Welcome! This blog contains research, information on lifestyle, nutrition, dietary supplements and health for those with MS, as well as continuing information on the understanding of CCSVI and cerebral hypoperfusion. 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 immune paradigm of MS, and continues the 15 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

Saturday, October 11, 2014

"We have confirmed Dr. Zamboni's results 100%"

It was only five years ago, September 2009, that I attended the very first CCSVI conference in Bologna, Italy.  Dr. Dake and I were invited as guests of Dr. Zamboni---and I was able to sit in on all of the sessions.  I took copious notes, and posted them on the internet.  I re-post the opening event notes  today, as a reminder of what has transpired.  I went to this conference, excited to see the cooperation of neurologists and vascular specialists.  I believed the benefits my husband received from his treatment would excite and encourage medical professionals in all fields.  I was naive.

I believe we have been let down and abandoned by a neurological community, which is intent on maintaining research funding and ties to the pharmaceutical industry.  I do not say this lightly.  I say it with a heavy heart. 
My bolding of the notes below illustrates my point.

The ISNVD will continue, and there are new members, mostly imaging and vascular specialists.  They are intent on understanding how restricted venous flow affects brain health.  They are not giving up on this investigation, despite the best efforts of others to thwart the reseach.  The Australian Alfred Hospital trial and Brave Dreams trials are still continuing.
And we are all older, wiser and most certainly not going away.
stay well,
Monday September 7, 2009
Bologna Italy
CCSVI PreCongress Meeting

Dr. Paolo Zamboni welcomes the gathered doctors and guests to the CCSVI Cenaculum Studiorum.
His topic is CCSVI, How to Move Forward-
He states that there are professionals gathered here from the studies of the blood’s path on the blood brain barrier side to the nervous system and that we all must share opinions and have exchanges. We need to dialogue and to learn from each other.

The origin of Dr. Zamboni’s work in Multiple Sclerosis began when he was a vascular surgeon in Sardinia, Italy. Sardinia is noted for its high level of epidemiology in MS in the general population. During 1987-1992, he noted a high prevalence in children with malformations of the jugular veins. His paper on this topic, “So-Called Primary Venous Aneurysms” was published in 1990. He noted AV fistula and a closed ring stenosis that could not be crossed by their blood in these children, external compression and this vascular anomaly appeared to be congenital. 20 years later, 90% of these children he studied have been diagnosed with MS.

In 2002, Dr. Zamboni noted that positive urine hemosiderin- a disease marker used to assess the severity of chronic venous disease- was administered to MS patients while they were in the midst of relapse. All of the MS patients tested positive. After he published a paper on this, he received an e-mail from Dr. FA Schelling- which referred him to Dr. Torben Fog’s paper- “Topography of Plaques in MS” The note from Dr. Schelling stated that perhaps Dr. Zamboni would now find what he was looking for...that the lesions of MS spread counter current from normal venous flow, and that there was where he should begin to study.

Dr. Zamboni then began to dedicate his work to develop a system of diagnosis of venous flow in the brain. He has found 100% correspondence with CCSVI and MS. He believes an international training program in Echo-Color doppler needs to be developed. and that there needs to be cooperation of neurologists and vascular surgeons. He mentioned endothelial disrupters such as smoking, cpn, EBV, and intracellular iron deposition as all being means of exacerbating this mechanism of disease. He spoke of his collaboration with neurologist Dr. Fabrizio Salvi of Bologna and the Jacobs Neurological Dept of SUNY Buffalo as being an example of such a collaboration.

Dr. Robert Zivadinov, Assistant professor of Neurology at Jacobs Neurological Institute at SUNY, Buffalo and Buffalo Neuroimaging and Analysis spoke next as to the Aim of the Meeting. He stated that we need to synthesize the current concepts about evaluation, pathogenesis and clinical relevance of CCSVI in MS. Individual variability in MS makes identifying the causative process very difficult.
He stated that the Journal of Vascular Surgery will soon be publishing the open label EVT intervention results of Zamboni, and that the current study at Jacobs, which will be completed in October ‘09 with the original 8 patients from America- has confirmed Dr. Zamboni’s results 100%. Dr. Zivadinov said that Jacobs is now recruiting and training new centers to test, diagnose and treat CCSVI in America.

He stated that he believes the next ten years will see 20,000 papers on CCSVI in vitro, vivo and animal studies. He reiterated that we need cooperation of various practices to find the solution. We need both the neurological and vascular perspective. He will be presenting at ECTRIMS after the Bologna conference.

Dr. Claude Franceschi- Director of the Paris Hospital Vascular lab spoke next on the Hemodynamic Factors of CCSVI.
The venous system is responsible for draining tissue, and the central parameter of drainage, transmural pressure, is changed when venous drainage is impaired. If TMP is too high, tissue suffers, edema and inflammation and vein dilation results.

Extra pressure on the nervous system comes from cerebral spinal fluid. Hydrostatic pressure is posture related- changing when the patient is supine or standing. The residual pressure- in which arterial blood surges into the venous system- is reduced in micro circulation. There is an increase in DR (downstream resistance) which is blocked by an obstacle. Obstacles can cause collateral veins to open as vicarious shunts and CSF will be excessive, causing edema and plaques. Cerebrospinal tissue is more sensitive to this. He believes the answer to CCSVI may lie in postural therapy, or a direct change in pressure via the Liberation technique or stenting.

Dr. Fabrizio Salvi- Head neurologist at the University of Bologna spoke of his clinical observations as a neurologist working with the CCSVI paradigm for three years. He told us that in 500 MS patients he has tested now, 100% have CCSVI. He stated the doppler is a wonderful tool of diagnosis and their needs to be training in the technique. He has a hypothesis as to why there are different varieties of screening in high risk subjects- because prognosis is related to the type of malformation. He wants to answer the question if the Liberation procedure is a disease modifying treatment in MS. He will give proof tomorrow that there is plasticity and remyelination in the CNS and the Liberation procedure have proven to activate remyelination in the CNS as shown by MRI.
“Yes!!!” stated Dr. Salvi...”no one is lost!!”

Dr. Patricia Coyle of Stony Brook University asks a question-
“How do we diagnose CCSVI?” 
The first answer comes from Dr. Zivadinov-
Doppler investigation is the beginning. If there is non-direction of flow in any body condition, or continual flow in the opposite direction- CCSVI is implicated. Transcranial doppler in the deep cerebral veins shows reflux. And then it is necessary to locate the stenosis. In MS, the jugular/Vertebral veins flow is consistently subverted. Dr. Zivadinov states that they had tested a 25 year old girl who had come into Jacobs as a control. A healthy girl, who presented with bilateral jugular occlusion. Months later, she had her first CIS attack of MS, and an MRI was done to show two lesions. She also has a familial history of MS. He reiterated that all of the doppler testing was blinded, yet it corraborated CCSVI in MS 100%.

Dr. Dake then stated that he had also tested a relative of a confirmed MS patient. A woman who had not been diagnosed with MS, but who presented at Stanford with jugular occlusion and a variety of neurological deficits, yet no MS diagnosis. She also showed lesion activity on an MRI, and he stented he occlusion the day before he flew to Bologna.

Dr. Zamboni makes the final statement to this question...he wants to articulate again that flow is more important than stenosis- especially as a preliminary diagnostic tool.
We are dismissed and all walk to a lovely formal dinner at the beautiful estate, Circolo della Caccia.

link to original post on Facebook September 7, 2009

How research has been manipulated:

Thursday, October 2, 2014

Systems Approach to healing-- Alzheimer's reversal!

I've written about the difficulty in conducting double-blind, placebo control trials for lifestyle.   As Dr. Roy Swank, Dr. George Jelinek and Dr. Terry Wahls could all attest,  the "gold standard" trial approach works best for drugs. But that doesn't mean a holistic approach to healing is invalid, or cannot be trialled.  It just means it takes more work for both patient and researcher.  

There is no way to patent or monetize a new lifestyle, so drug companies won't be paying for these studies.   However, a holistic approach addresses many different aspects of health, and some exciting new research shows that it can lead to disease reversal in Alzheimer's.

Published in the September issue of Aging, "Reversal of cognitive decline: A novel therapeutic program", a new study at UCLA shows exactly how a personalized "Systems Approach" helped Alzheimer's patients recover memory and health.

Dr. Dale Bredesen, Professor of Neurology at UCLA, authored the new paper.  Dr. Bredesen is one of many researchers who has questioned the pharmaceutical model of inhibiting beta amyloid plaques in Alzheimer's.  

In the case of Alzheimer's disease, Bredesen notes, there is not one drug that has been developed that stops or even slows the disease's progression, and drugs have only had modest effects on symptoms. "In the past decade alone, hundreds of clinical trials have been conducted for Alzheimer's at an aggregate cost of over a billion dollars, without success," he said.

The model of multiple targets and an imbalance in signaling runs contrary to the popular dogma that Alzheimer's is a disease of toxicity, caused by the accumulation of sticky plaques in the brain. Bredesen believes the amyloid beta peptide, the source of the plaques, has a normal function in the brain -- as part of a larger set of molecules that promotes signals that cause nerve connections to lapse. Thus the increase in the peptide that occurs in Alzheimer's disease shifts the memory-making vs. memory-breaking balance in favor of memory loss.


Dr. Bredesen believed that using a multiple target lifestyle therapy with his Alzheimer's patients might improve brain signaling.  Here are the main features of the program he created, which was adjusted for each individual patient.

(1) eliminating all simple carbohydrates (breads, pastas, baked goods)
(2) eliminating gluten and processed food, with increased vegetables, fruits, and non-farmed fish
(3) reducing stress with yoga
(4) as a second measure to reduce the stress, meditation for 20 minutes twice per day
(5) melatonin each night
(6) increasing sleep from 4-5 hours per night to 7-8 hours per night
(7) methylcobalamin (vitamin B12)
(8) vitamin D3
(9) omega 3 fish oil
(10) CoQ10
(11) Exercising for a minimum of 30 minutes, 4-6 days per week.

(Long time readers of this blog will notice that this program shares a lot with the Endothelial Health Program)

The results for 9 patients was better overall health, better body mass index, and a reversal of memory loss.   That's Alzheimer's Disease reversal!   Something no one drug has been able to achieve.

Yes, this is a small study, and yes, it is still anecdotal evidence.  But this program can be used in clinical trials.  It will be costly, and take time---but it may save brains.

What does this Alzheimer's research have to do with MS?  When we consider the link of the heart to the brain and the importance of cardiovascular health to cerebral perfusion, we can understand the need for endothelial health.  An oxygenated, perfused, cleansed and fed brain is a happy and healthy brain.

All diseases of neurodegeneration share hypoperfusion, or simply, reduced cerebral blood flow.  

There are lifestyle changes that can be made to aid healing.  Please note that I did not use the word "cure."  For more on how the "cure mentality" can hamper our efforts to heal--read 

The era of a "brain in isolation" research is ending.  More and more researchers, like Dr. Bredesen, are considering the body as a whole unit, and addressing cardiovascular function in brain health.

Thanks to Dr. Bredesen and UCLA for going up against the pharmaceutical companies, and bringing hope and healing to his Alzheimer's patients.

Where are the MS specialists ready to take on this challenge?
We're waiting,

Tuesday, September 30, 2014

REAL breakthroughs in MS research

It's been a busy month for MS research.  I wanted to give a brief overview of the new publications coming out in vascular journals, linking CCSVI and MS to slowed cerebral blood flow, changes in cerebrospinal fluid flow and coagulation factors.

As much as neurologists and immunologists continue to claim this exploration is dead, finito, over---there are still dozens of publications in press or being published which elucidate the vascular connection of CCSVI to neurological disease.  This exploration is far from over, as more and more international investigators join in the exploration.

1.  The International Society for Neurovascular Disease (ISNVD)--a multi-disciplinary group of researchers, has published their position statement on recommendations for multimodal noninvasive and invasive screening for detection of extracranial venous abnormalities indicative of CCSVI.

The full text is available here:

This position paper is extremely important, because it addresses the variablity of findings made by other researchers examining impaired venous flow in people with MS---and gives the first ever standardized imaging and evaluation recommendations.  It is written by some of the leading venous and imaging experts in the world.

The ISNVD recommends the use of a multimodal noninvasive and invasive imaging approach to optimally identify extracranial venous structural/morphologic and hemodynamic/functional abnormalities indicative of CCSVI. Creation of more quantitative imaging criteria are needed for further characterization of these venous abnormalities. Screening and monitoring of these venous abnormalities with the use of a combined noninvasive and invasive imaging approach should help establish the actual incidences and prevalence of extracranial venous abnormalities indicative of CCSVI in various populations. In addition, a multimodal imaging approach will address whether these abnormalities can cause significant hemodynamic consequences for intracranial venous drainage. The proposed noninvasive and invasive imaging protocols represent a first step toward establishing and validating the criteria for detection and monitoring of extracranial venous abnormalities indicative of CCSVI in open-label or double-blinded randomized controlled studies. The ISNVD recognizes that the rapidly evolving science and growing interest in this field will facilitate a refinement of these protocols in the near future.

2.  Another international collaborative effort looks at cerebrospinal fluid (CSF) dynamics in MS, using phase contrast MRI.  At the helm of this research is internationally recognized imaging expert, Dr. E. Mark Haacke.

This research separated pwMS into two groups, those with stenotic internal jugular veins (ST), and those without stenotic IJVs (NST) Changes in outflow was noted in those with stenotic veins.

The delay between the beginning of beginning of systole and the CSF outflow was higher in ST compared to NST MS. Less IJV flow was observed in ST vs NST MS. None of the measures was different between the different MS phenotypes. These results suggest that alterations of IJV morphology affect both IJV flow and CSF flow timing but not CSF flow amplitude

3.  Tying into this impairment of CSF outflow dynamics, another recent publication found that the third ventricle in the brains of those with CCSVI was much larger than in healthy controls on MRI.   The third ventricle is one of four ventricles in the brain, and is filled with cerebrospinal fluid (CSF).  In normal brains it is a narrow cavity and CSF flows freely through in a timely manner.  In those with hydrocephalus or normal pressure hydrocephalus, this ventricle expands.  

This buildup of fluid can damage the brain.  And the third ventricle is enlarged in those with CCSVI, indicating a lack of timely venous flow is impacting CSF flow.

In the MS–CCSVI group, the third ventricle diameter was 6.2±1.7 mm (from a minimum of 2.5 mm to a maximum of 9.2 mm, with a median of 6.3 mm, and a mode of 6.0 mm). Our data showed that 29 patients (88%) had an increase in third ventricle diameter, whereas only four patients (12%) had physiological size (less than 4 mm) comparable to all healthy control group subjects (27.28%). These results show that the increase in the third ventricle diameter could represent a criterion of positivity of neurological disease in patients with CCSVI.

4.  Finally, a group of vascular researchers look at how successful endovascular treatment of CCSVI changes the blood.  The fact that MS is related to higher levels of fibrin, ET1 and other markers of hypercoagulation and endothelial dysfunction has already been firmly established.

This group wanted to see if these blood markers changed, once normal venous flow was established.  They were.  In fact, lower coagulation activation status was associated with a better clinical outcome.  Another connection to the blood and endothelium.

Coagulation activation and endothelial dysfunction parameters were shown to be reduced at 1 month and stable up to 12-month follow-up, and they were furthermore associated with a good clinical outcome. Endovascular procedures performed by a qualified staff are well tolerated; they can be associated with other currently adopted treatments. Correlations between inflammation, coagulation activation and neurodegenerative disorders are here supported by the observed variations in plasma levels of markers of coagulation activation and endothelial dysfunction.

There is much movement in the study of how impaired venous return affects the brain for those with CCSVI/MS, and how treating this impairment improves clinical outcomes.  I live with anecdotal proof.  Jeff is now almost six years past his endovascular treatment and repair of malformed jugular veins and dural sinus.  He is jogging, traveling the world, working more than full-time, with a reversal of gray matter atrophy.  His third ventricle looks normal on MRI, he has had no further MS progression.  His coagulation numbers went from severe hypercoagulation, to normal.

There is a connection.  We will not let this research slip through the cracks.
stay tuned,