shared papers, programs and MS research.
4. Using pubmed and my local library, I eventually came to the intersection between the vascular and immune system I had been searching for---the endothelium. Using published and peer-reviewed science, I created The Endothelial Health Program for Jeff and shared it on This is MS in the summer of 2008. I saw a connection between many of his vascular issues (petechiae, high Crp levels, hypercoagulation, high liver enzymes), endothelial dysfunction, and his MS diagnosis. We found that by changing his diet to a Swank program, increasing his Vitamin D levels, including cardiovascular exercise, thinning his blood with proleolytic enzymes, getting him out in sunshine, reducing work stress, improving his sleep---he was doing much better, he did not have a relapse and his serum results normalized. http://ccsvi.org/index.php/helping-myself/endothelial-health
5. I wrote to endothelial researchers at USC and Stanford, asking if they had any knowledge of studies or published research on the function of the endothelium in MS. Both of them e-mailed me back. I began a correspondence with the researcher at Stanford, because he was the most interested in this connection. Here is part of his reply. I have all of the e-mails, if anyone aside from me ever truly wants to get this story correct.
"I enjoyed reading your treatise.
I quite like the hypothesis that MS is secondary to a derangement of the endothelium of the cerebrovasculature, that results in inflammation and local damage.
I am also in agreement with your contention that a functioning endothelium is a major key to health.
Furthermore, I agree that diet and exercise are critical for endothelial health."
6. It would be three months later I would send more research to this doctor. One of the papers was Dr. Zamboni's new publication on CCSVI, which had been shared with me, the "vascular hypothesis gal" on This Is MS. He was fascinated by the research, and suggested further testing for Jeff. Here's part of that e-mail.
"You could get more evidence for cerebral venous abnormalities (I would be particularly concerned about venous stenoses) by MR imaging, with attention to the cerebral veins. "
7. We would eventually bring Jeff up to Stanford for TESTING to see if he had any venous abnormalities. It took a few months to schedule, as he was busy composing and we needed to travel from LA to the Bay Area. He was tested in April, 2009. My mistake was that I wrote about all of this online, on the This is MS forum. I should not have done this. It is my one, deep regret. But it is also why I continue to blog and write. Because I feel hugely responsible for what would later happen.
8. Jeff had serious venous abnormalities, documented on MRV. link He had a 99% stenosis in his left jugular vein and an 80% closure of his right. The doctor we were consulting with felt this was a serious issue for his brain perfusion, and suggested we think about potential treatment. We went home.
9. After consulting with other physicians, Jeff scheduled his venoplasty treatment for May 2009. He went back up to Stanford and was treated for his venous abnormalities. He had a profound response on the table---he felt as though the "lights came on" after a stent was opened on his left side. He came home and slept soundly, without spasms, for the first time in over a year. He was dreaming again. He also had a terrible headache the first day, and would develop severe shoulder pain from having his accessory nerve pinched by stents. These side effects from the treatment would pass, but it was scary. Again, I wrote about it online.
10. People read what I wrote, called Stanford, were treated there or tried to get treated elsewhere. The press picked it up, and the rest is pretty well documented. What is never reported correctly is that I didn't force an IR to treat Jeff. We asked him to TEST Jeff for venous abnormalities. When we saw how bad they were, the IR suggested treatment, and we eventually agreed.
I never called venoplasty a cure for MS. I also never meant for people to get hurt, or travel for medical tourism, spend thousands of dollars (as Jeff was covered by our insurance) or most terribly, to die from complications. I certainly didn't want to be labeled the crazed wife who forced an IR to treat her husband. I always said this was only part of living a vascularly healthy life, to encourage healing and strengthen the heart-brain connection. I never used the word cure. I started the Facebook group because I was really concerned with how this research was being discussed as a cure. link I was also shocked with how vehemently the MS specialists were denying any link to the vasculature. I wanted people to know this was only a treatment, and it might not be right for them. Which is partially why I stayed online. That, and a huge amount of pride, I'm sure. Ego is never a good thing, and I know it complicated this issue.
But in all honesty, all I wanted were answers for the love of my life. And we hung around because we had hoped this could be helpful to others. But to be continually portrayed as cure seekers, zealots and wingnuts by the NY Times, the Wall Street Journal, and other publications (which will live online ad infinitum) and to have our names linked to false and incomplete reporting is simply too much.
So, there it is.
Going for a walk with my love, and our 17 yr. old dog, Angel (another medical anomaly)
Have a nice day,
Joan

Sunday, January 24, 2016
Jugular Veins are Important
Recently published in the Journal of Mutiple Sclerosis, a review paper co-authored by Dr. Paolo Zamboni and Dr. Massimo Pedriali on the "Pathology of the Internal Jugular Vein in Multiple Sclerosis". The complete paper is available on line for free---and I'd recommend it to all. It is a very thorough review.
http://www.omicsgroup.org/journals/the-pathology-of-the-internal-jugular-vein-wall-in-multiple-sclerosis-2376-0389-1000160.php?aid=63610
As this review outlines, there are observable and documented differences between the jugular veins of healthy controls, when compared to people with Multiple Sclerosis. These pathological differences involve the endothelial cells which comprise the veins' lining. Endothelial cell aptosis (death) and derangement, as seen in MS, changes the ability of the jugular veins to drain. Valvular and intraluminal abnormalities in the jugular veins of people with MS have hemodynamic implications. There is a shift in collagen in the jugular veins of people with MS which affects venous compliance.
Veins have received little attention and research, when compared to the study and understanding of arteries. Certainly, in terms of brain health, the carotid arteries are scanned and studied, and neurology and stroke researchers know that blockages, clots, and impairment in flow can be disastrous to the brain. There are treatment modalities developed to deal with carotid artery issues---from medications to open surgery, to interventional proceedures. No one questions the importance of healthy blood flow to the brain.
But the venous system and the removal of fluids from the brain is even more important than previously imagined.
During the past two years, international researchers have described a newly discovered lymphatic drainage system, which has actual draining vessels, and relies on the brain's draining veins. These vessels take lymph fluid, carrying metabolites, proteins and toxins, out of the brain. This process is aided by sleep. This science is brand new. It has reversed what we once believed was the brain's "immune privilege."
http://ccsviinms.blogspot.com/2015/06/rewrite-textbooks.html
This "stunning discovery" of a lymphatic drainage system relies on the jugular veins.
"Instead of asking, 'How do we study the immune response of the brain?' 'Why do multiple sclerosis patients have the immune attacks?' now we can approach this mechanistically. Because the brain is like every other tissue connected to the peripheral immune system through meningeal lymphatic vessels," said Jonathan Kipnis, PhD, professor in the UVA Department of Neuroscience and director of UVA's Center for Brain Immunology and Glia (BIG).
http://ccsviinms.blogspot.com/2015/06/a-stunning-discovery.html
The brain is like every other organ in our body---it needs drainage. Jugular veins are responsible for the exit of blood, cerebrospinal fluid (CSF) and lymph. Any delays can cause changes to the brain's immune functioning, oxygenation, glucose metabolism and health. Delays cause neuronal death and inflammation. Or, what we see in multiple sclerosis.
Dr. Jonathan Kipnis, the discoverer of these lymphatic vessels, will be the keynote speaker at the International Society for Neurovascular Disease. He will be presenting his research and proposals for studies in MS, alongside Dr. Zamboni and the other members of the ISNVD.
Here's the program. “How the Extracranial Venous System Influences Neurological Diseases.”
http://isnvd.org/sites/default/files/ISNVD-2016%20meeting%20outline%20program%20guide%209-21-2015.pdf
This is not going away.
jugular veins are important,
Joan
Notice the difference between the top panel---healthy endothelial cells lining the jugular veins in normal controls, compared to the endothelial cells of a person with MS (bottom)
http://www.omicsgroup.org/journals/the-pathology-of-the-internal-jugular-vein-wall-in-multiple-sclerosis-2376-0389-1000160.php?aid=63610
As this review outlines, there are observable and documented differences between the jugular veins of healthy controls, when compared to people with Multiple Sclerosis. These pathological differences involve the endothelial cells which comprise the veins' lining. Endothelial cell aptosis (death) and derangement, as seen in MS, changes the ability of the jugular veins to drain. Valvular and intraluminal abnormalities in the jugular veins of people with MS have hemodynamic implications. There is a shift in collagen in the jugular veins of people with MS which affects venous compliance.
Veins have received little attention and research, when compared to the study and understanding of arteries. Certainly, in terms of brain health, the carotid arteries are scanned and studied, and neurology and stroke researchers know that blockages, clots, and impairment in flow can be disastrous to the brain. There are treatment modalities developed to deal with carotid artery issues---from medications to open surgery, to interventional proceedures. No one questions the importance of healthy blood flow to the brain.
But the venous system and the removal of fluids from the brain is even more important than previously imagined.
During the past two years, international researchers have described a newly discovered lymphatic drainage system, which has actual draining vessels, and relies on the brain's draining veins. These vessels take lymph fluid, carrying metabolites, proteins and toxins, out of the brain. This process is aided by sleep. This science is brand new. It has reversed what we once believed was the brain's "immune privilege."
http://ccsviinms.blogspot.com/2015/06/rewrite-textbooks.html
This "stunning discovery" of a lymphatic drainage system relies on the jugular veins.
"Instead of asking, 'How do we study the immune response of the brain?' 'Why do multiple sclerosis patients have the immune attacks?' now we can approach this mechanistically. Because the brain is like every other tissue connected to the peripheral immune system through meningeal lymphatic vessels," said Jonathan Kipnis, PhD, professor in the UVA Department of Neuroscience and director of UVA's Center for Brain Immunology and Glia (BIG).
http://ccsviinms.blogspot.com/2015/06/a-stunning-discovery.html
The brain is like every other organ in our body---it needs drainage. Jugular veins are responsible for the exit of blood, cerebrospinal fluid (CSF) and lymph. Any delays can cause changes to the brain's immune functioning, oxygenation, glucose metabolism and health. Delays cause neuronal death and inflammation. Or, what we see in multiple sclerosis.
Dr. Jonathan Kipnis, the discoverer of these lymphatic vessels, will be the keynote speaker at the International Society for Neurovascular Disease. He will be presenting his research and proposals for studies in MS, alongside Dr. Zamboni and the other members of the ISNVD.
Here's the program. “How the Extracranial Venous System Influences Neurological Diseases.”
This is not going away.
jugular veins are important,
Joan
Notice the difference between the top panel---healthy endothelial cells lining the jugular veins in normal controls, compared to the endothelial cells of a person with MS (bottom)
Figure 5: Scanning electronic microscopy. Top panel: regular disposition of the endothelial cells in IJVs of healthy controls, respectively at 800x (right) and 1500x (left). Bottom panel: irregular arrangement of the endothelial cells in the IJV of a MS patient, respectively at 800x (left) and 1500x (right). The cells appear lifted with craters. |
Labels:
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Sunday, June 21, 2015
Rewrite the textbooks
UPDATE: October 2017
Confirmation of the Kipnis Lab and University of Helsinki finding in humans.
Researchers at NIH see the actual lymphatic vessels in the human brain.
“We literally watched people’s brains drain fluid into these vessels,” said Daniel S. Reich, M.D., Ph.D., senior investigator at the NIH’s National Institute of Neurological Disorders and Stroke (NINDS) and the senior author of the study published online in eLife(link is external). “We hope that our results provide new insights to a variety of neurological disorders.” link
*******************
The Journal of Experimental Medicine said it best in their recent tweet:
“Any neuroscience textbook that has ever been written will say that the central nervous system is devoid of a lymphatic system and that is one of the reasons the brain is immune privileged,” Louveau said. “When we started our project, our question was if there are so many immune cells surrounding the brain, how do they traffic there? By addressing this question we found vessels that weren’t supposed to exist. They were very well hidden and we think that is why it took so long to discover them.”
Confirmation of the Kipnis Lab and University of Helsinki finding in humans.
Researchers at NIH see the actual lymphatic vessels in the human brain.
“We literally watched people’s brains drain fluid into these vessels,” said Daniel S. Reich, M.D., Ph.D., senior investigator at the NIH’s National Institute of Neurological Disorders and Stroke (NINDS) and the senior author of the study published online in eLife(link is external). “We hope that our results provide new insights to a variety of neurological disorders.” link
*******************
The Journal of Experimental Medicine said it best in their recent tweet:
"The CNS is considered an organ devoid of lymphatic vasculature."
Ed. note: "NOT"
Not. Decades of medical theory which considered the brain as different from other organs of the body and without lymphatic drainage system were, well, simply wrong.
The University of Helsinki has independently published a paper in the Journal of Experimental Medicine which confirms the University of Virginia's paper on lymph vessels published just two weeks ago. Both universities have found:
A dural lymphatic vascular system that drains brain interstitial fluid and macromolecules
A dural lymphatic vascular system that drains brain interstitial fluid and macromolecules
How have researchers had it SO WRONG for SO LONG?
If you're like me, you figured that neuroscientists had looked long and hard for any signs of lymphatic drainage surrounding the brain, and had proven that it simply didn't exist, and that the brain was indeed immune privileged, and separate from the rest of the body's peripheral immune system.
“Any neuroscience textbook that has ever been written will say that the central nervous system is devoid of a lymphatic system and that is one of the reasons the brain is immune privileged,” Louveau said. “When we started our project, our question was if there are so many immune cells surrounding the brain, how do they traffic there? By addressing this question we found vessels that weren’t supposed to exist. They were very well hidden and we think that is why it took so long to discover them.”
link
Not coincidently, the EAE model for MS was developed around the same time as the theory of immune privilege, as an example of how t-cells could break through the blood brain barrier and attack the brain in an auto-immune reaction. It has been a prevailing theory in MS treatment development, which has also never been proven. Another 70 year old theory which has lead to disastrous assumptions about the brain.
The presence of mild scant lymphocytic infiltrates in the demyelinating lesions has been generally interpreted as the evidence of an inflammatory autoimmune process. Because specific T-cell mediated autoimmunity can be reproduced in animals after myelin protein sensitisation (Experimental Allergic Encephalo- myelitis (EAE)) it has been assumed (but never proven) that a similar T-cell driven immune mechanism is responsible for demyelination in MS.
The acceptance of EAE as a model for MS is an unfortunate error that has its basis on faith rather than science. Whilst EAE is a good example of an experimental organ-specific autoimmune disorder in animals, it cannot be accepted as a model for MS for a wide variety of reasons. This is particularly important in relation to the development of MS pharmacotherapy. We have analysed the literature on immune-modifying therapy in MS and it is clear that none of these agents can qualify as a candidate therapy under scrutiny.
link
The brain's relationship to the peripheral immune system is obviously much more communicative and complex than previously imagined. The discovery of lymphatic vessels by neuroimmunologists means we need a do-over in MS research, as this science writer comments:
For decades, several axioms have prevailed with respect to the relationships between the CNS and circulating immune cells. Specifically, immune cell entry was largely considered to be pathological or to mark the beginning of pathology within the brain. Moreover, local inflammation associated with neurodegenerative diseases such Alzheimer's disease or amyotrophic lateral sclerosis, were considered similar in their etiology to inflammatory diseases, such as remitting relapsing-multiple sclerosis. The ensuing confusion reflected a lack of awareness that the etiology of the disease as well as the origin of the immune cells determines the nature of the inflammatory response, and that inflammation resolution is an active cellular process. The last two decades have seen a revolution in these prevailing dogmas, with a significant contribution made by the authors. Microglia and infiltrating monocyte-derived macrophages are now known to be functionally distinct and of separate origin. Innate and adaptive immune cells are now known to have protective/healing properties in the CNS, as long as their activity is regulated, and their recruitment is well controlled; their role is appreciated in maintenance of brain plasticity in health, aging, and chronic neurodevelopmental and neurodegenerative diseases.
link
Israel Steiner, a neurologist at the Hadassah University Hospital in Jerusalem, agrees that EAE has blocked "effective progress" for decades. He thinks alternative theories should be put to the test. "I definitely believe it's high time to reconsider the entire field. It has not led us into understanding the disease or to a better therapy for patients," he says.
In fact, the whole concept of immune privilege of the brain and lack of lymphatic drainage was created 70 years ago and hasn't changed much in ensuing years. This was around the same time EAE was created as the animal model for MS. Why hasn't there been more exploration until recently? I believe one reason is because the old theories have made people very rich.
Let's learn the history:
The theory of immune privilege was invented to explain why foreign tissue grafts placed on brain tissue didn't cause an immediate immune reaction, as similar grafts did in other parts of the body, like the skin. It was believed that antigens in the brain were concealed from the immune system by the blood brain barrier. That's why it was assumed that when immune cells showed up in the brain--if they weren't there fighting an infection or as an inflammatory reaction after a stroke---there could only be one explanation--it was some sort of "auto-immune"and destructive inflammatory reaction.
This theory of immune privilege was developed in the 1940s and became the foundation of transplantation immunology---or the reason why we need to block the immune system when patients receive a donated organ or a skin graft. The body's immune response needs to be turned off, so that it will not reject the foreign tissue. This process was discovered by Sir Peter Medawar, who wanted to understand how to help skin grafts survive.
Let's learn the history:
The theory of immune privilege was invented to explain why foreign tissue grafts placed on brain tissue didn't cause an immediate immune reaction, as similar grafts did in other parts of the body, like the skin. It was believed that antigens in the brain were concealed from the immune system by the blood brain barrier. That's why it was assumed that when immune cells showed up in the brain--if they weren't there fighting an infection or as an inflammatory reaction after a stroke---there could only be one explanation--it was some sort of "auto-immune"and destructive inflammatory reaction.
This theory of immune privilege was developed in the 1940s and became the foundation of transplantation immunology---or the reason why we need to block the immune system when patients receive a donated organ or a skin graft. The body's immune response needs to be turned off, so that it will not reject the foreign tissue. This process was discovered by Sir Peter Medawar, who wanted to understand how to help skin grafts survive.
Sir Peter Medawar, whose experiments in the 1940s established the basic rules of transplantation immunology [2], placed skin and or other types of grafts in the anterior chamber of the eye and the brain [3]. Observing that many of these grafts, unexpectedly, survived for prolonged intervals of time, he invented the term ‘immune privilege‘ to refer to the unexpected and prolonged acceptance of solid tissue grafts at specialized sites in the body. At the time, it was believed that the brain and eye lacked lymphatic drainage pathways, and that both organs resided behind stringent blood-tissue barriers. In light of this knowledge, Medawar proposed that immune privilege results from ‘immunologic ignorance’ because, on the one hand, in the absence of lymph pathways antigens could not escape from the eye, and on the other hand, immune effectors in the blood could not pass the vascular barrier to enter the sites where antigen resides. He speculated that antigenic material placed in privileged sites is sequestered from the immune system, and that the system remains unaware of the existence of grafts in privileged sites. link
This speculation on immune privilege has continued on for seven decades, mostly due to the fact that no one could find any lymphatic drainage pathways or understand how or why immune cells might get through the blood brain barrier.
Not coincidently, the EAE model for MS was developed around the same time as the theory of immune privilege, as an example of how t-cells could break through the blood brain barrier and attack the brain in an auto-immune reaction. It has been a prevailing theory in MS treatment development, which has also never been proven. Another 70 year old theory which has lead to disastrous assumptions about the brain.
The presence of mild scant lymphocytic infiltrates in the demyelinating lesions has been generally interpreted as the evidence of an inflammatory autoimmune process. Because specific T-cell mediated autoimmunity can be reproduced in animals after myelin protein sensitisation (Experimental Allergic Encephalo- myelitis (EAE)) it has been assumed (but never proven) that a similar T-cell driven immune mechanism is responsible for demyelination in MS.
The acceptance of EAE as a model for MS is an unfortunate error that has its basis on faith rather than science. Whilst EAE is a good example of an experimental organ-specific autoimmune disorder in animals, it cannot be accepted as a model for MS for a wide variety of reasons. This is particularly important in relation to the development of MS pharmacotherapy. We have analysed the literature on immune-modifying therapy in MS and it is clear that none of these agents can qualify as a candidate therapy under scrutiny.
link
The brain's relationship to the peripheral immune system is obviously much more communicative and complex than previously imagined. The discovery of lymphatic vessels by neuroimmunologists means we need a do-over in MS research, as this science writer comments:
This data suggests that brain immune surveillance communicates with the immune system and can generate adaptive immune responses. The authors infer that previously characterized glymphatic washing of the brain likely connects to the lymphatic system; a testable hypothesis. The authors further suggest that this system will change the way we think about neurological disorders such as multiple sclerosis and Alzheimer’s.
The fact that MS has no disease-specific immune target, no specific antigen, and does not look like EAE in mice, should give us all pause. There has never been any concrete, scientific proof that MS is an autoimmune disease. Just a theory, which has been used to create a 20 billon dollar a year industry. And that theory has completely unravelled. The question is, will MS researchers let go of pharma money, in order to pursue the true etiology of MS?
If the brain requires immune cells for neuroprotection, stem cell regeneration and plasticity, than what are we doing suppressing the immune system with MS drug therapies? What if this immune reaction is, as Dr. Michal Schwartz's research has shown, "protective", and should be modified, not stopped? (notice that this paper was co-authored by Dr. Kipnis, a PhD graduate of the Weizmann Institute of Science, who now heads up the Kipnis Lab at the Univeristy of Virginia where these lymphatic vessels were discovered.)
For decades, several axioms have prevailed with respect to the relationships between the CNS and circulating immune cells. Specifically, immune cell entry was largely considered to be pathological or to mark the beginning of pathology within the brain. Moreover, local inflammation associated with neurodegenerative diseases such Alzheimer's disease or amyotrophic lateral sclerosis, were considered similar in their etiology to inflammatory diseases, such as remitting relapsing-multiple sclerosis. The ensuing confusion reflected a lack of awareness that the etiology of the disease as well as the origin of the immune cells determines the nature of the inflammatory response, and that inflammation resolution is an active cellular process. The last two decades have seen a revolution in these prevailing dogmas, with a significant contribution made by the authors. Microglia and infiltrating monocyte-derived macrophages are now known to be functionally distinct and of separate origin. Innate and adaptive immune cells are now known to have protective/healing properties in the CNS, as long as their activity is regulated, and their recruitment is well controlled; their role is appreciated in maintenance of brain plasticity in health, aging, and chronic neurodevelopmental and neurodegenerative diseases.
link
Israel Steiner, a neurologist at the Hadassah University Hospital in Jerusalem, agrees that EAE has blocked "effective progress" for decades. He thinks alternative theories should be put to the test. "I definitely believe it's high time to reconsider the entire field. It has not led us into understanding the disease or to a better therapy for patients," he says.
"Many people in the community who do not have a vested interest in the autoimmune hypothesis share my views, but I'm not sure they would like to step out."
New Scientist vol 176 issue 2369 - 16 November 2002, page 12
Dr. Steiner would later publish the paper: Experimental allergic encephalomyelitis: A misleading model of multiple sclerosis link
The MS neurologists with "vested interest in the autoimmune hypothesis" were the very same ones who shut down CCSVI research before it could even begin, or be done correctly. They were the first to say that veins would have nothing to do with MS, that it was an autoimmune disease, that the brain's drainage system was unimportant. They created the narrative that those of us pleading for collaboration with Dr. Paolo Zamboni and the International Society of Neurovascular Disease (www.isnvd.org) were wackos, a fringe element, a Facebook/YouTube phenomena that would pass.
But they were wrong. The brain's venous system is most certainly important for efficient drainage of CSF, blood and now, lymph. And the brain's immune system appears to be intimately tied to venous flow of the brain via newly discovered lymph vessels. link
In fact, the two large lymph vessels which collect the lymph drainage from the brain, head and neck can enter the blood stream at the internal jugular vein, the subclavian vein, or the junction of these two veins, called the venous angle. Lymph relies on the low pressure venous system for drainage. To say that this discovery has "nothing to do with CCSVI" is to blatantly ignore physiology. For patients, or neurologists, who would like to learn more about lymphatics: link
The writing is on the wall, in medical journals, blogs and even twitter.
In fact, the two large lymph vessels which collect the lymph drainage from the brain, head and neck can enter the blood stream at the internal jugular vein, the subclavian vein, or the junction of these two veins, called the venous angle. Lymph relies on the low pressure venous system for drainage. To say that this discovery has "nothing to do with CCSVI" is to blatantly ignore physiology. For patients, or neurologists, who would like to learn more about lymphatics: link
The writing is on the wall, in medical journals, blogs and even twitter.
And we are all watching, reading, and waiting.
Time to rewrite the textbooks and help people heal,
Joan
Sunday, March 8, 2015
New research on the Heart-Brain Connection in MS
More and more researchers are looking at the connection between heart health and brain health in Multiple Sclerosis. It was seven years ago I first contacted cardiovascular and endothelial specialist Dr. John Cooke at Stanford University regarding my theory that serum markers of endothelial dysfunction might be pointing to a connection between the heart and brain in MS.
Dr. Cooke was very kind in responding to me, and said that the research I had compiled appeared to point to an association, but that the MS specialists he talked to at his university asserted the autoimmune nature of the disease, and the lack of connection between the heart and brain health in MS. At that time, not many researchers considered endothelial dysfunction a component on MS disease progression. Endothelial dysfunction was a known contributor to heart disease and stroke, however researchers weren't really looking at it in terms of diseases of neurodegeneration.
In fact, when I wrote about the endothelium, most lay people and even some medical people I spoke to had never encountered the word, but thankfully, this is changing. The endothelium is the largest secreting organ in the human body. It is the layer of cells which line the 60,000 miles of blood vessels that nourish our bodies. When endothelial cells are damaged and die, we see markers of this in the blood. Endothelial health is essential to the health of the body's organs and tissues. The heart and brain included.
Today, more and more MS researchers are considering this connection.
There is about 30% higher risk of the myocardial infarction in patients diagnosed with multiple sclerosis (MS) than in people without MS. Increased risk of cardiovascular disease development positively correlates with levels of serum markers of an endothelial dysfunction, and may give rise to a global cerebral hypoperfusion. It appears that these complications precede progressive loss of axons, which mechanisms are complex and should be linked to a loss of β2 adrenergic receptors on astrocytes of demyelinating lesions. Consequence of this deficiency, the cause of which is not known yet, is a decline in energy metabolism of axons. Moreover, the loss of these receptors is linked to a reduced redistribution of potassium ions by astrocytes, glutamate excitotoxicity and increase of calcium ion concentration in the axon with subsequent activation of necrotic processes. In addition to immunological aspects we should take into account also parameters of the functional state of endothelium when appropriate targeted therapy for patient is considered. http://www.ncbi.nlm.nih.gov/pubmed/25702293
Patients with MS showed increased frequency of smoking (51.7% vs 36.5%, p=0.001) and hypertension (33.9% vs 24.7%, p=0.035) compared with HCs. In total, 49.9% of patients with MS and 36% of HCs showed ≥2 CV risks (p=0.003), while the frequency of ≥3 CV risks was 18.8% in the MS group and 8.6% in the HCs group (p=0.002). In patients with MS, hypertension and heart disease were associated with decreased grey matter (GM) and cortical volumes (p<0.05), while overweight/obesity was associated with increased T1-LV (p<0.39) and smoking with decreased whole brain volume (p=0.049). Increased lateral ventricle volume was associated with heart disease (p=0.029) in CIS.
Patients with MS with one or more CV risks showed increased lesion burden and more advanced brain atrophy.
Dr. Cooke was very kind in responding to me, and said that the research I had compiled appeared to point to an association, but that the MS specialists he talked to at his university asserted the autoimmune nature of the disease, and the lack of connection between the heart and brain health in MS. At that time, not many researchers considered endothelial dysfunction a component on MS disease progression. Endothelial dysfunction was a known contributor to heart disease and stroke, however researchers weren't really looking at it in terms of diseases of neurodegeneration.
In fact, when I wrote about the endothelium, most lay people and even some medical people I spoke to had never encountered the word, but thankfully, this is changing. The endothelium is the largest secreting organ in the human body. It is the layer of cells which line the 60,000 miles of blood vessels that nourish our bodies. When endothelial cells are damaged and die, we see markers of this in the blood. Endothelial health is essential to the health of the body's organs and tissues. The heart and brain included.
Today, more and more MS researchers are considering this connection.
There is about 30% higher risk of the myocardial infarction in patients diagnosed with multiple sclerosis (MS) than in people without MS. Increased risk of cardiovascular disease development positively correlates with levels of serum markers of an endothelial dysfunction, and may give rise to a global cerebral hypoperfusion. It appears that these complications precede progressive loss of axons, which mechanisms are complex and should be linked to a loss of β2 adrenergic receptors on astrocytes of demyelinating lesions. Consequence of this deficiency, the cause of which is not known yet, is a decline in energy metabolism of axons. Moreover, the loss of these receptors is linked to a reduced redistribution of potassium ions by astrocytes, glutamate excitotoxicity and increase of calcium ion concentration in the axon with subsequent activation of necrotic processes. In addition to immunological aspects we should take into account also parameters of the functional state of endothelium when appropriate targeted therapy for patient is considered. http://www.ncbi.nlm.nih.gov/pubmed/25702293
Serum markers of endothelial dysfunction which can be regularly tested are levels of c reactive protein (CrP), hypercoagulation (SED rate, ESR), and fibrinogen or thrombin (d dimer). In fact, researchers already know that all of these blood markers are found to be high in people with MS. When Jeff was diagnosed in 2007, his serum numbers for these markers were sky high. Which is why I started this line of inquiry in the first place.
http://ccsviinms.blogspot.com/2014/03/blood-matters.html
http://ccsviinms.blogspot.com/2014/03/blood-matters.html
Another new study has found that people with MS who also had one or more cardiovascular (CV) risk factor (obesity, smoking, inactivity, hypertension) had higher lesion load and more pronounced brain atrophy.
Patients with MS showed increased frequency of smoking (51.7% vs 36.5%, p=0.001) and hypertension (33.9% vs 24.7%, p=0.035) compared with HCs. In total, 49.9% of patients with MS and 36% of HCs showed ≥2 CV risks (p=0.003), while the frequency of ≥3 CV risks was 18.8% in the MS group and 8.6% in the HCs group (p=0.002). In patients with MS, hypertension and heart disease were associated with decreased grey matter (GM) and cortical volumes (p<0.05), while overweight/obesity was associated with increased T1-LV (p<0.39) and smoking with decreased whole brain volume (p=0.049). Increased lateral ventricle volume was associated with heart disease (p=0.029) in CIS.
Patients with MS with one or more CV risks showed increased lesion burden and more advanced brain atrophy.
What does this all mean? Living a cardiovascularly healthy lifestyle benefits more than the heart. It can keep the MS brain from atrophying and delay progression.
These are all things that can be done today with nutrition, exercise and lifestyle which will maintain brain health.
Here's the program I created for Jeff, based on the connections I saw all those years ago. He's still on the program, and it's still helping him keep his serum numbers in the normal zone, with no MS progression.
http://ccsvi.org/index.php/helping-myself/endothelial-health
http://ccsvi.org/index.php/helping-myself/endothelial-health
I hope this might encourage you to learn more about the connection between your heart and brain, and your amazing endothelium!
Joan
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