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

Monday, August 8, 2016

CCSVI included in Oxford Textbook of Vascular Surgery

"The Oxford Textbook series is the foremost international textbook of medicine. Unrivalled in its coverage of the scientific aspects and clinical practice of medicine and its subspecialties, it is a fixture in the offices and wards of physicians around the world."

The new edition of the Oxford Textbook of Vascular Surgery, edited by Matthew M. Thompson, professor of vascular surgery at St. George's Medical School in London, includes articles from "130 global experts."  The new edition features a full chapter on Chronic Cerebrospinal Venous Insufficiency (CCSVI).  Authored by Dr. Paolo Zamboni, Sergio Gianesini and Erica Menegatti from the University of Ferrara, this chapter is included in a section on diseases of veins and lymphatics.  link

While MS specialists and neuroimmunologists have disparaged and intentionally misrepresented Dr. Paolo Zamboni's vascular studies, he has continued to publish, undaunted.  He, along with the International Society of Neurovascular Disease,  have explored how the venous system affects neurodegenerative disease.  He has improved cerebral venous return using open surgery and venoplasty, and has documented benefits in the health of his patients.  He has created a brand new CCSVI diagnostic center at the University of Ferrara, while collaborating with international space organizations, to understand the affects of microgravity on the venous system.  As I have said before, if rocket scientists collaborate with Dr. Zamboni, why can't MS neurologists?  If the Oxford Textbook editors consider his research expert and important enough to include in this new publication, why the continued naysaying from neurology?

Heartfelt thanks to Dr. Paolo Zamboni and the entire vascular department at the University of Ferrara.  Thank you for continuing your research and exploration, even while confronted with unprecedented hysteria and vitriol from the neurological community.

CCSVI exists.  Slowed venous return to the heart harms the central nervous system, just as slowed venous return harms every other major organ in the human body.   This is scientific fact.  Whether or not MS specialists choose to acknowledge the science remains a moot point.  Vascular specialists understand this, and will continue to treat patients and push the research forward.  This is how medical science evolves, one peer-reviewed publication at a time, until the stack becomes undeniable.  Financial incentives, pharmaceutical payouts,  cognitive dissonance, and territorial medical silos cannot stop it.

Share this information with vascular specialists at your local universities and hospitals.  Fund research and support groups like the ISNVD.  Insist that "charities" and organizations who purport to be helping people with MS include vascular specialists on their medical advisory boards.  Question the status quo.

And most importantly, do all you can to improve your own heart and endothelial health.  Because this is real-- the heart and brain are connected-- and there are things you can do today to help yourself.  No prescription necessary.

Be well,
Joan







Saturday, August 6, 2016

Russia? сюрприз!


I recently found these new publications on PubMed.  Only the abstracts are available, as the articles are in Russian.


Multiple sclerosis and endothelial dysfunction (a review).
[Article in Russian]
Spirina NN, Spirin NN, Fadeeva OA, Shipova EG, Boĭko AN.
The endothelium plays an important role in the maintenance of vascular homeostasis, the tone and anatomical structure of the vascular wall. It is an essential component of the blood-brain barrier. In adverse conditions, damaged endothelium initiates many pathological processes in the human organism and plays a key role in the pathogenesis of a number of systemic diseases including multiple sclerosis. In this review, we discussed in detail the concepts of structural and functional features of a healthy endothelium and endothelial dysfunction, and present the basic theory of the damage mechanism of the blood-brain barrier and the role of endothelial cells, adhesion molecules, cerebral hypoperfusion in multiple sclerosis.


von Willebrand factor and adhesion molecules in patients with multiple sclerosis.
[Article in Russian]
Spirin NN1, Spirina NN, Boĭko AN
Based on a role of certain adhesion molecules and vascular endothelial damage in multiple sclerosis (MS), we explored C-reactive protein, von Willebrand factor, matrix metalloproteinase-9, sICAM-1, sPECAM-1, E-selectin and P-selectin in the blood of patients. One group of the patients received pathogenic therapy. There was the increase in the level of the von Willebrand factor in patients who did not receive the therapy. The levels MMP-9 and sE-selectin were correlated with the high activity of the disease. The authors suggest the presence of the endothelial dysfunction in some patients. MMP9 and sE-selectin may be considered as potential markers of the activity of multiple sclerosis.

I searched pubmed for Russian publications because this blog has been receiving an inordinate amount of traffic from Russia.  In the past several months, there have been hundreds of thousands of hits. I've now have more readers from Russia than the US or Canada.   I'm honestly not sure what this is all about, and whether these might be bots, or another variety of nefarious internet activity.

But I'm hoping it's more about actual Russians wanting to understand the vascular connection to MS, and being sent here by internet search engines.

So, if any of my Russian readers would like to pop on and say hi (or Здравствуйте) in the comments---I'd be honored. I first noticed endothelial dysfunction, high SED rate, C-reactive protein and hypercoagulation in my husband's serum results back in 2007, and created a lifestyle program to help address it.  link I keep writing all these years later, and my tracking results show that people all over the world are reading this blog.

Both sides of my father's family emigrated to America from Russia in the early 1900s.  They were escaping the pogroms and seeking religious tolerance and work opportunities.  I hope to visit their homeland under better circumstances, to honor my family's hard work and courage.  The world is much smaller today, thanks to our internet access.

I'd suggest that any interested researchers who visit this blog contact the ISNVD  www.isnvd.org  and submit your studies.  We're together in wanting to understand the vascular connection to MS--a disease which affects people all over the world.  Especially those of us in developed countries above and below the 40th parallel.

всего хорошего,
Joan



Thursday, August 4, 2016

7T MRI shows MS vascular connection

High powered MRI is allowing us to see the vascular connection to MS.  A recently published study used 7T MRI to compare the lesions of people with MS and those with Neuromyelitis Optica (NMO).  link

21 patients with MS and 21 patients with NMO were imaged.  There was one important difference between the two groups.  Only the patients with MS showed signs of "iron laden lesions" which contained a central vein.  None of the people with NMO showed this.

NMO is a truly autoimmune disease, in which immune cells attack the optic nerve and spine.   In contrast to MS,  NMO has a known antigen, called Aquaporin 4.  In NMO, the immune cells attack this antigen and cause demyelination.  However, there has never been a specific antigen discovered for MS.  In fact, MS lesions are very different from NMO lesions, as high powered MRI is showing us that inside MS lesions, there is a central vein which is allowing blood products, like iron, into brain tissue.

Here is how the researchers describe the difference:

Distinguishing MS from NMO lesions. 
Axial T2-weighted image from a representative patient with MS demonstrating a hyperintense lesion (black arrow) traversed by an ill-defined central venule adjacent to the inferior horn of the lateral ventricles. The lesion appears hypointense on a corresponding T1-weighted MPRAGE image. The lesion shows a hypointense peripheral rim and an iso- to hypointense central core traversed by a well-defined venule on GRE-T2*-weighted image. This lesion is hyperintense on QSM. Hypointense signal intensity within the lesion on GRE-T2*-weighted image and hyperintensity on QSM suggest iron accumulation (upper row). An axial T2-weighted image from a representative NMO lesion reveals 2 round hyperintense lesions (white arrows) in the subcortical WM region. The lesions appear hypointense on T1-weighted and hyperintense on GRE-T2*-weighted images. However, these lesions are isointense and therefore inconspicuous on QSM (lower row). The scale bar is for the QSM image with units of parts per billion.

Looking at the images, we can see the arrows pointing to the MS and NMO lesions.  All the images (on the top for MS and bottom for NMO) are of the same area of brain tissue.   It is the GRE-T2 image which clearly shows the MS lesion has a very small, yet well-defined vein (venule) going through the center.  The NMO lesion does not.  The QSM image shows that around this vein, in the MS patient, there is iron.  The researchers do not say that this is from blood leaking into tissue.  But this is the very obvious inference.  Blood, or heme, contains iron.  Microbleeds into brain tissue have been documented in MS. link   And here, once again, we have more proof.






For those of us who know our history, we remember that Rindfleisch saw the EXACT SAME THING through his microscope in 1863.

If one looks carefully at freshly altered parts of the white matter ...one perceives already with the naked eye a red point or line in the middle of each individual focus,.. the lumen of a small vessel engorged with blood...All this leads us to search for the primary cause of the disease in an alteration of individual vessels and their ramifications; All vessels running inside the foci, but also those which traverse the immediately surrounding but still intact parenchyma are in a state characteristic of chronic inflammation. 
Rindfleisch E. - "Histologisches detail zu der grauen degeneration von gehirn und ruckenmark". Archives of Pathological Anatomy and Physiology. 1863;26:474–483.

CW Adams published on damaged cerebral veins and the deposition of iron from blood in MS brains in 1988.
Yet, even after all the historical evidence, when Dr. Zamboni published on the link between venous disease, iron deposition into tissue, inflammation and MS lesions in his "Big Idea" paper in 2008---he was resoundingly ignored (or worse, mocked) by MS researchers. Here's the history of this research into the central vein sign, iron deposition and MS lesions-- link

Once again, we see the evidence of the vascular connection, in clear, high-powered MRI images. Iron deposited into brain tissue, creating inflammatory lesions, all around a small, central vein.

At a certain point, you simply have to say---
WAKE UP!

My family reached that point almost a decade ago, and because of this, my husband remains healthy. The evidence continues. There is a vascular connection to MS.
Whether or not MS specialists and immunologists will ever acknowledge this fact and help patients is moot. It is up to all of us to educate, inform, encourage, and move the research forward.


Be well,
Joan