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, August 30, 2014

Understanding Endothelial Dysfunction--learning from Ebola crisis

The horrific outbreak of the Ebola virus in West Africa is causing researchers and physicians around the globe to ask what can be done to slow the death rates in this vulnerable population.

A recent piece in the New York Times, titled "Can Statins Help Treat Ebola?"  is authored by Dr. David S. Fedson, a retired professor of medicine at the University of Virginia.  Dr. Fedson writes about the current crisis of the Ebola epidemic and the short supply of life-saving drugs.  He suggests that there are other treatments, aside from experimental and expensive drugs, that have already been tested in humans, are readily available and can modify the body's response to the virus.

How would these drugs help?  They target endothelial dysfunction.

More than a decade ago, clinicians noted striking similarities between patients with Ebola and those with bacterial sepsis. Both diseases involve severe dysfunction of the endothelial cells that line blood vessels throughout the body. This dysfunction in turn precipitates major abnormalities in blood coagulation. Both can eventually lead to the failure of internal organs, primarily the liver and kidneys, and organ failure often leads to death. 

Researchers have since discovered that abnormalities of endothelial function and coagulation can be modified or reversed by treatment with drugs such as statins, angiotensin-converting enzyme (ACE) inhibitors and angiotensin-receptor blockers (ARBs), which were developed to treat patients with cardiovascular diseases and diabetes. 

Dr. Fedson suggests that strengthening the endothelium with cardiovascular drugs may be the key to stopping organ failure and saving lives in the Ebola outbreak.

These very same statins have been suggested as a treatment for secondary progressive multiple sclerosis, as they reduced brain atrophy (from 0.6% to 0.3% per year) in pwMS when compared to placebo.  MS doctors are more accepting of a pill, rather than life-style modification, when treating disease, as a pill can be placebo-controlled and trialled.  And they most certainly never explain why cardiovascular treatments might slow brain atrophy.  But as we have all learned, it's because of blood flow to the brain.

In fact, all of the above mentioned cardiovascular drug treatments are now being tested in people with MS, to slow down neurodegeneration and brain atrophy; death of brain tissue due to endothelial dysfunction.  These drugs are not immune modulating---rather, they address blood flow, endothelial function and coagulation.  Here's more on the new medications being tested in MS.

What can those with a chronic and progressive disease like MS take away from this deadly Ebola outbreak?   There is a vascular connection to this terrible disease, as there is a vascular connection to MS.  A strong endothelium is the body's best defense.  Keeping the blood vessel lining healthy and impermeable is the surest way to maintain cerebral circulation for those with MS.   Endothelial health will slow brain atrophy and may even reverse it.

But you don't need a statin.  There is much that can be done with lifestyle, nutrition, and exercise.

Here's to more healing ahead!

Wednesday, August 20, 2014

Inadequate cerebral blood flow and loss of neurons in MS

A new study was recently been published in the JAMA Neurology journal.  One of the investigators is Yulin Ge, MD--a recent presenter at the International Society for Neurovascular Disease conference.  www.isnvd.org  Dr. Ge has been imaging the MS brain for over a decade at NYU, and he has found many vascular connections to MS.

The study looks at cerebrovascular reactivity, or CVR.  CVR is how the brain reacts or responds  with blood flow when there is vasodilation.  This function is extremely important, as neurons need adequate blood flow to provide glucose and oxygenation.  Without this response of adequate cerebral bloodflow (CBF), the brain will not function properly, and neurons can potentially die.


What this new study did to measure CVR was to look at how healthy controls and pwMS responded to a hypercapnia (too much carbon dioxide), which the researchers created by using 5% carbon dioxide gas.  This gas increases cerebral blood flow by creating vasodilation--or a widening of blood vessels.  A healthy endothelium (lining of the blood vessels) would normally respond to hypercapnia by widening vessels and allowing for more blood to flow to the brain.

Patients with MS had a significant decrease of cerebrovascular reactivity compared with controls. This decrease in CRV correlated to gray matter atrophy, but did not correlate with white matter lesions. 

Their conclusion was that there is an impairment in the cerebrovascular pathophysiology in pwMS, and that inadequate blood flow to neurons may indeed be the cause of neurodegeneration in MS.  And that this was a vascular problem, NOT a problem initiated by white matter lesions.

We know that impaired CVR is related to arterial stenosis and occlusion of the blood vessels in the neck.  http://www.hindawi.com/journals/rrp/2012/268483/

Note that this new study did not hypothesize why this is happening in people with MS. But this study could well be related to what the Columbia researchers saw when they damaged the vascular endothelial cells outside the brain.

The Columbia University study, which was published earlier this summer, found that when researchers damaged the vascular endothelial cells lining the blood vessels outside the brain using lasers to cause oxidative stress,  they could disrupt blood flow to the brain and affect neurovascular coupling.  http://ccsviinms.blogspot.com/2014/06/columbia-researchers-provide-new.html

Dr. Zamboni has noted that there is a derangement of the endothelial cell layer in the jugular veins and valves in people with CCSVI/MS.  This loss of endothelial cell integrity could well be causing the decrease in cerebrovascular reactivity seen in people with MS.

As an anecdotal side note, my husband's gray matter atrophy reversed after he was treated for dural and jugular venous stenosis and began following the Endothelial Health Program.
And he has had no further MS progression since 2007.

The heart and brain are connected, and a healthy endothelium is essential to both.
Something to consider,

Saturday, July 5, 2014

Ending a "Misadventure"

The following is an open letter to Dr. Dennis Bourdette in response to his editorial in the June 2014 issue of Neurology, entitled Venous Angioplasty for "CCSVI" in multiple sclerosis: ending a therapeutic misadventure.  This open letter has been sent to his university, as well.  I hope to continue a dialogue with the CCSVI advocacy community and neurology.

Dear Dr. Bourdette--

I was disappointed to see that your comments in Neurology only focused on one half of the two phases of the BNAC PREMiSe CCSVI trial.  The first phase, which has been largely ignored by the press and neurology,  was a case controlled study of venoplasty in 15 patients with RRMS.  Eight patients were treated with venoplasty to repair CCSVI, and the other seven had delayed treatment after 6 months.  There was an immediate improvement in cerebrospinal fluid flow in the treated group, a lessening of lesions on MRI, while the delayed treatment group showed continued MS progression, more lesions and altered CSF hemodynamics.  This phase of the study showed venoplasty, when able to restore venous flow to >75% of capacity,  created a measured improvement of CSF flow and better parenchyma venous drainage, which continued on for twelve months after treatment.   It was published in The Journal of Vascular Interventional Radiology.  (1)  Important to note that Phase 2 of PREMiSe DID NOT restore venous flow to >75%.. In fact, it only restored venous flow to 50%, and was a failure of treatment.  There are many more published studies finding a connection of CCSVI and MS and improvements after successful treatment, and they appear mainly in vascular journals and are ignored by neurology. This disconnect has become increasingly frustrating to those of us whose lives depend on the future of MS research.

As a neurologist with an endowed chair from the Swank Family Foundation, I'm sure you are well-versed in the vascular component of multiple sclerosis.  Dr. Roy Swank was documenting  "capillary fragility"  in Neurology's pages in 1958.  He found systemic subcutaneous hemorrhages in his MS patients, decades before the science of the endothelium.(2)  He also noted hypercoagulation, platelet abnormalities, and slowed cerebral blood flow in MS.(3)  Today, we understand much more about how the vasculature is involved in MS. (4)  To label research into CCSVI and the extracranial venous system as a "misadventure" is to do science a great disservice. 

In spite of the accumulating links of MS to cerebral hypoperfusion (5) and recent research as to how the vascular endothelium controls cerebral blood flow and neuronal health (6), neurological researchers remain wedded to Dr. River's EAE murine model of 1935.  This allegiance to EAE is a stranglehold far more damaging than Charcot's harness. (7)  The tragedy of PML occurred in patients receiving Tysabri infusions only because mice cannot be infected by the JC virus.  The murine model testing of Tysabri could not foretell the deadly results in humans. (8)  The mouse model of EAE is not spontaneous nor does not remit, as MS develops, relapses and remits in humans.(9)  It is time to admit that the EAE mouse model, while somewhat effective for testing immune modulating pharmaceuticals, is not helping us understand the disease process we call multiple sclerosis.  Nor is it addressing MS disability progression linked to gray matter atrophy.  

I am married to a man diagnosed with MS in 2007.  Due to his severe presentation, he was told not to expect many more days of mobility.  At the time, I noted vascular issues, including a petechial rash--the same rash Dr. Roy Swank had documented.  My husband also presented with extreme hypercoagulation and high liver enzymes.(10)  By making the connection of his disease to his vascular system, I was able to piece together peer-reviewed and published research to address these factors. Since his diagnosis seven years ago, he follows a diet and active lifestyle based on Dr. Swank's program-- combined with modern research into endothelial health and EDRF (nitric oxide), published by Dr. John Cooke, author of The Cardiovascular Cure. (11) 

He had venoplasty at Stanford University over five years ago, to resolve a severe stenosis in his left jugular vein and dural sinus. (12) Since this successful endovascular treatment, which is approved for dural sinus stenosis (13), his gray matter atrophy has reversed, as documented on MRI. This fact makes it difficult to claim his improvements are due to placebo.  He jogs, skis, mountain bikes, hikes and works full days.  Not bad for a 51 year old man with MS.  Since venoplasty, his heat intolerance is gone, his cognitive fog and fatigue hugely reduced.  His bladder issues and spasms have remitted. He no longer has central sleep apnea.  He has had no further lesions or MS progression.  And yes, he is a wonderful anecdote; as are the thousands of other MS patients who have received venoplasty and had benefit.  Or the thousands of other patients, like Dr. Terry Wahls and Dr. George Jelinek, who have changed their diets, increased aerobic exercise, stopped smoking, utilized UV ray therapy, and found hope in "alternative" cardiovascular treatments.

Where is the intellectual curiosity of neurologists?  Why the continued disassociation of the brain with the cardiovascular system and blood vessels?  

It is time to admit---neuroimmunology has failed MS patients.  This is exactly why so many patients and caregivers are turning to treatments outside the EAE autoimmune paradigm.  Neurologists must reach out, across academic silos, to include the new research of the endothelium and the vascular component of MS.  CCSVI investigation is only just beginning.  Neurology has had eighty years of EAE, and many, many failures.  The vascular endothelium and extracranial venous system deserve a bit more time and effort, before you proclaim the exploration over.

I invite a dialogue, Dr. Bourdette-- and would be happy to share your thoughts on this letter- in my blog and with the online CCSVI community.  I also invite you to consider the continuing research of the International Society for Neurovascular Disease. (14)

most sincerely,

Joan Beal

Disclosure:  Joan Beal is not a doctor.  She receives no money for her MS advocacy work.  She funds her own endeavors.  Her personal reward is seeing her husband thriving.  She writes about current MS research on her blog, Multiple Sclerosis-the vascular connection.  Joan's theory of MS is that it is a disease of endothelial dysfunction, cerebral hypoperfusion and reperfusion injury, and she invites researchers to consider the scientific evidence. Multiple Sclerosis--the vascular connection: Multiple Sclerosis -- Hypoperfusion/Reperfusion Theory


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2. Swank RL. Subcutaneous hemorrhages in multiple sclerosis. Neurology. 1958; 8: 497-498. 

3.. Swank RL: Plasma and multiple sclerosis - past and present; in: Multiple Sclerosis: Immunological, Diagnostic and Therapeutic Aspects. London, John Libbey Eurotext, 1987, pp 217-220.

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  • Elizabeth M. C. Hillman, PhD     
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    9. Gold, R Linington, C Lassman, H.  Understanding pathogenesis and therapy of MS via animal models: 70 years of merits and culprits in EAE research.  Brain  doi:10.1093  2006.

    10. Tremlett H, Seemüller S, Zhao Y, Yoshida EM, Oger JD, Petkau J.    Liver test abnormalities in multiple sclerosis: findings from placebo-treated patients.  Neurology. 2006 Oct 10;67(7):1291-3.  

    11. Cooke, JP. Therapeutic interventions in Endothelial Dysfunction.  Clin. Cardiol. Vol. 20 (Suppl. II), II-45–II-51 (1997)

    12. Dake MD,  Dantzer N, Bennett WL, Cooke, JP.   Endovascular correction of cerebrovenous anomalies in multiple sclerosis: a retrospective review of an uncontrolled case series.   Vascular Medicine 2012 Jun;17(3):131-7. doi: 10.1177/1358863X12440125. E2012

    13. Arac, A  Lee, M  Steinberg, G   Efficacy of endovascular stenting in dural venous sinus stenosis   Neurosurg Focus 27 (5):E14, 2009 

    14.  www.isnvd.org