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 15, 2014

Report from the AAN conference---What Do They Know?

Please read the transcript and/or watch this Medscape video from the recent American Academy of Neurology's 66th Annual Meeting in Philadelphia.  It is sobering.

(You can join for free to view the videos and read articles.)

All of the panelists are MS specialists.  These are the experts. 

In it, we learn that:

1. MS disease progression and disability appear to be tied to brain atrophy, not new lesions or relapses.
A drug for MS, called laquinimod, appeared to help slow disease progression and atrophy in MS, although it had no effect on relapses and lesions.  In fact, laquinimod failed to slow relapses or lesions any better than placebo in the initial trial of RRMS.   No one really knows how laquinimod works.  That's right, the Mechanism of Action (MOA) is unknown.

It could be that laquinimod is increasing brain derived neurotrophic factor (BDNF) and preserving neurons.   Increasing BDNF is known to help the brain by preserving brain tissue.
You can increase BDNF levels yourself, without laquinimod--by exercising.

Bottom line--the MS specialists really aren't sure what is going on, or why laquinimod worked....but they'll be happy to try it out on people with progressive MS.  And as their disclosure statements show us, all of them have received honoraria, speakers fees, consultant fees and funding from Teva Neuroscience, the company developing laquinimod.

2. Genetics really do not play into the risk of developing MS.  The new genes associated with MS only add about 1% more to risk of susceptability.  Genetics studies have, for the most part, been a dead-end.

3. In fact, environmental factors, like sunlight exposure, vitamin D and Epstein Barr exposure, appear to be more important.  

4. Smoking is not good for people with MS.  It hastens disease progression.  There are lifestyle changes that people can make, which will slow disease progression.  And smoking appears to be the most "modifiable" risk.  Why is smoking bad for people with MS?  They don't know.  It could be how the "mucosa of the lungs interacts with the immune system during smoking."  

Or it could be, hmmm...just maybe... how smoking, a known risk factor for stroke and cerebrovascular disease, impairs blood flow and oxygenation of the central nervous system?

Watch this video and see behind the curtain of the great and powerful Oz.  View the emperor in all of his regal clothing.  These guys are basically saying, we don't know what MS really is or what to do about it.  If I have learned anything about MS in the seven years since Jeff's diagnosis, I have learned that the EAE model of MS is wrong, and the current treatment of MS is not helping patients live longer, more vital, less disabled lives.
Here is more on the futility of EAE in MS research.

"... a false orthodoxy claiming that multiple sclerosis is an autoimmune disorder has developed and formed the present basis of treatment, drug trials and research. The outcome of this misplaced creed has been truly catastrophic.” 

However, I have witnessed how pioneers who actually have MS---people such as Dr. Terry Wahls, Dr. George Jelinek and all of you---have taken measures into your own hands.  You have found the direct correlation of your disease to slowed cerebral blood flow from venous malformations.  You have had venoplasty and changed your lifestyles.  You are getting more sunshine, UV rays and vitamin D.  You have quit smoking, started moving more.  You have gotten off sugar and gluten,  are eating more whole foods and are dealing with life's stresses.   You are healing your gut with whole foods and probiotics.  You are lessening your exposure to toxins.  You are healing your endothelium! You have explored other avenues and differential diagnoses.

And you are living, wonderful, anecdotal proof of the ability to slow, stop and reverse MS disease progression!  Proof of the fact that there are things we can do to reduce inflammation and maintain gray matter.  Lifestyle changes, like smoking cessation, exercise and nutrition-can really make a difference.

Don't wait another minute, let alone a decade, for these guys to figure it out.  Take care of yourself, today!


Thursday, May 8, 2014

Why do women have higher MS rates? S1PR2 and the Endothelium

In the news---researchers find another connection of MS to blood vessels.  
New research from the Washington University School of Medicine outlines how higher levels of the blood vessel receptor protein S1PR2 in women might be creating higher MS rates in women. 

S1PR2 is a receptor which signals the endothelium (the cellular lining of our blood vessels).  It tells the endothelium which cells and molecules can pass through into tissue.  In the case of MS--this process affects the brain and spine.  An overexpression of this receptor may be behind MS.

The research, conducted at Washington University School of Medicine in St. Louis and published in the Journal of Clinical Investigation, found higher levels of a blood vessel receptor protein called S1PR2 in both female mice and women who were vulnerable to MS. What's more, S1PR2 was even higher in the parts of the brains of the women and mice that MS usually affects.
"It was a 'Bingo!' moment –- our genetic studies led us right to this receptor," senior author and associate professor of medicine at Robyn Klein, M.D., Ph.D., said in a statement. "When we looked at its function in mice, we found that it can determine whether immune cells cross blood vessels into the brain. These cells cause the inflammation that leads to MS."
Among the female mice, Klein and her team found 20 genes in areas of the brain typically affected by MS that were active at different levels than in male mice. Previous research had identified S1PR2 as a protein that dictates the ease with which cells and molecules pass through the walls of blood vessels. In the new research, S1PR2 was found to also regulate which cells cross from the blood vessels into the brain, which could allow the inflammatory cells that lead to MS to enter the central nervous system, according to the press release.
The highest levels of S1PR2 in human brain tissue samples were in two female MS patients who had "relapsing and remitting MS", meaning their symptoms flared irregularly.

Vascular researchers have been studying the role of the overexpression of S1PR2 in inflammation:
The endothelium, as the interface between blood and all tissues, plays a critical role in inflammation. Sphingosine-1-phosphate (S1P) is a bioactive sphingolipid, highly abundant in plasma, that potently regulates endothelial responses through interaction with its receptors (S1PRs). Here, we studied the role of S1PR2 in the regulation of the proadhesion and proinflammatory phenotype of the endothelium.
What can cause this overexpression of S1PR2?
Obesity and hypoxia (or low oxygen environments) are linked to higher levels of S1PR2.    http://www.ncbi.nlm.nih.gov/pubmed/24212262
Adipose tissue is linked to higher levels--  This might explain the connection to women.

S1PR2 is overexpressed during hypoxic stress

S1PR2 is over expressed during reperfusion, after an ischemic event.

We would experct to see these high levels of S1PR2 in those having relapses, if the hypo perfusion/reperfusion injury theory of MS is correct.

In fact, the hypoxic conditions we see in CCSVI, due to slowed venous return and hypoperfusion of the MS brain- with the resulting reperfusion injury- could well be linked to the overexpression of this protein.


While pharmaceutical companies look for ways to regulate S1PR2 and strengthen the endothelium---there are lifestyle modifications which can accomplish this--- for free.
If you are new to this page, please consider the Endothelial Health Program, and talk to your own physician about changes you can incoporate into your own lifestyle, to help strengthen your blood brain barrier.   http://www.ccsvi.org/index.php/helping-myself/endothelial-health

And when neurologists tell you MS has nothing to do with cerebral blood flow, hypoperfusion and the endothelium, you can point them to yet another study which contradicts this claim.  
There is most certainly a vascular connection to MS.
Heal the endothelium, heal the blood brain barrier, heal the brain.

Thursday, May 1, 2014

An ischemic stroke treatment--to be trialled for MS

Add a new medication to the ever-growing list of MS drug trials that address cerebral blood flow -not the immune system--3K3A-APC
With the growth of research into the connection of MS to cerebral blood flow,  we've seen an interest in exploring new ways to address hypoperfusion (slowed blood flow), endothelial dysfunction (damaged blood vessels) and brain atrophy (loss of brain tissue).

Why is this?  Because MS specialists, neurologists and advocacy groups are much more comfortable designing, testing and recommending a drug for MS, rather than encouraging healthy lifestyles and treating venous malformations.  It's almost impossible to have a placebo-controlled clinical trial for lifestyle.  

3K3A-APC is a modified form of human protein C.  Human protein C is an anti-inflammatory which protects the endothelial barrier.  3K3A-APC was created to strengthen the endothelial barrier--to prevent reperfusion injury and microbleeds in the brain after stroke.

3K3A-APC was created by Dr. Berislav Zlokovic.  Dr. Zlokovic was the keynote speaker at the ISNVD two years ago.  He is an endothelial researcher I contacted in 2008 regarding the potential connection to MS.  I reached out to him while he was at my alma mater, and he kindly replied.   Dr. Zlokovic is now at the University of Southern California, where he has continued his research on the blood brain barrier, stroke and neurodegenerative disease.  

Zlokovic is the scientific founder of ZZ Biotech, a Houston-based biotechnology company he co-founded with USC benefactor Selim Zilkha to develop biological treatments for stroke and other neurological ailments.
ZZ Biotech’s 3K3A-APC is a genetically engineered variant of the naturally occurring activated protein C (APC), which plays a role in the regulation of blood clotting and inflammation. 3K3A-APC has been shown to have a protective effect on the lining of blood vessels in rodent brains, which appears to help prevent bleeding caused by tPA.  http://news.usc.edu/56646/experimental-drug-reduces-brain-damage-in-rodents-afflicted-by-stroke/
Dr. Zlokovic's team has reached phase II this week, and they have just received and $8 million dollar grant from the NIH to test this drug in those who have had ischemic stroke.  I truly hope it can help these patients.  Dr. Zlokovic is a brilliant researcher, and this new drug has the potential to save brains.   http://www.acrpnet.org/MainMenuCategory/Resources/News/ACRP-Wire/CampusConnections.aspx

But the story does not end here....
ZZ Biotech's 3K3A-APC will also be tested for MS by USC's Neurology Dept.  

This is from the Erase MS website, where they discuss research they are funding.

The fourth research study is Dr. Weiner’s at USC. He plans to test a drug that works on multiple disease processes that are observed in MS, including inflammation, changes in blood vessel functions and neurodegeneration. This drug is known as human 3K3A-APC, and is modified from a protein called activated protein C (APC). 


Here is what Dr. Weiner says about the drug...

Although anti-inflammatory drugs are clearly beneficial, there is a great need to develop treatments that can also protect brain cells from injury or death and subsequently, prevent neurodegeneration and disease progression.

To this end, and with the help of the Race to Erase MS, we have begun to test the possibility that a new neuroprotective drug can be developed for the treatment of MS. The drug, named 3K3A-activated protein C (3K3A-APC), provides potent protection for brain cells against injury and death in models of stroke and Alzheimer’s disease. 

Why does Dr. Weiner not even mention the fact that this drug's method of action is on the vascular endothelium?  That it is made to strengthen the blood brain barrier?   Why does he skirt around the fact that the anti-inflammatory/immune-modulating DMDs are NOT preventing neurodegeneration and disease progression?  Calling 3K3A-APC "neuroprotective" is not the whole story.  Dr. Weiner has spoken out against CCSVI research, calling those who have been successfully treated with venoplasty as benefiting from placebo affect.  But why did my husband's gray matter atrophy reverse?  Why no more progression?  Isn't adequate blood flow to the brain also "neuroprotective?"

Once more, 3K3A-APC was created to strengthen the endothelial barrier--to prevent reperfusion injury and microbleeds in the brain after an hypoxic event.

Is this further tacit proof of the connection of MS to cerebral blood flow?
I believe so.

(For those who enjoy hypotheses and research--here's my hypoperfusion/reperfusion injury theory of MS.  I still believe this is what we are seeing in the disease.  I believe this is MS.  If so, this medicine may be very helpful.)