Monday, April 27, 2015

Biotin for Progressive MS

UPDATE:  December 2017---
Medday, the company developing high dose biotin for progressive MS, has told the European Medicines Agency that it wishes to withdraw its licence application for the treatment of progressive multiple sclerosis.The European Medicines Agency (EMA) has been examining data on high dose biotin (MD1003, Qizenday) since the application was accepted in September 2016. At a meeting last week, the EMA's Committee for Medicinal Products for Human Use (CHMP) concluded that the clinical data from two trials that enrolled 253 patients was not sufficient(link is external) to assess the effectiveness or the safety of biotin.  link
Recent research and press releases on the use of super-high dosages of biotin (300 mg a day, also known as MD1003) for progressive MS are all over the internet, after moderate improvements in MS symptoms were announced at the annual American Academy of Neurology meeting last week.  MS boards and patient blogs describe how people are considering trying this therapy on their own, by securing high dosages of biotin from compounding pharmacies or health food stores.   But strangely absent from this online discussion is the method of action implied for biotin, which is targeting the results of a decrease in cerebral blood flow, as well as the actual results of pilot studies.  I think it's vitally important to look behind the MS research headlines, and consider the science.  Especially before investing time, money and hope in a new product.

 I simply do not think it's wise to take mega-doses of biotin.  Although I do think it's important to deal with slowed cerebral blood flow in the MS brain.  Please take 5 minutes to read this note, and I believe you might feel the same way.

 I first wrote about biotin at the beginning of April, on the CCSVI in MS Facebook page, after one of our administrators posted a link to an abstract.
High doses of biotin in chronic progressive multiple sclerosis: A pilot study.

 Here's what I posted below the link from Sandro:
"Biotin is also known as vitamin B7. It is found in peanuts, leafy green veggies and egg yolks. It is naturally produced by healthy intestinal bacteria. Smoking and drinking can deplete it. Thanks to Sandro for this link.  
All of these ideas can be found in the Endothelial Health Program, which recommends probiotics, B vitamins, dietary increases in leafy veggies, and smoking cessation. It's not a pill, it's a lifestyle. Joan"

 At that time, readers were asking for more information, so I dug a bit deeper and found the patent application for this new "drug."
http://www.google.com/patents/WO2014016003A1?cl=en

 "A pharma company is patenting this high dosage of biotin, to market this vitamin as a drug. Here's the patent. I suggest you read it, it is enlightening. They are also patenting this "drug" for ischemic stroke damage and hypoperfusion. Drug companies understand the vascular connection."
In fact, if you read the entire patent application, the method of action for high dosages of biotin in multiple sclerosis is explained--biotin is targeting the damage from ischemia.  This vitamin addresses the results of  decreased cerebral blood flow, which creates ischemia, oxidative stress and reduced ATP production in the brain's cells.  From the patent application:

  The major responsibility for the evolution of the ischemic penumbra is the status of local cerebral blood flow. It is assumed that a decrease in cerebral blood flow yields reduced ATP production and failure of Na+/K+ pumps, increasing extracellular glutamate and activating glutamate- mediated channels, ending in an increase of intracellular calcium that is deleterious for the cell. It is widely accepted that the ischemic penumbra is a target for neurorepair and neuroprotective therapies.

 Once again, we see quite clearly that drug companies understand the fact that the MS brain is hypoperfused and suffering from ischemia.  They know there is a vascular connection in MS, and that the damage to the MS brain is very similar to ischemic stroke.  

 The results of the biotin study were somewhat compelling, but I was surprised at how many people were ready to take high doses of a vitamin, without understanding the mechanism of action, or the fact that this treatment was created for a very specific type of MS--mainly optic neuropathy.  In fact, the major improvements in patients in the trial were not in motor abilities, but in vision.  The changes is EDSS were incredibly minor. All of this information is very specifically addressed in the patent application.

 I've often said that it is much easier to placebo control one compound, one drug, one treatment modality at a time, rather than an entire lifestyle. Because of this fact, drug companies are able to test high dosages of biotin in the gold standard method, against placebo,  and publish results.  But this does not mean that the best method of addressing the damage of a hypoperfused brain is high dosages of biotin.

 There are side effects noted with high dosages of biotin, and serious interactions with other drugs.

 Interactions. Biotin negatively interacts with anti-seizure medications and medications that help lower cholesterol, causing these medications to work less effectively. While biotin is helpful in regulating your metabolism and blood sugar levels, it can have a distinct effect on the overall blood glucose level in your body. If you are taking medications like cholesterol medication or anticonvulsants or treating a condition like diabetes, taking biotin can have an impact on your symptoms.
http://www.md-health.com/Biotin-Side-Effects.html

Best results are found in a complete lifestyle approach, with cardiovascular exercise, physical therapy, whole food nutrition full of leafy greens and phytonutrients from plants, stress reduction, probiotics,  UV ray therapy, vitamin D supplementation, vitamin B supplementation, smoking cessation, hydration, adequate sleep,  and addressing venous malformations which may be impacting cerebral blood flow.

 There is no one miracle pill or supplement or drug which can replicate the results of a complete lifestyle.

Here's the complete program I created for Jeff, which takes all of this into account.  It was created to deal with oxidative stress, hypoperfusion and energy depletion in the brain.
http://ccsvi.org/index.php/helping-myself/endothelial-health

 The Endothelial Health Program was created to increase cerebral blood flow, via healthier blood vessels and cardiovascular function.  All of the steps are proven, scientifically, to increase cerebral blood flow and oxygenation of the brain.  It is preventative and reparative medicine.  And it works.  Jeff's going strong, now 8 years past his MS diagnosis, with no MS progression and a reversal of brain atrophy on MRI.  He's still jogging and working full days. Always consult with your own physician before beginning a new lifestyle program.  Jeff works with our GP, to make sure all of his blood numbers are good, and that he is doing well on his program.

 Be well, be hopeful, but understand that there is not one pill or compound or vitamin that will ever replace a multi-modal, systems approach to healing.

 Joan





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Wednesday, April 22, 2015

Independent review of new MS Drugs--Must Read

Prescrire ("to prescribe" in French) is a French medical journal, which uses evidence based science to make recommendations on drugs.  It is written by health care professionals for health care professionals,  but it is unique in that it does not accept any pharmaceutical monies for advertising or for payment to reviewers.  This journal makes money by having 33,500 subscribers---medical professionals who turn to this journal for unbiased information. This is a completely independent journal---they have signed a "Non, Merci" (no, thank you) charter to maintain no conflicts of interest.  
http://english.prescrire.org/en/82/173/0/0/About.aspx

Prescrire’s subject matter mainly consists of critical reviews of medicines and other treatment options. Prescrire’s editorial staff is made up of healthcare professionals, most of whom are in active practice. Editors are specially trained and are free from any ties to pharmaceutical or other companies doing business in the healthcare arena. Prescrire’s reviews therefore help healthcare professionals to prescribe for their patients in an informed and fully independent manner.

Prescrire is also completely independent of all national and supernational institutions that determine or implement healthcare policy. Prescrire is therefore free to make recommendations in matters of ethics, public health and national and international healthcare policy.
Prescrire is written and edited by and for healthcare professionals. You could say that it’s just what the doctor ordered.
http://english.prescrire.org/en/82/169/0/322/About.aspx


And Prescrire's March issue has some startling information on MS drugs.  The reviewers names are not published (to keep them safe?) but they stand behind their recommendations.  Each article submitted has been reviewed by 20-40 other peer-reviewers.   And what they say is that when looking at all of the data we now have, these new drugs are too dangerous, with too many side effects and known and unknown risks.  That people with MS are much better off using the first line meds (interferon and copaxone), because these new, more powerful drugs have had biased trials, and have not proven any long term benefit.
1.  Tysabri and MS.  With longer follow-up:  even more toxic than suspected.
http://www.ncbi.nlm.nih.gov/pubmed/25897454
Post-marketing data confirm the adverse effects identified in clinical trials, including serious and life-threatening opportunistic infections, particularly progressive multifocal leukoencephalopathy in about two per thousand treated patients (an incidence twice as high as initially estimated), and potentially severe hypersensitivity reactions. An increased risk of cancer in the long term cannot be ruled out. Post-marketing data also show that natalizumab can cause severe liver damage. In addition, natalizumab withdrawal because of progressive multifocal leukoencephalopathy almost always triggers an immune reconsti- tution syndrome that can lead to neurological complications or even death. In practice, regardless of the severity of multiple sclerosis, it does not seem reasonable to expose patients to the many serious adverse effects of natalizumab for such an uncertain benefit.

2. Lemtrada and MS.  Biased evaluations, evidence of serious risks
Clinical evaluation in multiple sclerosis is based on three unblinded trials comparing alemtuzumab with interferon beta-1a. These trials were all biased in favour of alemtuzumab and thus fail to establish the potential value of this immunosuppressant. Overall, adverse effects, including the most severe, were more frequent with alemtuzumab than with interferon beta-1a. The adverse effects of alemtuzumab reported in these trials had already been observed in cancer patients. They included potentially severe reactions to the infusion, as well as a risk of infections and cancer due to profound and prolonged immunosuppression. At the dosage authorised in multiple sclerosis, autoimmune disorders such as thyroid disorders and immune thrombocytopenic purpura are particularly frequent and serious. In practice, patients with multiple sclerosis already have difficulty coping with the troublesome consequences of their underlying disease. They should not be subjected to the serious adverse effects of alemtuzumab, especially given the absence of any proven benefit.

3. Aubagio and MS.  just a metabolite of leflunomide.
Clinical evaluation of teriflunomide is based on a comparative trial versus interferon beta-1a in 324 patients and on two placebo-controlled trials in a total of about 2300 patients lasting 1 to 2 years. In these trials, oral teriflunomide at a dose of 14 mg per day led to a statistically significant decrease in the average annual number of relapses compared to placebo, but teriflunomide may be less effective than interferon beta. No impact on the progression of disability has been shown during less than 2 years of follow-up. The burdensome adverse effect profile of teriflunomide is similar to that of leflunomide and includes hepatotoxicity, infections, leukopenia, arterial hypertension, peripheral neuropathy and alopecia. The long half-life of teriflunomide (about 19 days) complicates the management of its adverse effects and multiple drug interactions, and has important implications for patients wishing to have children. Teriflunomide is teratogenic in animals and should not be used by pregnant women. Fetal toxicity via semen cannot be ruled out. In practice, the adverse effects of teriflunomide in multiple sclerosis are disproportionate to its efficacy. It is better to choose interferon beta, despite its limitations.

Their April issue includes a paper called "Tecfidera and MS: Too many Long-term Unknowns

I'm thankful that the researchers of Prescrire are speaking out and publishing their findings.   But I wonder how many neurologists will heed their warnings and inform their patients?  While the MS drug machine continues to crank along, now making 20 billion dollars a year in profits, people with MS are rarely given the facts.  These new drugs are exceedingly dangerous, and they do not prevent disease progression. 

Please spread the word in your own community and help others understand the risks of these drugs are known, while the benefits remain unproven. 

Take care of yourselves and be well,
Joan






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Thursday, April 16, 2015

Glial Cells, "Glymphatics" and the Nedergaard Lab

Jeff and I are spending the week at our alma mater, the Eastman School of Music, where we've been in residence and working with the wonderful students. On Sunday, Jeff is conducting a concert of his film music.  


While we're here, I wanted to visit the world-renowned laboratory of Dr. Maiken Nedergaard at the University of Rochester.  Suzanne Stover, Director of Development at Eastman, contacted her for me.  Dr. Nedergaard graciously invited us over for lunch, a tour and round table discussion on her research.  

Many of you may have read the Nedergaard Lab's ground breaking publications on the "glymphatic system" and the waste clearing work which is accomplished while we sleep.  The glial cells are the most abundant cells in the human brain, and they include oligodendrocytes and astrocytes. They surround neurons, yet do not carry any electrical impulses.  Glial cells had been considered supporting players in brain health, but thanks to Dr. Nedergaard's research, we now know how important these cells are in removing waste from the brain.

Dr. Nedergaard's lab continues to receive much attention for the discovery of the cleansing process of the brain, and the importance of these overlooked glial cells.

This 'peri-vascular' route for CSF-ISF exchange constitutes a complete anatomical pathway, which we dubbed the glymphatic system due to its dependence on glial cells performing a 'lymphatic' cleansing of the brain interstitial fluid. Further characterization of the involvement of the glymphatic system in a number of neurological diseases and neurodegenerative disorders is underway. 

And in 2013,  research on "Sleep Drives Metabolic Clearance from the Adult Brain" was published in Science.  http://www.sciencemag.org/content/342/6156/373

A good night’s rest may literally clear the mind. Using mice, researchers showed for the first time that the space between brain cells may increase during sleep, allowing the brain to flush out toxins that build up during waking hours. These results suggest a new role for sleep in health and disease. The study was funded by the National Institute of Neurological Disorders and Stroke (NINDS), part of the NIH.“Sleep changes the cellular structure of the brain. It appears to be a completely different state,” said Maiken Nedergaard, M.D., D.M.Sc., co-director of the Center for Translational Neuromedicine at the University of Rochester Medical Center in New York, and a leader of the study.Their results, published in Science, show that during sleep a plumbing system called the glymphatic system may open, letting fluid flow rapidly through the brain. Dr. Nedergaard’s lab recently discovered the glymphatic system helps control the flow of cerebrospinal fluid (CSF), a clear liquid surrounding the brain and spinal cord. http://www.nih.gov/news/health/oct2013/ninds-17.htm

This paper was awarded the 2014 American Association for the Advancement of Science (AAAS) Newcomb Cleveland Prize.  This discovery is changing the way researchers are thinking about clearance of the brain's waste products and how sleep, or a lack of sleep, may be compounding issues in neurological disease. 
http://www.aaas.org/news/paper-sleeps-restorative-effects-wins-2014-aaas-newcomb-cleveland-prize

We were able to tour her vast and well-funded research facilities and speak to students and staff researchers there, who are working on a myriad of murine models and brain imaging experiments.  Dr. Nedergaard and two of her research team put together a wonderful powerpoint presentation of their new work for me and I had the opportunity to speak with them about how their discoveries might impact Multiple Sclerosis research.

The glymphatic system relies on timely transport of waste products alongside the venous system, and the lesions we see specific to MS happen to run along this very same clearance system to exit,  or the "paravenous" spaces.   There appears to be a connection between the demyelinating patterns of MS and the glymphatic system.  And any slow down in venous flow when the body is supine, as we see in CCSVI, would certainly be impacting the body's ability to cleanse the brain during sleep, as these metabolites and toxins are eventually swept out into the venous blood.

This research is essential in understanding MS disease etiology!  I was so excited to hear Dr. Nedergaard present her proposal to continue this research into MS and the glymphatic system.  She was quite energized to see the connections, and is making a proposal for more research specific to MS, and thanked me for bringing in the vascular research of MS to her attention.  I hope to aid her lab in securing funding for this very important work, and will be asking for funding ideas and assistance once her research proposal has been formalized.  Establishing the basic science and foundation necessary to understand how brain diseases develop will only aid progress.  And of course, I introduced her to the International Society of Neurovascular Disease!  www.isnvd.org

Dr. Nedegarrd's husband, Dr. Steven Goldman,  has his own research lab down the hall at the University of Rochester, where he has been looking at neural regeneration in the human brain; focusing on neural stem cells and proginator cells.   His research brilliantly intersects with his wife's;  as he is honing in on how the glial cells, these worker cells in our glymphatic system, might be a viable stem cell treatment for demylinating diseases like MS. 

The diseases of myelin are among the most prevalent and disabling conditions in neurology. These diseases include both the vascular and inflammatory demyelinating disorders of adulthood, as well as the childhood leukodystrophies and cerebral palsy. These fundamentally glial disorders may be amenable to treatment by glial progenitor cells (GPCs), which give rise to astroglia and myelin-producing oligodendrocytes. Given the development of new methods for generating and isolating human GPCs, the myelin disorders may now be compelling targets for cell-based therapy. In addition, the efficient engraftment and expansion of human GPCs in murine hosts has led to the development of human glial chimeric mouse brains, which provides new opportunities for studying the species-specific roles of human glia in cognition, as well as in disease pathogenesis.

As Dr. Nedergaard said to me, before stem cell applications will be truly viable for MS, we need to calm down the inflammation in the brain. Implanted glial progenitor cells will not thrive in an inflamed brain with a faulty glymphatic system, or a hypoperfused brain with low oxygenation.

For instance, the chronically ischemic brain tissue of diabetics with small vessel disease may require aggressive treatment of the underlying vascular insufficiency before any cell-replacement strategy may be considered. Similarly, the inflammatory disease environments of MS and many of the leukodystrophies present their own challenges, which need to be overcome before cell-based remyelination can succeed .
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3548656/


However, a brain which has a working glymphatic system, a working venous system, and a calming of inflammation might be able to be remyelinated with stem cells. This may well be the future of treatment for multiple sclerosis, and I was honored and thrilled to speak to Dr. Nedergaard about these possibilities.

I am so thankful to Dr. Nedergaard, for what she has already accomplished, and what her research will accomplish in the future. The best and brightest scientists I have had the honor of meeting have a similar openess and curiosity. They are gracious enough to speak to simple laypeople, and they also listen. If I were a young scientist, I would look into joining her team. This is from the Nedergaard Lab website:
If you have an inquisitive mind, and if you are passionate about science, than we have a place for you in the Nedergaard Lab. We are constantly looking for talented and motivated scientists to join our team. We have opportunities for any level of education – enthusiasm and curiosity are the only pre-requisites.
Enthusiasm and curiosity.  Open-mindedness--which is not adherence to a credo based on dogma-- but a willingness to investigate new ideas, no matter their source.  This is what a scientist is and does.  This is how we learn and advance.
Thanks, Dr. Nedergaard!!   
Joan









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Friday, April 10, 2015

Endothelial cell dysfunction

New research from the University of San Diego is looking at something all diseases of neurodegeneration share, a breakdown of the endothelial lining of the blood brain barrier.  This includes stroke, ALS, MS, and traumatic brain injury.  In each of these diseases, the endothelium is not working properly.
http://www.sciencedaily.com/releases/2015/03/150330173827.htm

To protect the brain from harm, endothelial cells lining the blood vessels around the brain form a barrier that lets only very specific molecules move from the blood to the brain. In people with certain diseases or brain injuries, the barrier doesn't work properly and can allow dangerous molecules or pathogens into the brain.
Using an animal model, researchers are in the process of identifying the genes behind this disruption of the endothelial cells, and they are finding a common pathway.
"Even though the diseases we looked at all have different triggers, we see very similar genes changing in all the different diseases within the brain endothelial cells," said Daneman. "The fact that we found a common pathway means we could potentially find a single therapeutic target that could stop these different neurological diseases from occurring or progressing."

This is a promising area of research.  Finding ways to strengthen endothelial cells and maintain their integrity would help millions of people.  The endothelium exists not only in the brain's blood vessels, but extends throughout the body.  These vascular cells are found outside the blood brain barrier.  Endothelial cells (ECs) line all 60,000 miles of our blood vessels.   In the vessels which protect the blood brain barrier, these endothelial cells are specialized.

Vessels of the BBB are composed of specialized endothelial cells that lack fenestration (pores that allow rapid exchange of molecules between vessels and tissue), have few pinocytic vesicles to minimize uptake of extracellular substances, and have extensive tight junctions that severely restrict cell permeability.

When I first posited that Multiple Sclerosis was a disease of endothelial dysfunction, similar to the situation seen in cardiovascular disease, I contacted a premiere endothelial cell scientist at Stanford University and sent him my summary of the research, current to 2007.   His comment to me was that not many neurologists were interested in looking at the disease from the vascular angle, as they were already convinced MS was a purely autoimmune disease.

Much has changed in seven years.  The research continues to come in.  

We now know that people with MS show signs of endothelial dysfunction and increased vascular permeability in their blood levels, with raised levels of fibrin, ET-1, inflammation and hypercoagulation.  People with MS have endothelial cell dysfunction.

Can endothelial cell dysfunction be reversed?  Cardiovascular research says yes.

Cardiovascular research also says that endothelial cell dysfunction is systemic.
There is a new specialty of researchers looking at this---called neurocardiologists, who are finding connections between heart disease and cerebrovascular disease.

While the understanding of the blood brain barrier endothelial cells continues, changing the things we can change in our own lives, today, to reverse endothelial cell dysfunction, can make a difference.

The heart and brain are connected, and endothelial cells matter--

Joan


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Wednesday, April 8, 2015

An Apology Letter to Dr. Roy Swank from the National MS Society

Dear Dr. Roy Swank,

 We would like to apologize.  Remember how we denigrated your cardiovascular health program for people with MS because it wasn't placebo controlled?   We laughed at you for implying that MS might be a vascular disease?   You had the audacity to suggest that people with Multiple Sclerosis would live longer, healthier lives by limiting saturated and trans fats, eating more fruits and vegetables, removing processed foods and exercising, and you had published research to back up your claims.

We assured everyone that you were spinning hope, not science.  We told people with MS to ignore your research.  Since we knew MS was a purely an autoimmune disease,  addressing cardiovascular health would make NO DIFFERENCE in disease progression.  How would heart and blood vessel health change an autoimmune disease???  C'mon!  You have to admit, it even now, it seems too simple.  

 Yes, you published 170 scientific papers from 1934-2003,  LINK   But food and exercise helping MS disease progression?  Too easy.  It was placebo effect, obviously.

 Here's what we said to the NY Times about programs like Dr. Swank's "diet and whatever" in 2008.  We called it placebo. 

 Patricia O’Looney, vice president for biomedical research at the Multiple Sclerosis Society, said in an interview: “There’s a strong placebo effect in MS. With any change a person makes — in diet or whatever — they’re likely to feel better because they’re taking some action. Eating less saturated fat and more fish oil is good for all of us. But we’d never suggest changing one’s diet in place of taking a therapy approved by the FDA.
“Thus far, no researcher has been interested in taking this (nutrition for MS) on,” Dr. Kalb said. “The medications seemed to show more promise.”
link

We have recommended expensive FDA approved chemotherapies and those promising immune ablating and modulating drugs, in the hopes of wiping out all the nasty, aberrent immune cells. We used double blind placebo controlled gold-standard science--not as easy to do for your "diet." 

 Here's a news story from 1989, where we scientists discuss how our chemotherapies are going to conquer MS.  We compare our science to your quaint lifestyle program.  We look like the future.  You look like a friendly, small town doctor.  We are really taking dramatic risks,  and we chuckle at your program for MS.  Of course, this particular chemo treatment failed in future trials,  and left the participants in worse shape, with cancer or heart disease,  but hindsight is 20/20, right?
link to video

 Well, gosh.  All these years later, it appears we might have been wrong and you were on to something!

 Turns out nutrition, exercise and cardiovascularly healthful pursuits can make a difference in quality of life, and slow disease progression in MS, without the side effects.  And your peer-reviewed and published research was actually right.  Because even more research is being published on the connection, and your papers are being cited.  Obesity in linked to faster MS progression, processed and highly fatty foods are linked to faster MS progression, and nutritional and lifestyle strategies are making a difference.  People with MS show plasmic differences, related to endothelial dysfunction.  Environmental factors like nutrition and exercise really affect disease progression.  Cardiovascular exercise even reversed brain atrophy in progressive MS...

 Huh.  Who would have thought?


We won't give you any credit, mention your name and research, or make any public apologies.  Because, well, we don't really want people to know that you were publishing this science on the cardiovascular connection to MS in the 1950s, and we could have saved millions from undue suffering.

 Well, anyway.  Bygones, OK?

 your friends,
The National MS Society

(note:  just so I won't get sued, this letter isn't real.  It's satire.  But it's really not that funny.  I find it tragic.)
For those who wish to learn more, here is Dr. Swank's website.
http://www.swankmsdiet.org

Dr. Aston Embry developed the Best Bet Diet for his son Matt, using Dr. Swank's principals.
Matt is now 20 years past his MS diagnosis, using diet, exercise and treatment for CCSVI,  with no disease progression.  Here's his program.
http://www.mshope.com

Here is Dr. George Jelinek's program, Overcoming Multiple Sclerosis, based on Dr. Swank's foundational research.  http://www.overcomingmultiplesclerosis.org

And finally, here is the Endothelial Health Program.  I used Dr. Swank's documentation of "capillary fragility" in MS, and brought his research into 21st century science with the recent discovery of nitric oxide as endothelially derived relaxing factor (EDRF), and how nutrition, lifestyle and exercise impact brain health.
http://ccsvi.org/index.php/helping-myself/endothelial-health

 The vascular connection to MS is real.  It was real in the 1850s when Dr. Rindfleisch saw inflamed and engourged veins in MS brain tissue under his microscope, it was real in the 1940s when Dr. Putnam created MS lesions by blocking venous blood flow, it was real in the 1950s when Dr. Swank found the dietary connection, it was real in the 1980s when Dr. Schelling noted the venous connection and still real in 2005 when Dr. Zamboni saw on doppler ultrasound how blood was refluxing in jugular veins.

 Please take care of yourselves.  Eat well, move as much as you are able, don't smoke, get UV rays and plenty of sleep, laugh, pray and meditate, find support, and live your best life.  Because science says these things can make a difference.

 Be well,

 Joan





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