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

Tuesday, July 4, 2017

Interferon β almost doubles the risk of stroke and migraine in MS. Why?

An important observational study on long term use of interferon β and increased risk of stroke and migraine in MS was just published by one of my favorite MS researchers, Professor Helen Tremlett at the University of British Columbia.  Current interferon beta drugs prescribed for MS are Avonex, Betaseron, and Rebif.  

The complete paper is available here:
Evaluating the Safety of B Interferons in MS

Dr. Tremlett does not represent any drug company or MS treatment.  Dr. Tremlett simply studies people with MS, to understand disease progression and environmental factors, like gut microbia, vascular commorbidities, liver enzymes, Vitamin D, sun exposure, fatigue and pregnancy.  link

She has been studying the adverse affects of MS drugs and documenting many things pharmaceutical trials marginalize, or completely ignore.  In her publications, she highlights MS DMDs' modest efficacy, and the fact that clinical trials are of short duration and in a highly selected patient group, and do not give us a complete picture of long-term adverse events.

The IFN-βs are modestly effective, reducing relapse rates by about one-third and having a beneficial effect on imaging outcomes,2 but findings regarding longer-term effects on disability have been mixed.3,4The IFN-βs are generally considered safe, especially compared to newer agents for MS.5 However, few studies have systematically assessed their safety in real-world clinical practice (appendix e-1 at Neurology.org).5 A meta-analysis of 9 clinical trials estimated that patients treated with IFN-β had a 2.8-fold increased risk of discontinuing drug because of an adverse event compared to the placebo group. The most common adverse events were flu-like symptoms, injection-site reactions, leukopenia, lymphopenia, and elevated liver enzymes.6 However, because of their short duration and relatively small sample sizes, clinical trials cannot identify all potential adverse effects of a drug treatment or predict the safety of the drug in clinical practice. Furthermore, participants in clinical trials are highly selected in terms of comorbidities and concomitant medications and often differ substantially from patients who use the drug once it reaches the market. We identified signals of potential adverse events related to IFN-β treatment in a large population-based cohort of patients with RRMS.

This new study looked at patients with RRMS, registered at the UBC MS Clinic from 1995-2004, who were treated with interferons.  2,485 eligible patients were followed up until death, until they left BC, or until they stopped taking interferons.  After compiling the data, the study showed that patients who had taken interferons, there was a 1.8 fold increase (almost double risk at 180%) of stroke or migraine.  There was also a 1.3 fold increase in depression and hematologic abnormalities.

I realize this might be an obvious observation to many of my readers, but I feel like it will be overlooked by neurologists.  All of these adverse affects are vascular.  Stroke, migraine, blood issues --and yes, even depression---are related to blood flow, cerebral perfusion, coagulation and endothelial health.  Interferon B changes platelet adhesion to the endothelium and appears to raise blood pressure.

Here's more on this from the paper:

Our study is a comprehensive assessment of the potential risks for a broad range of adverse events related to IFN-β in the real-world clinical setting. Several of the adverse events that we observed to be associated with IFN-β exposure such as migraine, hematologic abnormalities, and depression are included in the known safety profile of the IFN-βs. Stroke, on the other hand, is not well recognized as a potential adverse event, being limited to a few case reports.19,20 Nonetheless, it is biologically plausible that this event is associated with IFN-β because this drug may alter wall competence or enhance the major histocompatibility complex-1 molecule expression of platelets and other cells,21,22 resulting in enhanced platelet adhesion to the endothelium.22,23 
Hypertension can also increase the risk of both migraine35 and stroke, and we observed a higher risk for hypertension among current users of IFN-β, which might point to a common pathway.

Other researchers are also studying the long term vascular side effects caused by interferons---
including thrombotic microangiopathy, which is a disease of endothelial injury resulting in thrombosis.  These clots can cause stroke, chronic kidney disease and renal failure.  

Also being studied is how interferons affect blood clotting and cause hypertension

There have been case studies where people with MS who were treated with interferon B had subsequent strokes.

Previous studies have shown that people with MS already have a two fold increase in risk of venous clots, independent of drug treatment.

Perhaps long-term use of Interferon β-- which further increases the risks of clotting, hypertension,  stroke and endothelial dysfunction, while only reducing relapse risk by 1/3-- isn't the best approach for people with MS.

The vascular connection to MS is real.
Endothelial health is essential.


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.

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,

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.

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:

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.

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.


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.

Friday, April 28, 2017

The Endoplasmic Reticulum (ER), Rab32 and MS

Once again, the medical news headlines are full of "breakthrough!" "cause of MS!" "new way of looking at the disease!" and even "Cure!"

Researchers in the UK and Canada have found the protein Rab32 appears in large quantities in autopsied brain tissue of those who had MS.  Higher levels of this protein cause a disruption of communication between cells, and lead to mitochondrial malfunction and neurodegeneration.  Researchers say they do not know what causes this increase in Rab32, but they believe that by inhibiting this protein with new treatments,  they can slow MS progression.  However, neurovascular researchers have been studying this mechanism for many years in Alzheimer's, ALS, Parkinson's and dementia---and vascular researchers know why this happens (keep reading.)

I find it's always a good idea to read the actual research, rather than rely on click bait or fake news headlines.  Many medical reporters have only a basic understanding of science.  The researchers who send out press releases like to keep it that way. The news stories continue to mention the autoimmune theory of MS right at the start, yet this new discovery has little to do with autoimmune disease, and almost everything to do with inflammation of the vasculature and endothelial dysfunction.

Here is the complete paper:

Together, using multiple patient tissue samples, our findings indicate that Rab32 increases dramatically in neurons and macrophages/microglia localized within active MS lesions and that high amounts of Rab32 coincide with the expression of CHOP. In contrast, chronic MS lesions show Rab32 predominantly in neurons.

Simmen and his colleagues were quick to note that it’s not yet clear what actually causes the surge of Rab32. They also note that Rab32 is likely not the only important protein when it comes to unraveling the mystery of MS.
Rab32 is just one of the proteins that is having the effect of drawing the ER and mitochondria too close. There are dozens of other possibilities,” he said.

So,  as we learn when digging a bit deeper into the research, it's not just about the increase of Rab32.  This just makes a great headline, and will fund ongoing research for these labs.  But there are other unfolded proteins causing cellular disruption.

At the center of this "discovery" is the endoplasmic reticulum (ER) and ER stress.  The ER is a membraneous structure of a cell, it connects to the nucleus and provides a protective and cleansing function.  Red blood cells do not have ERs...but the liver or pancreas cells have lots of them.  So does the brain.  This is because the ER allows for protein synthesis. And we've known about ER stress in other disease for quite a while.  So, to catagorize this as a "discovery" is not really true.  It's just new for MS researchers to look at how ER stress is linked in Rab32 increases in the MS brain.

The link of ER stress and neurodegeneration is not new.
The ER stress-associated cell death pathways have been recognized in the numerous pathophysiological conditions, such as diabetes, hypoxia, ischemia/reperfusion injury, and neurodegenerative disorders, including Alzheimer's disease, Parkinson's disease, and bipolar disorder.

Under various pathological conditions, the perturbation of any of the three physiological functions of the ER results in so-called ER stress and can lead to an accumulation of the newly synthesized unfolded and misfolded proteins in the ER. Among the stimuli that promote ER stress are ischemia, inflammation, and disorders that impair the ER’s ability to properly fold polypeptides or eliminate unfolded proteins ().

Thanks to the work of vascular researchers, we know a few things which can create ER stress.  I suggest reading this complete paper.  link
But to summarize:

ER Stress, Endothelial Dysfunction and unfolded protein response are caused by:
1. High levels of homocysteine
2. Disturbed blood flow and lack of good shear stress
3. High levels of bad cholesterol (LDL) and low levels of good cholesterol (HDL)
4. High levels of glucose
5. High blood pressure and obesity

All the stuff mentioned in the Endothelial Health Program.
There are things you can do today to improve health and reduce ER stress.

A final thought for blog readers---targeting one misfolded or rogue protein without considering the mechanism which leads to this perturbation may not be the most successful approach. This is my main concern, and why I wrote this post. We have learned this through years of Alzheimer's research and treatment targeting the beta amyloid protein, which still has no success in alleviating the disease process. In contrast, a multimodal lifestyle approach employed at UCLA led to Alzheimer's disease reversal. link

Big picture: why do cerebral hypoperfusion, cerebral endothelial cell aptosis, a breakdown of the blood brain barrier, ER stress and neurodegeneration occur? 

Continue to dig deeper, past the MS News headlines.
There is truth beneath all of the hyperbole.


Monday, March 20, 2017

Fast Mimicking Diet (FMD) for MS

In the name of research, and with a bit of curiosity,  I tried a fast.   I've recenly completed the ProLon Fast Mimicking Diet.    More details about the specifics later, but first, you may well be asking---why would someone who LOVES food (yes, a lot link) voluntarily go on a five day fast?   Believe me, I asked myself the same question.

Honestly, I wanted to check out the program before sharing more research with you all.  I really think this is an interesting approach for MS, as it potentially reduces inflammation, boosts cellular rejuvenation, and resets the immune system.  This program has had great success for patients with diabetes and cancer, as well.  It's beginnings were in anti-aging therapies, and clinical trials in many chronic conditions related to aging are ongoing.

Fasting is not something people with MS should do without a doctor's supervision.   I had to get approval from the ProLon nurse (over the phone) before starting the program---and I'm healthy.  People with MS will need even further approval from their doctors, which is a really good thing.  But it might be worth exploring.  You can take the research and links to your doctor and see if this might be right for you.   Jeff said he's interested after watching me last week, so we'll clear it with his doctor and do it together later this year.

Here's the science.  In 2016, a study at the University of Southern California researched fasting and multiple sclerosis, and found that caloric reduction with a fast mimicking diet (FMD) did all sorts of wonderful things for the body, which specifically helped those with MS.

The USC study in mice with EAE and humans with MS found that a fast mimicking diet (FMD) made the body produce more of the hormone corticosterone, which in turn killed off damaging and inflammatory immune cells, and led to a production of new, healthy stem cells.  This study also saw regeneration in myelin producing cells, and reduction of MS symptoms.  All amazing stuff!  Here's more on his study in layman's terms   link    Here is the complete paper, which I suggest reading, and sharing with your doctor if you're interested.    Cell Reports FMD in MS publication

It's potentially an affordable alternative treatment for MS --so get ready for pharma to try and take it down with their own "trials" ( link to "Pragmatic Trial" of fasting with Tysabri )  You know something is worthwhile when pharma gets involved in debunking.

The lead USC researcher, Dr. Valter Longo, also discovered that fasting does not necessitate complete avoidance of food, but a fasting state can be reached by restricting caloric intake in a specific manner.  Thus the "fast mimicking" part.   This is something which might be easier for most of us to accomplish, and this was a key point for me.  I could never do a liquid fast.  I simply get too light headed and tired from low blood sugar.  But I found this program to be much different, and very doable.

I'd had some nice back and forth e-mails with Dr. Longo when this research was first published last year.  We both share a love of music and medicine.  He was a young music student in Italy before coming to the states to study jazz guitar.  He became interested in the study of aging, and got his PhD in biochemistry at UCLA, then joined the USC Davis School of Gerontology.  He is also Director of the USC Longevity Institute.  His focus is on how caloric restriction and fasting kills damaging cells while inducing healthy stem cell production.    link to Dr. Longo's story

I had wondered if any of his FMD studies had looked at markers of inflammation related to endothelial improvements.  I had found prior research looking at this connection.  link  He replied that his group wasn't looking at that specific aspect. He felt that the benefit of FMD was more about reduction of damaging autoimmune cells and a rejuvination of stem cells. But I have a hunch the increase in cortisone is also helping strengthen endothelial cells and reduce cell permeability--as well as helping the microbiome.   The FMD has been shown to reduce C reactive protein in other studies, so there is a vascular connection. I hope more research will be done on these other aspects of the program.

Since I wanted to remain impartial in my analysis of Dr. Longo's FMD, I didn't ask him for a sample.  I purchased the $300 ProLon FMD for myself online.  (Still can't believe I shelled out big bucks to starve myself.)  I hoped for benefit.  I have some pain from a bit of osteoarthritis in two fingers and my neck, and lowering inflammation might help me.  Losing weight wasn't my primary objective, but I figured it would be a nice side effect.  I'm turning 55 this week,  and my vanity continues.   Jeff and I already follow the Endothelial Health Program.  We eat whole, organic foods, mostly plants and no processed food, no dairy or gluten, so I was already in the right dietary zone.  Just had to halve my daily caloric intake.  Gulp.

The things I liked about ProLon were that it is a plant based and gluten free diet, shipped in a box right to my front door.  It was very easy to follow.  Each day had a separate carton, which was clearly labled with nutritional information and instructions.  You can learn more about the specifics of this diet here:   https://prolonfmd.com   The reason it is a five day fast is because it takes that long for the body to reprogram and for cells to rejuvenate.  Dr. Longo recommends doing this fast every three to four months.  I think I could handle it a few times a year.

I believe it would be pretty easy to hack this program and do it on my own now.  I have all of the caloric and nutrient info.  But it's nice to have the supplements and energy drink and everything timed and packaged.  Makes it easier to follow,  and you're less likely to stray, when you think about how much you spent.   The food was surprisingly palatable.  I loved the kale crackers, and the instant soups were hearty and filling.  The breakfast bar was nutty and satisfying to chew.  Olives for snacks was fine with me.  And the herbal teas were nice.   I felt better knowing Dr. Longo is donating the proceeds to charity.  He's a good guy.   Anyone who studies jazz guitar and wants people healthier without drugs is OK in my book.   link

How did I feel after 5 days of eating under 800 calories?  It's odd, I wasn't really hungry, except for one day.  I was surprisingly energized, and not fatigued.   The hardest part of this program was giving up my usual three cups of caffeinated coffee a day.  Prolon allows only one caffeinated drink per day, and this left me with a nasty caffeine withdrawal headache after day 1. However,  I didn't feel sluggish without the coffee and I guess that must be from the cortisone coursing through my body.   I was really hungry on day 3, and wanted to quit, but curiosity kept me going.  That, and a bit of pride.

Jeff said he felt guilty eating in front of me.  But he got over that and ate just fine!  I also had to prepare a big dinner for some friends who happened to be in town on Day 2,  and that was pretty hard.   Standing over the stove, cooking and serving a delicious meal and then sitting and watching eveyone happily eating while I sipped herbal tea is not something I want to do again.

Now for the good stuff.  I slept really well, and am still having very vivid, lucid dreams.   I wake up ready to go, not groggy at all.   And my skin looks great!  It could be the fact I didn't had any alcohol, sugar or animal products for 5 days, but my eye bags are less noticeable and my complexion looks rosy.  And my arthritis pain is much, much better.  My knuckles are less stiff, and my neck has been feeling great.  I was able to keep active, out walking, running errands and doing my normal routine, without feeling faint. I didn't have any recording or performing work during this week, so I could take it relatively easy.  And I lost three pounds!  Not as much as many others report (average loss is 5 lbs.) but hey, I'll take it.

Final thoughts.  What we eat matters.  Our bodies are miraculous machines, and it makes sense that the manner in which we fuel ourselves has repercussions on our health.  By putting the body in a fasting state, we kick it into survival mode.  We were created to withstand periods with limited caloric intake, and our body knows how to utilize our stored sugars and fats reserves. Most of us in the industrialized western nations eat much more than we need, far too many processed foods,  too much animal protein and sugar,  and not enough plants.

But this isn't to cast blame for being sick!  No one gives themselves MS, cancer, osteoarthritis, or Alzheimer's.  We don't control our genetic predispositions, and we all will die eventually.   Here's Dr. Longo's TedX talk about how "if one disease doesn't get you, another one will!"   He shows that it is possible to live longer, healthier lives.  link   There are things in our control which we can do to feel better, function better, and maybe even heal,  including fasting. I believe the future will provide more understanding of our microbiome and brain, and how they are connected via the thousands of miles of lymph and blood vessels which keep our organs protected, nourished and cleansed.  And a lot of that depends on food.

Also, as it is the Lenten season, I couldn't help but feel more meaning to the fast.  Christians are taught to fast or give up something during Lent, to remind ourselves of Christ's forty days of fasting, praying and temptation in the desert before his eventual arrest and crucifixion.  This is practiced, not as an exercise in self-denial, but in order to draw closer and more reliant on God. And for that reminder, I am thankful.


Wednesday, March 15, 2017

Tony Traboulsee and the Lemtrada story

It is now quite obvious that Anthony Traboulsee meant what he said back in 2010. He does not believe the venous system has anything to do with Multiple Sclerosis, and that people with MS should not worry about their vascular health.  They simply need to take their drugs.

This is in sharp contrast to peer-reviewed research conducted in labs around the globe; redefining the connection of the brain to the vasculature.  link

Commenting on the failure of the UBC trial to prove any benefit in (under) treating stenotic veins, he gave patients the bright side.
“Fortunately, there are a range of drug treatments for MS that have been proven, through rigorous studies, to be safe and effective at slowing the disease progression.”  

Macleans Magazine journalist Anne Kingston questions why the UBC CCSVI trial released results before the study was actually completed.  Read her well-researched article here:  link

I think it's important to understand exactly why Tony needed to stop further exploration of the vascular connection to MS and state that the UBC study was the final word which debunked CCSVI research--- even though his study was not complete, and there are other placebo control CCSVI studies currently in Australia and Italy.  He wants this research over.  Tony's whole life, lab and career hinge on the maintenance of the EAE autoimmune model of MS, and the success of drugs.  Especially one monoclonal antibody which targets the protein CD52 found on t and be cells, called Lemtrada.

Tony has been working hard for the Sanofi Genzyme Company for several years, as a saleman for Lemtrada.  He is a paid researcher and spokeperson for Lemtrada.  He has been touting this wonder drug around the world.  Don't believe me?   Behold, the google results of Traboulsee + Lemtrada.

Genzyme Corp. paid out over 5 million dollars to US doctors from 2013-15 for promoting Lemtrada.  This information is not available for Canada--but I believe we can assume that payments were equally high.   link

Lemtrada is Dr. Traboulsee's "Top Pick" for his MS patients.  Here's a blogger sharing this news.
Today is my 3rd MRI. I have a new neurologist.....Dr. Traboulsee also gave me some new options to check out, including his top pick called Lemtrada.  Lemtrada sounds like an interesting choice, as it is administered one or twice a year.   link
Tony believes that Lemtrada is the future of MS treatment.    
But this isn't actually true.  Lemtrada can't the future, because it's the past.  It has a very well-documented research history since the mid 1900s, and has been used as an MS treatment since 1991, when it was called Campath.

Campath (alemtuzumab) was developed to treat B cell leukemia, but there were problems with that, so it was tried for immune suppression for organ transplants, and had a few too many side effects there, so it was tried in autoimmune diseases.   It never became the big money maker drug companies had hoped for.  It was first used as an off-label drug for multiple sclerosis in the UK.

The problem with using Lemtrada/Campath as an MS treatment was that it did not help people who were already progressive.  In fact, as researchers were dismayed to find out, people with progressive MS disease worsened on the drug.

“We realised that, although we had stopped disease activity in terms of new inflammatory brain lesions and had reduced the number of attacks that people were having, most of our patients were continuing to deteriorate.” The problems that the patients had when they started Campath-1H treatment were slowly progressing. This observation puzzled the researchers. If MS is an inflammatory autoimmune disease, why was Alemtuzumab treatment failing to help people in the progressive phase of the disease even though the treatment seemed to turn off inflammation?

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. This particular group of patients who showed continuing disease progression had the highest inflammatory load prior to commencing alemtuzumab therapy. This group of patients were followed up with MRI scanning many years later (14 years post treatment) and did not demonstrate any increase in lesion load but did demonstrate further cerebral atrophy [Coles et al. 2006]. This was reflected in their EDSS score, the median being 7.5 (range 4.5–9) at latest follow up [Hill-Cawthorne et al. 2012].

Campath 1H treatment was associated with a sustained and marked reduction in the volume of Gd enhancement, indicating suppression of active inflammation. Nevertheless, many patients developed increasing brain and spinal cord atrophy, T1 hypointensity, and disability. 

Disability in all but one of the 37 patients continued to worsen progressively despite alemtuzumab treatment, as previously reported.8 9 At the last recorded follow-up, a median of 14 years post-treatment, the median disability estimated in 35/37 patients was EDSS 7.5 (range 4.5e9). Relapses were uncommon but were not systematically captured.  link

So, as you can see from these studies, to claim that Lemtrada slows progression or reverses MS is simply (excuse me) bullshit.  What has changed?  Campath has been renamed and rebranded.  It's being given to a very specific population of people with MS.  Lemtrada is helpful for people with highly inflammatory, brand new MS, because it wipes out the immune system and halts inflammation.  As I've referred to this kind of immune ablation before--it's like "using a sledgehammer to swat a fly."   This early intervention is being touted as a "window of opportunity."

Treatment response to alemtuzumab is strongest as long as active inflammation is the predominant pathophysiological feature, and it is becoming less efficacious in neurodegeneration-dominated later stages of the disease. Thus, the optimal placement of alemtuzumab within treatment algorithms of MS is crucial. The impressive efficacy of alemtuzumab is counteracted by a less favorable safety profile. link

Tony knew how to get around that problem of MS progression.  He only enrolled young people and people with early RRMS in his Lemtrada trial.  And voila!  Success!  It's amazing what drugs can do when you get rid of those pesky older and progressive patients.  He saved them for the CCSVI trial, where the median age was 50, and most were progressive.

Now that he’s managed a trial of 80 patients on Lemtrada (alemtuzumab), Traboulsee believes the future of MS is very treatable. Traboulsee believes he’s part of a movement that’s 10 years ahead of the curve and thinks this treatment might be resetting the immune system in patients who receive it. -link

What a trend setter Tony is with his deadly drug from the 1900s!  It is because of Tony's work that Lemtrada became available in Canada in 2013.  Tony's trials at UBC paved the way.  Yet even with all of this hoopla in Canada, the FDA panel in the US was concerned about adverse effects and lack of evidence and decided not to approve Lemtrada.

They then voted almost unanimously that the sponsor had not provided sufficient evidence of a reduction in disability with alemtuzumab, but then subsequently decided that, assuming the efficacy results were as they appeared, safety results would not preclude approval. The panel also voted unanimously (with 2 abstentions) that if the drug were approved, it should not be indicated as a first-line agent in MS.

The FDA panel mentioned the fact that Lemtrada had only been tested in young patients, those with a new MS diagnosis, and that the adverse effects of this drug were too risky.  Like me, they read the prior research on Campath.  They did not think it was an appropriate first line treatment for those newly diagnosed.  And then, after pressure was put on the FDA by the National MS Society with some help from Genzyme,  in a surprise turn-around ruling, Lemtrada was accepted by the FDA with black box warnings.  Sadly, since 2013,  we have a better understanding of the long-lasting side effects of Lemtrada.

Like a severe B-cell mediated disease of enhancing demyelination, which was caused by Lemtrada, and is even worse than just MS. link

or death from cancer, ITP and thyroid disease and a slew of other problems that come from destroying immune cells....
Patients did have serious, even fatal, side effects while using Lemtrada, including viral infections and infusion reactions, and the drug may cause malignancies such as thyroid cancer, melanoma, and lymphoproliferative disorders. As a result, it is only available through a restricted distribution program, the Lemtrada REMS (Risk Evaluation and Mitigation Strategy), to ensure that patients prescribed Lemtrada are enrolled in the program and undergo periodic monitoring to detect potential health risks. 

Which makes sense, when you consider the Kipnis Lab's recent discovery of a new lymphocyte which protects the gut and the brain.  These type 2 lymphocytes are called "powerful defenders" and may be essential for the brain to heal after injury or an MS relapse.  We have no idea on how destroying them with Lemtrada may affect long term health.

Don't believe me?  Let's hear from some of Tony's patients--- from public reviews.

I've had R-R MS for 18 years. I've been symptom free for 5 years. My previous MS Specialist, Dr.Hoogie retired and the doctor he referred me to was on mat leave when it was time for my annual check-up so I went to see him. He's well reputed as a researcher and is head of the MS Clinic at UBC, so I thought I was in good hands. I found out he is not what I want in a Doctor. He pushed his drug study on me really hard. I went home and researched the drug he's studying and it has caused death due to massive organ failure in one patient the UK. I don't have severe enough MS to want to try that kind of drug. When I asked him questions, he didn't really answer them clearly. I went back to my GP and asked for another referral to another MS Specialist. I strongly believe he should not be a practicing Doctor - he does it to pressure and try to recruit more patients for his studies and because he has to. I'm sure he's a good clinician and researcher. If you have a severe case and want to try to get access to what will be expensive, and hard core drugs that are not yet available to the public, go see him. But I don't want to be a lab rat.
To begin, I was diagnosed with MS just over 18 years ago, a mere six months after graduating high school. Following a couple of weeks in the hospital, I was referred to the UBC MS Clinic and assigned to Traboulsee. He lied to me from the start, insisting there were no treatment options for the neuropathic pain and muscle spasms I suffered. Instead he claimed that there were only clinical trial studies and that he could do nothing more than sign me up to become a lab rat. Out of desperation, I enrolled on one clinical trial which saw me bed ridden from the side effects of that drig that was later proven to be useless for MS. When telling Traboulsee this during the trial, he ignored my severe reactions to the trial study drug and tried to convince me that I was actually doing better because of the experimental drug, though he should have been able to know that since the study was double-blinded. At one point I was able to procure a copy of my records from the clinic, only to find that Traboulsee had falsified many portions of my records, including one that indicated he had recommended various medications to me which I had refused. In reality, I had requested one type of medication for my MS symptoms which Traboulsee had refused me on the basis that he didn't like my attitude in not wanting to take part in further trial studies. Traboulsee should also set he watch as he is always an hour late for every appointment. He never answers any questions, is always reading the patient file, and ignore basic human rights.
I believe that the behaviour of this Doctor is unacceptable, he was rude, condescending and at times devoid of any compassion or empathy. Moreover, he has extremely poor communication skills. I believe he is quite brilliant in his research, however, he should not be dealing with patients on a one on one basis. The sad part is he truly sees nothing wrong with his behaviour and can be vindictive and arrogant if you question what he has said. By not listening to his patients and showing them compassion he is doing a disservice to those looking to him for help.
This doctor is horrible and a complete jerk. If you care about your health of that of a loved one you will seek medical expertise elsewhere. Nightmare treatment and responsible for the loss of my loved one. Only cares about research and treating patients as guinea pigs. Arrogant, condescending and doesn't care about human life or treatment - he only cares about MRIs and research not the person. Unsympathetic and a complete jackass of a person.
Horrible. Saw him in summer, I have been so upset about his lack of care his and condescending tone that I am only now able to write this. Cares about money not about treating patients. Avoid this "doctor". He has to look things up on Google. Smug, wants you to join a clinical trial, otherwise dismisses you.
You can read more here:

So, where does this leave us?  
I have no idea where it leaves you, but I hate having to write about this man.  I hate his arrogance, his lack of compassion, his lack of morals, ethics, and his tunnel vision.   This is why I said I was walking away earlier this year...because I abhor these people and what they do to others, and it's upsetting. 

But I keep writing and staying involved, because I love other people more.  I was recently told by a commentor on this blog that I have no right to say anything about MS, because I do not have it.  She said that I do not understand how it feels to have an incurable disease.  And I agree with her.  I have no idea.  But I don't think that means I can't discuss new research, or walk alongside people with MS and encourage them.   Nor do I think I need to say that there is no vascular connection to the MS disease process, when more and more peer-reviewed science continues to show this reality.

I've been going thru test results with a girlfriend this week.  Her husband was just diagnosed with MS.  She's asking for more blood panels, allergy tests, consulting with a vascular doctor and neurologist, and working with her GP.  I'm going through all the various diet and lifestyle programs with her as her family comes to grips with this diagnosis.  This week I also had a delicious seafood dinner overlooking the Pacific with another girlfriend who has MS, and she is thriving and healthy and amazing. I answer e-mails and phone calls, and try to encourage others.  Because I live with proof of the importance of dealing with vascular health.  I tell everyone, I AM NOT A DOCTOR.  But I can read, and I can write.  And I can encourage.

Jeff reminds me every single day that people with MS have more control than the Traboulsees of the world tell them.  That the vascular connection is real.  It may not be the complete picture, but it is part of the answer.

I hope there is an investigation into conflicts of interest with Dr. Traboulsee and the UBC Clinic.
If you have MS, and you love Lemtrada, and it's changed your life, no need to flame me.  If you love Dr. Traboulsee. good for you!   I'm happy for you!  Honest!  Be well, and continue in good health.   My concern is that the UBC clinic is not looking at the big picture in MS treatments and manipulating research.  And we all want the complete picture, right?

Just doing some "debunking" of my own.


Thursday, March 2, 2017

UBC CCSVI Clinical Trial

I want to say upfront, I am not hopeful regarding the results of the University of British Columbia (UBC) CCSVI trial.  The preliminary results may be most dramatically revealed at the Society of Interventional Radiologist conference on March 8th in the Marquis Ballroom of the Marriot in Washington DC.  I have a pretty strong hunch they will be negative and will not show any benefit in venoplasty for CCSVI.  

I wish I could be more upbeat and say that this trial will give CCSVI venoplasty intervention a fair shot, but I've been concerned about bias and an ill-conceived trial since the beginning.  Anne Kingston wrote the best article on this topic back in 2012--
"Finally, CCSVI Clinical Trials.  So Why is Everyone So Pissed Off?"  link

Here is what I thought about Traboulsee's 2014 CCSVI imaging study- Scientific Misconduct?

Fast forward to 2017.  Even though the UBC CCSVI study is still on-going, preliminary results have been fast-tracked for a release at a vascular conference in the US.  This research was submitted to the SIR conference after the deadline for submissions in September. This is from the SIR website, where the investigators are allowed to explain why their presentation deserves consideration.  

Please provide a justification below for this abstract's eligibility to be considered for late-breaking submission.

This will be the first presentation of a randomized, double blind clinical trial of jugular and azygos venoplasty in MS, including patient reported, clinical, and MRI outcomes. The presentation will include all data from the first 48 weeks in all patients after their first procedure only, comparing sham to venoplasty.

This is a multicenter trial with an independent trial coordinator. The database was locked December 23, 2016 and the authors were (and still are) blinded to the outcome. It is a trial of sufficient magnitude and scientific rigor that it deserves presentation at a major society meeting
link  (search "Traboulsee" to see the submission)

Get that? The trial coordinators and authors claim to still be blinded to results. Seems odd, right? Why submit to SIR, a "major society meeting" without knowing the results? And why now? Why not wait until all the data has been collected and collated?

I believe the reason the UBC study was submitted to SIR, before completion and after the SIR deadline, is because Dr. Zamboni announced, at the Veith Conference in November 2016, that his Brave Dreams Trial had been completed and results would be published in mid-2017.

The UBC team submitted their abstract after Dr. Zamboni's announcement, as I believe they wanted to get out in front of the Brave Dreams published study results and put the final "nail in the coffin," ring the last "death knell", be the "last word" (or fill in any of the other hyperbolic titles for anti-CCSVI publications over the last five years.) I honestly think they want to kill this research and be done with it.

I have a hunch we will be reading a lot of negative CCSVI stories in the media in the next few days. Here's a first example from Vox:  
This is why you shouldn't believe that exciting new medical study

Joan, wait... (you say to me) this UBC study is gold-standard research! You sound like a conspiracy theorist. Science is science. Blinding and placebo controlled trials are what you have been asking for! This is exactly what the vascular connection to MS needs---independent study. That doesn't mean you get the results you want! Also, didn't you say you're done with all of this???

Yes, you're absolutely right.  And I am done, but felt it was important to go on record.  Here's my problem. This study does not look at blood flow before and after treatment.  They did not measure venous pressure--so how could they possibly know if stenosis had been treated?

The results of this study are not all objective.  Dr. Zamboni has stated that the Brave Dreams trial results are objective.  Objective results are numbers and stats and things that can be measured and tallied using unbiased machines.  Venous pressure is an objective measure.  Not questionaires from subjective humans compiled by even more subjective humans. 
There was no retreatment for restenosis in the UBC trial (a problem for 50% of patients) or suggested aftercare and lifestyle intervention.  Jeff had to be retreated at Stanford, as he developed intimal hyperplasia.  He also had aftercare treatment and drastically changed his lifestyle, diet and exercise program.  
Angioplasty for carotid artery stenosis has had placebo control trials, and you know what metric they used to measure success?  Size of stenosis and blood flow.  That's it.  Not a questionaire asking "how are you feeling?"  The researchers measured blood flow before and after and at monthly intervals up to a year.  They used ultrasound to see how carotid stenosis looked, if there was restenosis it was re-treated.   And most importantly, after treatment,  they put the study participants on an aftercare program, making sure they had blood thinning treatment and that they exercised and ate better.  Trial participants quit smoking or lost weight, if warranted.  Because without aftercare and lifestyle changes, restenosis can be immediate, and all gains from angioplasty are lost.  IRs know this.   link

Take my husband's reversal of gray matter atrophy on MRI.  No one can call that placebo!  He doesn't just feel better or have less brain fog.  His brain shows objective healing on MRI.   He has had no new lesions, and his old ones have shrunk. Another objective measurement from Jeff's venoplasty treatment was blood flow.  His jugular vein blood volume doubled after being stented.  Other research has shown that CSF flow increased after treatment for CCSVI.  link  These are all benefits which can be measured using medical equipment, and are not part of the UBC data.

I fear the UBC researchers are going to say any subjective benefit after treatment is placebo. That there are no objective benefits in those treated, because they have not measured blood flow, CSF flow and gray matter atrophy. They certainly didn't retreat restenosis. And Charcot will be laughing, once again, at how easily he is able to control the mind of the hysteric, labile, desperate MS patient. link

To recap my concerns:
1. Not objective results.  Too easy to claim "placebo"  No measurement of blood flow before/after
2. No treatment for restenosis (as in angioplasty trials)
3. No aftercare or lifestyle changes required (as in angioplasty trials)
4. Timing of release is suspicious
5. A history of bias and nay saying against CCSVI from trial lead investigator
Don't be discouraged. No matter what the UBC researchers claim, or how loudly they say it, it isn't over. Italy and Australia still have their trials. And we have other reseachers looking at the vascular connection. This research is not going away. Not with the ISNVD, not with The Gladstone Lab, The Kipnis Lab, the Nedergaard Lab and others--all committed to getting to the bottom of the vascular connection to diseases of neurodegeneration.

And I may be wrong!! Let's hope for that! Please let me be wrong!!!!
In the meantime, live your best, vascularly healthy life.
(Because I'm right about that part :-) )


Monday, February 6, 2017

Gladstone Labs and Nrf2 protein

Gladstone Labs is at it again!   Finding a single protein which limits neuronal death.  How much do we love this innovative lab!  Thanks to Dr. Terry Wahls for tweeting about this paper today, I had missed it.

"I am very enthusiastic about this strategy for treating neurodegenerative diseases," said Finkbeiner, a senior investigator at Gladstone and senior author on the paper. "We've tested Nrf2 in models of Huntington's disease, Parkinson's disease, and ALS, and it is the most protective thing we've ever found. Based on the magnitude and the breadth of the effect, we really want to understand Nrf2 and its role in protein regulation better."

In this new research, Gladstone Labs have shown how the protein Nrf2 serves as a housekeeper for our brains, by cleaning up damaging proteins.  Nrf2 actually protects neurons from cellular death by regulating other proteins.  

For those new to this super protein, the Nrf2 signaling pathway (nuclear factor erythroid 2-related factor) is how your body defends and protects itself against damaging proteins, toxins, oxidative stress and inflammation.   I have blogged about it before--since Nrf2 had been shown to reduce oxidative stress in MS.  This blog post is from 2012  link

There are actually ways to turn on our body's Nrf2 protein defenses, by using Nrf2 activators. 
Nrf2 activators are PRO-oxidant---meaning they introduce an oxidizer, so that your body create its own antioxidant protection.  Kind of like "fighting fire with fire."  This compound activates the enzymes in your own cells to fight oxidative stress in your body.  These enzymes then protect your oligodendrocytes (myelin forming cells), and keep them from dying during an attack of oxidative stress.   And now we know that Nrf2 protects neurons from harmful proteins.   A win/win for those with MS.

Three of the plants I recommend in the Endothelial Health Program as anti-oxidants, which also have published research as Nrf2 activators-

Curcumin--the golden powder that gives Indian curry its color, is extracted from the tumeric plant.
link  link  link
Silymarin--or milk thistle, known to protect liver cells and produce glutathione
link  link  link
and EGCG, or green tea. Known for its antioxidizing and metal chelating effects.
link  link   link  link

More ways to increase Nrf2:

Dr. Bernhard Juurlink has spoken and published on the power of broccoli sprouts as Nrf2 activators.  Here is information on his book on the health benefits of broccoli--

Paul Thornalley, from the University of Warwick (United Kingdom), and colleagues have observed that sulforaphane in broccoli, and quercetin in onions, are capable of increasing Nrf2 movement. Observing a continual movement cycle of Nrf2, which sees the protein oscillate in and out of the cell nucleus once every 129 minutes, the team found that sulforaphane and  quercetin sped the cycle up to 80 minutes.  Writing that: “We discovered cytoplasmic refresh rate of Nrf2 is important in maintaining and regulating the transcriptional response and links stress challenge to increased cytoplasmic surveillance,” the study authors aim to develop new food supplements – superfoods that stimulate Nrf2 activity.

The supplement Protandim is a scientifically recognized Nrf2 activator, as well--although Jeff has not used it, so I don't have any experience with it, but I know many other pwMS do.  link

Always talk to your own doctors before adding any supplements to your program, as there may be contraindications for you.  And, it bears repeating...I am NOT a doctor!

Hope you find this research encouraging!   I know I do.
Go, Gladstone Labs!!  
Thanks to Dr. Finkbeiner  (left) and Dr. Skibinski (right)