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

Thursday, May 26, 2011

Restricted Blood Flow, Moyamoya Disease and MS

May 26, 2011

From my friend Mark--someone with MS who was treated at Stanford after my husband--a story in his local paper caught his eye this morning.

When they first met in 1991, Corona residents Douglas Wang and Lizabeth Tso didn't know of the love and heartache that would follow them over the next 20 years.

Eight years later, they met a second time and fell in love.

In December 2001, Wang was diagnosed with multiple sclerosis. Nine months after that, at age 28, he suffered a massive stroke that left him paralyzed on his right side. He was then diagnosed with Moyamoya disease, a rare disorder that constricts blood flow to the brain.

Mark wondered, what the heck is Moyamoya Disease, and how is it like MS?  
Turns out, this disease, which restricts blood flow in the brain, is often MISDIAGNOSED as MS.

Moyamoya is a disease of the intracranial arteries which deliver blood inside the brain.  CCSVI is a disease of the extracranial veins.  But the mechanism of injury is hypoxia, not the immune system.

And to add another interesting layer to this tale...here is research from Stanford University, where Dr. Steinberg looked at pwMS and those with Moyamoya.

Misdiagnosis of Moyamoya Disease as Multiple Sclerosis Variants in a Case Series of Seven Patients
Omar Choudhri MD; Teresa Bell-Stephens RN; Robert M. Lober MD PhD; Nancy Fishbein; Gary K. Steinberg MD, PhD

Multiple sclerosis is a relatively common demyelinating condition of the brain and spinal cord that can present insidiously with multiple neurological symptoms.Some multiple sclerosis symptoms could be mimicked by transient ischemic attacks in the setting of a vasculopathy such as moyamoya disease.

Moyamoya disease is an idiopathic chronic cerebrovascular disorder, characterized by progressive occlusion of vessels comprising the circle of Willis and clinical presentation can vary depending on the ischemic territory. Here we present a series of patients managed as having multiple sclerosis for many years before being correctly diagnosed with moyamoya disease.

This study investigates the radiographic, laboratory and clinical overlap between the two clinical entities and outcomes after surgical revascularization.

Seven patients found in retrospective review of the 448 patients in the Stanford Moyamoya Database from 1991-2010 to have initial diagnosis of multiple sclerosis on presentation. MRI imaging, angiograms, CSF results and clinical follow-up data were reviewed.

Male : Female ratio of our patients was 1:6 which correlates with female preponderence in both conditions. The average age of patientsmwas 35 years and duration of diagnosis for presumed multiple sclerosis varied between 6 months to 20 years. Extremity paresthesia was the most common neurological symptom in these patients. MRI periventricular FLAIR or T1 changes were the most common diagnostic clue to multiple sclerosis and a repeat MR angiogram or formal angiogram subsequently confirmed the diagnosis of moyamoya disease.

Greater than 60% of patients had improvement of their neurologic symptoms following cerebral

We believe that moyamoya disease should be considered in multiple sclerosis variants who present with paresthesias and do not respond to traditional immunosuppressive therapies.
Early diagnosis and revascularization procedures could help prevent further neurologic sequelae. Furthermore, subtle MRI findings should suggest obtaining a CTA/MRA or a formal angiogram to identify moyamoya vessels.

Given that Moyamoya is yet ANOTHER DIFFERENTIAL diagnosis for MS which involves the cerebrovasculature, I believe those with an MS diagnosis deserve to be tested with angiograms and MRVs, to learn if they have a vascular component to their disease.  The evidence continues to grow.


Friday, May 20, 2011


May 20, 2011 at 9:41am

Dr. Giedrius Buracas is a Functional MRI (fMRI) researcher at University of California, San Diego. He presented new research the Hubbard Foundation is conducting into the MS brain before and after angioplasty.  The study utilizes functional magnetic resonance imaging to study how the brain is activated when doing specific tasks.

fMRI  is a type of specialized MRI scan used to measure the hemodynamic response (change in blood flow) related to neural activity in the brain. It is one of the most recently developed forms of neuroimaging. Since the early 1990s, fMRI has come to dominate the brain mapping field due to its relatively low invasiveness, absence of radiation exposure, and relatively wide availability.

In the Hubbard study, there were many differences in how normal vs. MS brains responded to tasks.  The MS brains showed an "undershoot"---or less bloodflow and neural activity.

There were changes in the subcortical gray matter response from before venoplasty and after.  PwMS were able to complete tasks in a more "normal" manner, and their brains showed improved blood flow and activation after treatment for CCSVI.

Here is Dr. Buracas' presentation at the Hubbard conference

"The most surprising outcome of this angioplasty intervention is that it eleviates some symptoms of MS which presumably has to do with structural damage.  The structural damage stays there, but people feel better---so, it looks like one of the contributors to the neural basis of eleviated symptoms is recovery of default mode network suppression."

Certainly, impeded blood flow into the cortical areas of the brain, as shown on these fMRI studies, could be part of the reason for slowed responses.  And repairing this flow, by getting rid of extracranial blockage, could very well be the reason for improved bloodflow  and a more normal response of the brain after angioplasty.  The brain needs normal cerebral perfusion---delivering O2 and glucose--in order to function.   Thanks again to the Hubbard Foundation for this important work.


Thursday, May 19, 2011

Viagra in the MS news (again)

May 19, 2011 at 9:59am

Reading MS news is like having deja vu everyday (all over again...)

The same old stories, regurgitated.  Most "innovations" in MS research involve the EAE mouse model and some NEW!  EXCITING!  PHARMACEUTICAL!

About two years ago, there were stories about how viagra could help relieve MS symptoms.
And, today, there are more stories. 
I'm not even going to bother linking them.  Just google it, if you're interested.

The point is, viagra affects the nitric oxide in our bodies.  It creates vasodilation via the endothelium.  It's yet another connection of the vasculature to MS. 

If you want to learn more about how you can enhance nitric oxide and achieve symptom relief for free, without a prescription, without side effects from drugs that mess with your body's natural chemical balance--
check out The Endothelial Health Program and increase your own nitric oxide.

I wrote it up for Jeff and have been sharing it online for free since 2008.  It's recommended for all, and can help with cardiovascular disease and many other modern, western lifestyle diseases.

It is not a cure.  It is not the full-story.  But it will help relieve symptoms, and will maintain vibrant natural health.  Without another prescription.  Remember, always speak with your own doctor before beginning a nutritional or supplemental program.  I based this research on Dr. John Cooke's book, The Cardiovascular Cure.  I hope it may be of help.


Wednesday, May 18, 2011

Zonulin and gluten: the link to the blood brain barrier

May 18, 2011 at 2:49pm

Dr. David Hubbard discussed research into zonulin in his presentation at the Hubbard Foundation conference.  As many of you know, the Hubbard Foundation recommends a gluten-free diet to maintain endothelial integrity and a healthy blood brain barrier.

Another neurologist named David--Dr. David Perlmutter-- also recommends a gluten free diet.  Here is his newly published book, Grain Brain  http://drperlmutter.com/about/grain-brain-by-david-perlmutter/

So, what is gluten? Gluten is a special type of protein that is commonly found in rye, wheat, and barley. Therefore, it is found in most types of cereals and in many types of bread. Not all foods from the grain family, however, contain gluten. Examples of grains and seeds that do not have gluten include wild rice, corn, buckwheat, millet, amaranth, quinoa, teff, oats, soybeans, and sunflower seeds.

If you're like me, you've probably wondered, "What the heck does gluten have to do with the brain?"
Well, there is a very interesting connection, and it's based on research being done at the University of Maryland on a protein called zonulin.

Tuesday, May 17, 2011

EAE in mice vs. the new Stanford animal model of CCSVI by Dr. Michael Dake

May 17, 2011 at 7:39pm
Here is part of Dr. Dake's lecture from the Hubbard Foundation conference:

First, Dr. Dake explains how the current model of EAE is created in mice.  It is a rather convoluted procedure--

"There's an animal model, but it's not really, unfortunately, like most animal models, it's not really a human model.  Basically, you take like a mish of ground up spinal cord and brain from some other species, you mix it with some oily substance, some TB bacilli, and some bordadella pertussis, some whooping cough toxin, and inject into peridium,  and what you get is this whopping inflammatory response, and that's good because you get the accelerated disease process, but obviously in humans, it's a much more chronic and progressive thing.  

So, what we've done is taken mice and ligated (the jugular veins)  and we're going to move now up to marmosets, because that's the next level of the species, and marmosets you can actually partially occlude the veins and keep them open without totally ligating them.

 And these mice and their veins, we've got a recipe that we think is right where we want it.  We're starting to see not only clinical performance differences between mice that are ligated and mice that aren't  ligated, but now there's a way to tomographically, in a little mouse brain, to make these wafer thin micron sections thru the whole brain and we're learning a whole lot.  I think it's going to be very interesting as we move up to a larger model to really see....but we think that we're seeing an accentuation of the venous ligation on the disease process."

No words to describe how much I respect this man.  He listened to us and was interested, treated my husband's venous malformations,  and continues to speak out on CCSVI.  Thanks, Dr. Dake.

Friday, May 13, 2011

Jugular venous reflux could influence cerebral blood flow and neurological disease

May 13, 2011 at 8:18am

Anyone who has been following this page for awhile knows about the research in Taiwan by Dr. Chung and his associates into jugular valve insufficiency and transient global amnesia.  I wrote to Dr. Chung in '09 and sent him all of Dr. Zamboni's research, noting that I thought he would find some interesting and complimentary discoveries to his own research on the jugular veins.

Dr. Chung and his associates are different in their studies, in that they employ valsalva manuever (exerting pressure against a closed airway-- which happens during straining, sneezing, breath-holding, etc) in order to create jugular reflux, and as we all know, Dr. Zamboni finds reflux in those with CCSVI during normal breathing.

It appears Dr. Chung's team is now looking at CCSVI.  We can only hope they bring further understanding into how jugular venous reflux affects cerebral blood flow and perfusion---
 Acta Neurol Taiwan. 2011 Mar;20(1):1-3.
Jugular venous reflux and neurological disorders.
Hsu HY.
Department of Neurology, School of Medicine, Chung Shan Medical University, Taichung, Taiwan 

  • Abstract
    Usually, disturbance of arterial blood supply and circulation of cerebrospinal fluid are considered more clinically relevant, though accumulating data suggest that cerebral venous insufficiency does have important pathophysiological consequences in various neurological diseases(1-5). Hindrance of principal and collateral cerebral venous outflow will cause elevation of venous pressure, insufficiency of cerebral blood flow (CBF), increase of intracranial pressure, and eventually lead to parenchymal abnormalities. Disorders involving cerebral venous circulation, such as cerebral sinus thrombosis, dural arteriovenous fistula, and surgical sacrifice of the cerebral veins, may lead to serious complications. However, most physicians do not assign practical importance to cerebral venous circulation.