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

Wednesday, February 24, 2016

Turf War

If all you read are neurological journals, you would assume CCSVI research is over and done. But CCSVI venoplasty studies are continually being published in peer-reviewed vascular journals---and the results are encouraging.

Here is a recent study from a university cardiovascular disease center, published this month in the Journal of Cardiovascular Interventions--looking at quality of life (QOL) one year after treatment to relieve venous stenosis.

Does an Endovascular Procedure Improve the Quality of Life in Patients with Multiple Sclerosis

There were 94 MS patients tested for CCSVI (22 RRMS, 44SPMS and 26PPMS). 2 patients did not present with any vascular abnormality (that's 2%) and were not treated. Most patients had left IJV stenosis. The more disabled patients were, the more areas of venous abnormalities which needed treatment. The remaining 92 patients were all treated with balloon venoplasty.

By treating the venous abnormalities, cerebral venous drainage was increased.

There was a reduction in bladder disfunction, reduction in fatigue, improvement in disability and QOL for all of the treated patients, and these 4 parameters were maintained a year after treatment.There are other papers showing similar positive results after treatment. You will note that most are published in vascular journals, because this is a vascular treatment for a vascular problem.

Here are the some of the most recent ones on successful treatment for CCSVI:



Why don't we hear about these published CCSVI studies? Primarily because MS immune modulating drugs are a $20 billion dollar a year business.  Yes, that's $20 BILLION dollars....with a B.   And this kind of money has created a disastrous turf war.
The value of the multiple sclerosis therapeutics market will rise slowly from $17.2 billion in 2014 to approximately $20 billion by 2024, at a Compound Annual Growth Rate (CAGR) of 1.5%, according to research and consulting firm GlobalData.

We have known about this dilemma in medical research for decades. Vascular departments at universities simply do not receive the grant and pharma funding which is readily available to neuroimmulogical departments for drug development.  This has lead to an imbalance of power, and a betrayal of multiple sclerosis patients.

Read "Social constructionism and medical sociology: a study of the vascular theory of multiple sclerosis" a paper specifically addressing this divide, which was published in 1988.


brief excerpts below:

"A recent debate surrounding the pathogenesis of multiple sclerosis is analysed in terms of the skills, interests and backgrounds of the medical personnel involved. It is noted that the proponents of the vascular theory possess developed expertises in interpreting disease in structural, vascular terms, whereas their opponents' skills lie in immunology or neurology. Different observers have produced different conceptions of the disease because modes of observation, and the points from which observation takes place, differ. It is also noted that the debate over the causation and treatment of MS has occurred between a large and powerful social group (neurology) and a weak and marginal one (vascular specialists). The effects of this power inequality on the production an assessment of knowledge about MS are investigated. "

The paper goes on to discuss the very real turf war between vascular researchers and neuroimmunologists:


"Support for the idea of early vascular involvement in the aetiology of MS has also come from researchers working with the tomographic scanner. One of the standard techniques used in sectional radiography is a process whereby a radio-opaque dye is injected into the bloodstream, thus enabling any leakage through the walls of the blood-vessels to be readily observed. In other words tomographers possess well-developed skills in the study of lesion events within the vascular system. When these skills have been applied to the investigation of MS they have revealed fresh vascular features. "

"The dominant anatomic feature of multiple sclerosis is the relation of plaques to the venous component of the vascular system. The plaques, at least in the early stages, are almost always perivenular, extending as slender sleeves of demyelination. "


"Furthermore, the clinicians who treat MS patients have always been neurologists - who tend routinely to conceive of MS as being essentially, as well as symptomatically, a neurological disorder.

Also the therapeutic implications of the auto-immune theory are generally pharmacological - involving modes of treatment with which most neurologists are already very familiar and in which they possess developed skills. A new drug treatment for MS, even the trial of a new drug, could be accommodated into existing clinical routines with little difficulty."

It is now almost 30 years since this paper was written. And very little has changed in mainstream MS treatments.
Not since Dr. Zamboni's discovery of CCSVI, Dr. Michal Schwartz's discovery of the brain's protective immune system, Dr. Jonathan Kipnis' discovery of the brain's lymphatic vessels which rely on veins, The Gladstone Institute's revelation that a singular drop of blood in brain tissue creates MS lesions, or Dr. Yulin Ge's visualization of microbleeds in the MS brain with 7T MRI.

The vascular connection to MS is still being swept under a very large $20 billion dollar rug.
MS has a quantifiable vascular component. However, I'm not planning on blogging about this for 20 more years.  Jeff's doing well, now nine years past an MS diagnosis with no disease progression. He has returned to his performing and conducting, as well as increasing his compositional output. We've been traveling the world, and enjoying his renewed health and vigor. His brain is healthier than it was when he was diagnosed with MS in 2007 and treated for CCSVI in 2009---with a reversal of gray matter atrophy and remyelination of his cervical lesion documented on MRI.

He is very fortunate, and he is not alone.

Let's hope that all of us, working together, can change MS research and treatment.

Coming up---information on an opportunity to donate to CCSVI Alliance's matching donation drive, and double your dollars to fund neurovascular research.



Tuesday, February 2, 2016

The brain needs immune cells

In 2010, Dr. Alasdair Coles, an academic neurologist at Cambridge University, said to the press:
'We know MS is an auto-immune disease because if you block the immune response with drugs, people get better.'
This now infamous quote from Dr. Coles came when he was asked to comment on Jeff's treatment for CCSVI, as reported in the UK's Daily Mail.

In my mind, linking the cause of MS to how the drugs work (for some) is akin to saying, 
"We know the earth is flat because we don't fall off!"
The relationship between the brain and immune system is much more complex than ever imagined.

Labeling MS a classic autoimmune disease is a serious misnomer--since we see the same immune cell reaction to myelin after hypoxic injury and stroke.

Demyelination and axonal injury are characteristics of MS but are also observed in stroke. Conversely, hallmarks of stroke, such as vascular impairment and neurodegeneration, are found in MS. However, the most conspicuous common feature is the marked neuroinflammatory response, marked by glia cell activation and immune cell influx

There are no antigen specific antibodies in MS. There is no specific immune target in Multiple Sclerosis.  

And, thanks to new research, we now know that immune cells are vital to a functioning brain.  

1.They provide healing after a break of the blood brain barrier, as we see in MS.
2.They aid healing of axons after injury to the central nervous system, via glial scar formation
3.The "autoimmune" t cells often ablated in MS treatment are also responsible for neuroprotection.

At the time of his quote, Dr. Coles was bringing his life's work to market--the chemotherapy drug Alemtuzumab, repackaged for MS as Lemtrada.  Cole's overarching premise in his research is that the immune cells in multiple sclerosis are completely damaging to the brain, and need to be entirely removed.

And his theory then that "people get better" when the immune system is ablated is actually not true.  Yes, inflammation is tamped down in those with RRMS.  But, just like swatting a pesky fly with a sledgehammer, there is a lot of residual damage.   Immune ablation with chemotherapy has a host of horrific side effects, including fatal cancers, fatal viral and bacterial infections, worse autoimmune reactions in other parts of the body including kidney failure, lung tissue swelling, and hypothyroidism.  Not necessarily "all better!"  Which is why this medication has a black box warning, 

Meanwhile, Dr. Coles is busy trying to create an antidote to stop the new autoimmune diseases his drug has caused.  That's right...Lemtrada actually causes autoimmune disease!
The principal adverse effect of alemtuzumab (Lemtrada) is autoimmunity, which arises when reconstitution of the immune repertoire after alemtuzumab occurs by homeostatic expansion of residual lymphocytes. Therefore we are now testing the ability of keratinocyte growth factor to promote thymic lymphopoiesis and so prevent autoimmunity after alemtuzumab, in a MRC-funded clinical trial.

Even worse,  the MS disease process does not stop with Dr. Cole's Lemtrada.  Cerebral atrophy and disability continue, even without any new lesions.

Unfortunately, this did not lead to a clinical improvement in the disability in these patients. In fact, their disability worsened with time at a rate of 0.02 EDSS points for each patient each year. Evidence for continued neurodegeneration in these patients was shown by progressive cerebral atrophy on follow-up MRI scanning. 

In the past decade, a narrative developed in the MS drug industry by MS researchers like Dr. Coles:  the idea that the immune system is at fault, and needs to be halted.   This has led to the creation of a class of drugs which create "lymphocyte sequestration" and "lymphocyte depletion"---meaning they keep the white blood cells walled off in the lymph tissue or deplete them, keeping them out of the body's circulation.  Instead of allowing immune cells protective entry into the body and around the brain, they are held back.  This new class of more powerful disease modifying drugs include Tysabri, Gilenya and Tecfidera.  

Not surprisingly, there is a price to pay when you hold back immune cells, deplete them, and don't let them do their job.  And one of those side effects is the reactivation of latent viruses and bacterial infections, including the John Cunningham virus (JCV).  This virus causes the deadly brain infection, progressive multifocal leukoencephalopathy (PML).  

Neurologists have comforted their patients regarding their PML risk and Tysabri use, telling them that if they were tested as JC virus negative, they would remain that way and not to worry.   But this was simply not true.  

The JC virus is very common in the general population, infecting almost 90% of us in childhood.  It stays under control and latent because our immune system keeps it in check.  This means we have a JC negative status.  The virus is able to cross the blood brain barrier where it attacks myelin and destroys brain tissue.  

New research shows that the risk of JCV reactivation due to Tysabri use is ten times higher than previously estimated.  That not 1%, but 10% of all patients on Tysabri were seen to go from JCV negative status to JCV positive status while taking Tysabri.  The drug is apparently what turns people from JC virus negative to positive.  This makes sense, if you understand that what Tysabri is doing is holding back immune cells, and rendering them unable to stop a virus from reactivating.

It also makes sense as to why Tecfidera and Gilenya have now been linked to PML...and I fear it's only a matter of time until real world reporting comes in showing JCV reactivation on these drugs.

Dr. Michal Schwartz has been publishing on the importance of immune cells for brain health for decades.  Both she and Dr. Nedergaard are two of my research heros.  They are brilliant, determined women who have challenged the neurological status quo and are actively publishing their findings.

Dr. Schwartz explains her decades long search in understanding the importance of the immune system for the brain in her new book,  Neuroimmunity: A New Science That Will Revolutionize How We Keep Our Bodies Healthy and Young.

This book is simply wonderful!  It is written clearly and simply, so that lay people might understand her research.  But it is also in-depth enough to appeal to researchers.  All of her publications are cited.

Scientists long believed that there was no communication between the brain and the immune system; in fact, it was thought that any infiltration of immune cells into the brain was a major threat to our health. Based on this assumption, the standard treatment for inflammation associated with neurodegenerative diseases, such as Alzheimer’s, was to totally suppress the body’s immune system.

Prof. Schwartz turned this theory on its head by proving that the immune system and the brain do “speak” to each other – and that, in fact, neurodegenerative diseases are the result of a communication breakdown between the brain and the immune system. Instead of suppressing the immune system, she argues that the most effective way to treat Alzheimer’s and other chronic neurodegenerative diseases is to do the opposite: boosting targeted immune cells in the brain. 

The brain needs immune cells.

Please, if you have MS--- until we understand more about the immune system and brain health, make sure to discuss this new research with your neurologist, especially if they are putting pressure on you to try these new immune ablating and lymphocyte depleting drugs for MS.  New research is coming in every single day, showing that this method might not be the best approach for long-term brain health.

Be well, be curious.
The earth is not flat.