Welcome! This blog contains research & information on lifestyle, nutrition 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 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

Friday, June 9, 2017

Caution and concern: minocycline and antibiotics for MS

There are new reports and publications advocating for use of minocycline as a "safe and inexpensive treatment for MS"--as well as a new publication on combined antibiotic treatment for CCSVI.

There is no doubt that antibiotics have been helpful for many with MS.

However, I have serious concerns about using antiobiotics as an MS treatment, due to a side effect which can go undetected, causing damage to the brain and vision.

First, a bit of history.  When Jeff was diagnosed with MS in 2007, I found a publication which considered use of minocycline as a low-risk MS treatment.  Yes, this antibiotic has been touted before.  What's old is new.  link

I brought in the research in and asked his neurologist if she would prescribe the antiobiotic for him, and she agreed.

Jeff took minocycline for a couple of days, and developed serious pressure headaches.  He kept on with it, even though he was in agony,  as we had read some articles about "herxing" and bacterial "die-off" and thought maybe that might be the issue.  But the headaches got worse.  After consulting with his neurologist, we learned that Jeff's headaches were most likely due to a KNOWN side-effect of minocycline.

Minocycline is believed to hamper reabsorption of cerebrospinal fluid in the brain,  potentially creating intracranial hypertension and vision loss.  In fact, doctors know about this side effect, and it has been well documented.   For someone with already slowed venous flow and build-up of CSF (as a patient with CCSVI),  this side effect could be even more harmful.

As intracranial hypertension does not always manifest in vision loss or headache, it might be difficult to know if this antibiotic is hampering CSF flow in the brain.   link
For those who wish to learn more about how all tetracyclines, like minocycline, create intracranial hypertension. link

Jeff's neurologist advised him to stop taking minocycline, and the headaches went away.  He was lucky, he had a very obvious side effect, and knew to stop.  But not everyone gets headaches.

So, please be careful.  Something which seems "benign" as a treatment for MS, may actually have side effects that we still do not understand.

We also do not clearly know the impact of antibiotics on the gut's microbiome.  And this is another area of concern for me.

The study, recently published in mBio, found that just one weeklong course of antibiotics changed participants' gut microbiomes, with the effects sometimes lasting as long as a year. After all, antibiotics don’t discriminate—as they attack the bad bacteria, the good ones are vulnerable too.
link

For people who have benefitted from antiobiotic protocols, I'm truly happy for you!  MS is indeed a snowflake disease, and chronic infections are known endothelial disrupters.   This post is for the folks who have not had benefit, or had damage, or who want to know more.

Because people with MS do not always get the complete story,
Joan






Tuesday, May 30, 2017

Jugular anomalies and collateral flow in multiple sclerosis

There is a new paper recently published in the American Journal of Radiology from Dr. Haacke's superb radiology team at Wayne State University in Detroit, called Jugular Anomalies in Multiple Sclerosis are Associated with Increased Collateral Venous Flow

The complete paper is here:  link

As many of my readers know, there has been very little study of the outgoing venous system, especially when compared to the ingoing arterial side of blood flow.  We have a well-documented understanding of how problems with carotid arteries, the main inflowing blood vessels to the brain, can cause disease.  link  There are many papers on carotid arterial stenosis and stroke, dementia, Alzheimer's and other diseases of neurodegeneration.  And carotid artery scans are quite commonplace.  Angioplasty treatment for carotid arterial disease is an accepted and even routine practice today.

But in contrast, the venous system, specifically the internal jugular veins which are the main drainage route for the brain, has been under-researched and is not well understood.  A common thought from doctors has been that the brain can utilize collateral veins to drain, and that when the jugular veins are blocked, it's no big deal, since there are other veins to take up the flow.  This paper is one of the first which is looking specifically at how blockage of the IJV changes venous flow patterns.


Research on venous abnormalities in MS thus far has been limited to the IJV, and little is known about extracranial venous collateralization. The extrajugular drainage system consists of the vertebral venous system; the deep cervical veins, which anatomically are paraspinal toward the heart; and the anterior and external jugular veins, which receive blood from facial and superficial areas.8 Although the presence and structure of collateral veins have been assessed by using time-resolved imaging of contrast kinetics venography, flow values were not quantitatively evaluated.9-11 The purpose of this work was to examine the relation of extracranial venous anatomy and flow in a large cohort of patients with MS and healthy controls (HCs) taken from our neuroimaging data base.12 Because of the complexity of the extracranial venous system, we have classified these vessels into 3 groups based on anatomic MR information and their drainage path: primary (ie, IJV), paraspinal, and superficial. We hypothesized that increased venous paraspinal and superficial flow will also be observed for cases that evidence abnormal IJV structure and flow. In contrast, a subset of patients with MS may have a distinct collateral venous flow pattern compared with patients with MS and HCs without structural venous anomalies. 

In a study of 153 people with MS, 55% of the MS group exhibited jugular venous stenosis.  In the healthy control group of 105 people, 20% had stenotic veins.  Both of these groups had collateral venous flow, either through the vertebral or paraspinal veins.   The anatomic assessment of these vessels really isn't the complete picture.  Remember Dr. Zamboni's quote--"It's not the architecture, it's the flow."

Collateral flow has hemodynamic consequences.   This collateral system is like taking a winding country road when the main highway is blocked.  It is slower, less direct and has consequences for the brain, including venous hypertension and venous insufficiency.  There will be further research on the hemodynamic consequences of collateral venous flow.

One of the leading researchers publishing on this link is ISNVD member Professor Clive Beggs.

Professor Beggs has been able to show that MS is associated with changes in the dynamics of the CSF pulse in the cranium, and that the normal relationship between this and the jugular veins is profoundly altered in MS patients. He has also found that venous drainage anomalies in patients with Alzheimer's disease are associated with blood retention in the cerebral veins, suggesting that constricted venous outflow might be a generic phenomenon implicated in the pathophysiology of other neurological diseases.   Professor Beggs said: “My work suggests that vascular anomalies can profoundly alter the biomechanics of the intracranial space. This is important because there is a growing body of evidence that altered haemodynamics in the cranium are associated with a wide range of neurological conditions.  link
I know it has been frustrating for those waiting for CCSVI science to come in.  In the ten years since Dr. Zamboni first published his initial papers on CCSVI, we have seen an unprecedented pushback from the neurological community to even consider venous flow and the brain.

But we have also seen new publications like this one from radiologists,  and contributions from groups like the Nedergaard Lab, the Kipnis Lab, the Gladstone Lab and the ISNVD.  These groups are publishing on the newly discovered lymphatic system, which relies on the venous system of the brain.  We are now seeing how absolutely vital the brain's veins are--and how problems in venous flow are linked to all diseases of neurodegeneration.  This is real, and the science is coming in.  link

For those who are "out of wait" and frustrated by the pace of this research--it is best to consider the vascular connection to MS and live your most  endothelially healthy life today.  Talk to your own doctor about eating whole, colorful natural foods, exercising or physical therapy, getting UV ray exposure,  increasing quality sleep, reducing stress,  and finding joy and community.  Maybe consider NUCCA or atlas orthogonal treatments, having your venous system scanned for irregularities and getting treatment from a respected IR.

Be hopeful, and be well.
Joan

My husband's MRV from Stanford University, April 2009
Showing 99% and 70% obstructed IJVs and collateral flow (those curly, small veins) before his venoplasty treatment

Wednesday, May 17, 2017

MS is vascular


MS is caused by a breakdown of cerebral endothelial cells.  The loss of these vascular cells, which line all 60,000 miles of our blood and lymph vessels, is why the blood brain barrier becomes open, how immune cells are called in creating inflammation, why the coagulation cascade occurs increasing fibrinogen, what allows for death of neurons,  what causes MS to progress.

For those who hate medical language, find it confusing, and like easy to understand explanations, I wrote up a simple post on the endothelium and how it works here:  link

I'm not the only one saying the endothelium is central to MS.

A new paper, edited by MS neurologist Lawrence Steinman at Stanford University states the following:

Endothelial cells (ECs) in the CNS form a unique blood–brain barrier (BBB) that is broken down in multiple sclerosis (MS). New therapies are sorely needed to restore BBB function in this disease.

Disruption of the blood–brain barrier (BBB) is a defining and early feature of multiple sclerosis (MS) that directly damages the central nervous system (CNS), promotes immune cell infiltration, and influences clinical outcomes. There is an urgent need for new therapies to protect and restore BBB function, either by strengthening endothelial tight junctions or suppressing endothelial vesicular transcytosis.

This paper is a collaborative review from Columbia University, UC Irvine, Stanford and the Albert Einstein College of Medicine.  You can read the abstract here:
link

I really don't know how else to say it.  Your endothelium is important.  I've been blogging about this scientific reality since my first post on this blog.  Hundreds of my posts are about endothelial cells, why they are important, why they die, how to maintain them.  Obviously, I didn't do the research, I just put it together.  

Yes, I am gratified that universities acknowledge the importance of the endothelium in MS.  But so much of this remains a continued search for industry funding and "pharmacologic enhancement" rather than a search for the etiology, or cause of MS.  Or an understanding of how the endothelium is damaged by a variety of lifestyle, vascular and disease factors.  

I wanted to understand how to protect and strenghten the endothelium, which is why I originally contacted Dr. John Cooke, a researcher at Stanford University who had published a book on nitric oxide and lifestyle measures to heal the endothelium in cardiovascular disease.  He is now at Houston Methodist, heading up a lab which is creating endothelial cells from stem cells, for use in regenerative medicine.  He's getting there!  link

Below are the interventions we discussed, which I compiled for Jeff and others with MS.  The endothelium can heal by using these strategies.   Jeff has done really, really well following this program.  I have also heard from other people with MS who are employing these measures, and finding health and stability.  Please talk to your own doctors before beginning any lifestyle program, to make sure it is right for you.  I am not a doctor.  But I trust people like Dr. Cooke.
http://ccsvi.org/index.php/helping-myself/endothelial-health

The International Society for Neurovascular Disease recently had their 7th annual conference.  This year, the President of the ISNVD was Dr. Stephen Alexander.  I originally met Dr. Alexander online and later in person at the first meeting of the group which would become the ISNVD, back in 2009 in Bologna, Italy.   Dr. Alexander is an endothelial researcher who studies endothelial cells in MS and inflammation.  He and his fellow researcher, Dr.  Alireza Minagar, have published many papers on the vascular connection to MS.

This is their paper, which caught my attention ten years ago:
Multiple Sclerosis as a Vascular Disease


Their most recent effort is a chapter included in the book "Inflammatory Disorders of the Nervous System" called "Emerging Roles of Endothelial Cells in Multiple Sclerosis Pathophysiology and Therapy"

The complex pathogenesis of MS can only be appreciated when and if vascular contributions are recognized as a significant part of MS etiology. Indeed, many novel therapies for MS target the mechanistically relevant vascular inflammatory features of these conditions and implicate cerebrovascular endothelial cells (CECs) as the “failing gatekeeper” of the blood-brain barrier (BBB).    link


And yes, CCSVI is a factor.  When blood flow is disturbed, due to venous hypertension or stenotic blood vessels,  there is a lack of shear stress over endothelial cells, and they die.  Endothelial cells need constant moving blood.  Here is a paper from Dr. Alexander on Venous Endothelial Injury in Diseases of the CNS.   https://bmcmedicine.biomedcentral.com/articles/10.1186/1741-7015-11-219

While researchers continue to put together the pieces and find pharmacological means to strengthen the endothelium, there are things you can do today to help yourself.

I know, I repeat myself.  A lot.  Because this is important.

Heal the endothelium, heal the vasculature, heal the body.

Joan





The brain’s blood vessels are lined with endothelial cells that are wedged tightly together, creating a nearly impermeable boundary between the brain and bloodstream.