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Saturday, May 2, 2015

AAN 2015: low testosterone level in the womb increase risk of MS


Low androgens in utero linked to increase risk of MS in males #AAN2015 #MSBlog #MSResearch

"I note there has been some recent discussions about testosterone and MS. Two presentations at the AAN link low testosterone levels in utero or early childhood with an increased risk of MS. The first study shows that the ratio of the length of the ring finger to the index finger, the so called 2D:4D ratio, is higher in male MSers than controls. A lower 2D:4D ratio is associated with lower prenatal (before birth) or in utero (in the womb) androgen levels (testosterone is one of the androgens). The second study, done by the brilliant Julia Pakpoor (still in medical school) using NHS hospital records report a strong positive association (a five-fold elevation of rates) between testicular hypofunction and the subsequent development of MS in males. If these studies are correct this is another emerging risk factor that can be targeted when thinking of preventing, or at least lowering, the risk of developing MS. The latter must not be confused with the hypothesis that testosterone may be used as a disease-modifying therapy to treat MS. I am aware that there is emerging evidence for this, but until properly designed and powered studies are done we can't be sure. We also need to be aware that testosterone supplementation comes with risk, the most concerning include cancer and cardiovascular events (myocardial infarction and stroke)."




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MS ambassador says she doesn't see herself as disabled



Lizelle Mendoza, a Multiple Sclerosis Society ambassador, was diagnosed with MS eight years ago at the age of 18, seven years after she had begun to show symptoms. 
Faced with the fear that came with her diagnosis, Mendoza kept her relapsing-remitting MS a secret, afraid that her friends wouldn't want to support her. 
"I was just afraid," she said. "I was very self-conscious. I had symptoms since I was 11."
Mendoza's symptoms started in her eyes, with complete, but temporary, blindness. The disease has since spread through her body and has affected her mobility, she now walks with a limp. 
It was hard for Mendonza to find support and answers since no one else in her family had the disease. 
"I kept to myself, I was very isolated."
Speaking out
Her advocacy started when she was 18. She signed up for the MS walk and brought her friends along. They continued the tradition ever since and Saturday's walk marks nine events they've taken part in together. Mendoza also began to volunteer with the MS society. 
But Mendoza didn't tell her friends she herself had MS for another two years after they started walking.
"I wish I would have told myself not to be afraid, to kind of just open up. If I had spoken to other people earlier, I would have gotten help sooner and I wouldn't have been so self-conscious and so alone," Mendoza told CBC's Radio Noon.  
"Disability has such a negative stigma attached to it, I don't see myself as disabled."
Not only did Mendoza struggle with the stigma of having a disability, she said she also struggled with the misconception that MS is only found in older people. In fact, the Multiple Sclerosis Society of Canada says the most common period of diagnosis is between the ages of 15 and 40. 
Statistics Canada estimates that 93,535 Canadians are living with MS. 
"It's an individual disease and it's invisible," she said Friday. 
One foot in front of the other




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Thursday, April 30, 2015

Protein may offer key to remyelination

Protein may offer key to remyelination
Kick-starting a process that might repair the damage done in multiple sclerosis could start with disabling a process that blocks myelin regeneration, according to Baylor College of Medicine researchers.

Daam2 and another protein, PIP5K, comprise a pathway regulating Wnt signaling and myelination. Wnt signaling plays an essential role in developmental and regenerative myelination of the central nervous system. Wnt signaling pathways are present at high levels in precursors of myelin-making oligodendrocyte, and Wnt blocks the ability of cells to differentiate. Cells that differentiate are mature and can carry out their prescribed function.

Daam2 promotes Wnt signaling and receptor complex formation through PIP5K-PIP2. Analysis of Daam2 function in oligodendrocytes revealed that it suppresses oligodendrocyte differentiation during development, after white matter injury, and is expressed in human white matter lesions.

Results of mouse model studies sometimes do not translate to humans and may be years away from being a marketable treatment. The authors note that the results suggest drugs that inhibit Daam2-PIP5K function may stimulate remyelination after white matter injury.


The report appears in the journal Neuron.







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Julie from the USA shares her experience of LDN as a treatment for Multiple Sclerosis (MS) Low Dose Naltrexone





        Julie's LDN Testimonial is found here: video https://vimeo.com/121541736





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Wednesday, April 29, 2015

Cytokine may play major role in multiple sclerosis

Source:
Thomas Jefferson University
Summary:
Multiple sclerosis (MS) is caused by immune cells that activate a cascade of chemicals in the brain, attacking and degrading the insulation that keeps neuronal signals moving. These chemicals, called cytokines, drive the inflammation in the brain, attracting more immune cells, and causing the debilitating disease marked by loss of neurological function. Researchers have now discovered the role of a major cytokine in multiple sclerosis that could be a target for new therapy against the disease.
Multiple sclerosis (MS) is caused by immune cells that activate a cascade of chemicals in the brain, attacking and degrading the insulation that keeps neuronal signals moving. These chemicals, called cytokines, drive the inflammation in the brain, attracting more immune cells, and causing the debilitating disease marked by loss of neurological function. Researchers have long debated which cytokines drive the disease and which are merely accessory.

Now, a study published online April 27th, in the Journal of Immunology, confirms that the cytokine GM-CSF (Granulocyte macrophage colony-stimulating factor) likely plays an important role in human disease and offers a new explanation for why the MS treatment interferon-Beta (INF-β) is often effective at reducing MS attacks.

"After our animal studies showed that GM-CSF was important in the development of an MS-like disease, we were excited to see these results confirmed using samples from MS patients in the current study," says Abdolmohamad Rostami, M.D., Ph.D., Chair of the Department of Neurology at Thomas Jefferson University and director of its neuroimmunology laboratory.

A few years ago, MS researchers were focused on a new type of immune cell called the Th-17 cell, which appeared to be a key player in driving the neuronal damage in MS. Because Th-17 cells produce the cytokine IL-17, researchers likewise thought this chemical was essential to the disease. IL-17, however, turned out to be something of a red herring. In a paper published in Nature Immunology in 2011, Dr. Rostami and colleagues showed that the Th-17 cells also produced another cytokine called GM-CSF, which created a chain reaction with another cell type ultimately increasing the GM-CSF levels in the brain of mouse models significantly. In addition, the researchers showed that in experimental models of MS, mice that were unable to produce GM-CSF never developed the disease, whereas mice lacking IL-17 did develop the disease, though generally developed a milder form.

In the new study, to test whether the same observation was true in humans, Dr. Rostami and colleagues tested blood samples of patients with MS who had not yet received therapy, and those currently being treated with INF-β, a commonly used therapy. On average, untreated patients had two to three times as many immune cells producing GM-CSF as did patients being treated with INF-β, or normal subjects. In addition, the researchers looked at brain samples of deceased patients with MS and found increased numbers of GM-CSF-producing cells in comparison to normal brain samples. "The study demonstrates a new mechanism of action for INF-β therapies," says Dr. Rostami.

In addition, a recent Phase 1 clinical trial of an antibody that blocks GM-CSF showed early signs of effect. Phase 1 trials are typically only designed to determine if a new drug is safe, and can't answer whether a new drug works. However, these results together with the work from the Rostami lab suggest that GM-CSF is a target worth pursuing for the treatment of MS.

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FDA Accepts Biologics License Application For ZINBRYTA (Daclizumab High-Yield Process) For Treatment of MS

CAMBRIDGE, Mass. & NORTH CHICAGO, Ill.--(BUSINESS WIRE)--

Today Biogen (BIIB) and AbbVie (ABBV) announced that the U.S. Food and Drug Administration (FDA) has accepted for review the companies’ Biologics License Application (BLA) requesting marketing approval of ZINBRYTA™ (daclizumab high-yield process) for relapsing forms of multiple sclerosis (MS).
“We are pleased by the FDA’s acceptance of our BLA for ZINBRYTA, which we believe has the potential to help people living with MS,” said Gilmore O’Neill, Vice president, Multiple Sclerosis Research and Development at Biogen. “We look forward to working with both U.S. and European regulatory authorities to bring this investigational treatment to MS patients as soon as possible.”
Biogen and AbbVie announced in March 2015 that their Marketing Authorisation Application for ZINBRYTA was validated by the European Medicines Agency for review in the European Union.
The BLA included results from two pivotal trials, DECIDE and SELECT, in which ZINBRYTA 150 mg was administered subcutaneously every four weeks in people with relapsing-remitting MS.
“This is an important milestone in the development program for ZINBRYTA and moves us a step closer to potentially bringing a new treatment option to patients with MS,” said Michael Severino, M.D., executive vice president, Research and Development and Chief Scientific Officer at AbbVie.

About ZINBRYTA™ (daclizumab high-yield process)
ZINBRYTA (daclizumab high-yield process) is an investigational treatment and is a new form of a humanized monoclonal antibody that selectively binds to the high-affinity interleukin-2 (IL-2) receptor subunit (CD25) that is expressed at high levels on T-cells that become abnormally activated in MS. ZINBRYTA modulates IL-2 signaling without causing general immune cell depletion. ZINBRYTA is believed to work by decreasing abnormally-activated T-cells and pro-inflammatory lymphoid tissue inducer cells, and increasing CD56bright natural killer (NK) cells, important cells that help regulate the immune system.
Biogen and AbbVie are jointly developing ZINBRYTA.

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Tuesday, April 28, 2015

Little-known drug may halt multiple sclerosis, Gladstone study finds

Apr 27, 2015,
Blocking a specific protein with a little-known, experimental drug restored balance in the immune systems of lab mice, preventing them from developing multiple sclerosis, researchers at San Francisco's Gladstone Institutes found.
The early research, published Monday in the Journal of Experimental Medicine, could chart a new course for the drug against MS, a potentially fatal disease where the immune system runs amok and attacks nerve cells' protective covers. But the researchers note that some scientists — including one now at Google Inc.-backed Calico Life Sciences LLC — have thought that enhancing the same protein could slow the aging process.
Much research remains to be done, said Dr. Eric Verdin, co-senior author of the study and a senior investigator at the University of California, San Francisco-affiliated Gladstone Institutes. "I don't want to raise false hopes," he said.
Still, it is the balance between the potential anti-aging promise of activating the protein — called sirtuin 1, or SIRT1 — and its harmful role in inflammation in MS patients that makes it intriguing, Verdin said.
The findings also underscore the delicate seesaw action of the immune system in protecting us from disease without going hyperactive and attacking our bodies instead.
"It is a very complex but significant target," Verdin said about SIRT1.
Gladstone researchers found that an experimental drug called EX-527, which was developed by shuttered Elixir Pharmaceuticals Inc., inhibited production of SIRT1 in laboratory mice engineered to develop MS. That blocking action protected the mice against the onset of MS, researchers said.



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Monday, April 27, 2015

Effect of Genzyme's Multiple Sclerosis Treatment Lemtrada® (alemtuzumab) on Slowing Brain Atrophy and MRI Lesion ...

April 27, 2015

- Approximately 70 per cent of Lemtrada Patients Had Not Received Any Additional Lemtrada Treatment in the Prior Three Years -
MISSISSAUGA, ON, April 27, 2015 /CNW/ - Genzyme, a Sanofi company, announced new magnetic resonance imaging (MRI) data from the Lemtrada® (alemtuzumab) clinical development program at the 67th American Academy of Neurology (AAN) Annual Meeting in Washington, D.C. last week.
In relapsing remitting multiple sclerosis (RRMS) patients treated with Lemtrada in the Phase III pivotal studies, MRI effects observed in the two-year trials were maintained through two additional years in the extension study (years three and four). After the initial two courses of treatment in the pivotal studies, which were given at month zero and at month 12, approximately 70 per cent of Lemtrada patients did not receive additional Lemtrada treatment during the following three years, through month 48.
The Phase III trials of Lemtrada were randomized, two-year pivotal studies comparing treatment with Lemtrada to high-dose subcutaneous interferon beta-1a (Rebif®) in patients with RRMS who had active disease and were either new to treatment (CARE-MS I) or who had an inadequate response to another therapy (CARE-MS II).
Through year four, the adverse event profile of Lemtrada was consistent with that observed during the pivotal studies. The new data presented at AAN on Thursday, April 23 included:
  • The rate of brain atrophy, as measured by brain parenchymal fraction (BPF), decreased progressively over four years among Lemtrada patients in CARE-MS I. Among CARE-MS II Lemtrada patients, the rate of brain atrophy decreased progressively over three years and remained low in year four. In both studies, the median yearly brain volume loss was less than -0.20 per cent in years three and four, which was lower than what was observed during the two-year pivotal studies.
  • In CARE-MS I and II, treatment with Lemtrada significantly reduced the risk of developing new lesions compared to interferon beta-1a. In the extension study, most of the Lemtrada-treated patients from CARE-MS I and II were free of new lesions and MRI activity in years three and four (approximately 70 per cent).
Brain atrophy is a measure of the most destructive pathological processes that occur in MS.1 It is seen from the earliest stages of disease and may lead to irreversible neurological and cognitive impairment.  Given its association with disability, control or prevention of brain atrophy is an important target for MS treatment. In addition, MRI measures including lesion activity are considered useful tools when evaluating the effect of MS therapies, and lesion activity is among several prognostic factors for unfavorable clinical outcomes. 2
"It is very promising that most Lemtrada patients experienced slowing of brain atrophy and remained free of new lesions despite receiving their last treatment course three years previously," said Dr. Alasdair Coles, Professor, Department of Clinical Neurosciences, University of Cambridge. "These new MRI data are consistent with the clinical data from the extension study that provide additional evidence of the sustained efficacy of Lemtrada on both relapses and disability."  
Safety results from the second year of the extension study were previously reported. No new risks were identified. The most common side effects of Lemtrada are rash, headache, pyrexia, nasopharyngitis, nausea, urinary tract infection, fatigue, insomnia, upper respiratory tract infection, herpes viral infection, urticaria, pruritus, thyroid gland disorders, fungal infection, arthralgia, pain in extremity, back pain, diarrhea, sinusitis, oropharyngeal pain, paresthesia, dizziness, abdominal pain, flushing, and vomiting. Other serious side effects associated with Lemtrada include autoimmune thyroid disease, autoimmune cytopenias, infections and pneumonitis. A risk management program incorporating education and monitoring helps support early detection and management of these identified risks.
"The four-year MRI data support the prolonged efficacy of Lemtrada," said Genzyme President and CEO, David Meeker, M.D. "These results are encouraging, as they provide further evidence of Lemtrada's potential to change the treatment approach for people living with relapsing forms of MS."
More than 90 per cent of the patients who were treated with Lemtrada in the CARE-MS Phase III trials enrolled in the extension study. These patients were eligible to receive additional treatment with Lemtrada in the extension study if they experienced at least one relapse or at least two new or enlarging brain or spinal cord lesions. MRI scans were taken at CARE-MS baseline, and at 12, 24, 36 and 48 months.
In CARE-MS I, Lemtrada was significantly more effective than interferon beta-1a at reducing annualized relapse rates; the difference observed in slowing disability progression did not reach statistical significance. In CARE-MS II, Lemtrada was significantly more effective than interferon beta-1a at reducing annualized relapse rates, and accumulation of disability was significantly slowed in patients given Lemtrada vs. interferon beta-1a.

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Multiple Sclerosis, Crohn's Drug Used in HIV Targeted Therapy -

Apr 26, 2015    |    Rachel Lutz


Multiple sclerosis (MS) and Crohn’s disease drug Tysabri (Biogen Idec Inc.) can be used to fight against human immunodeficiency virus (HIV), according to research published in PLOS Pathogens.




  Researchers from Boston College treated 4 monkey models of HIV with high plasma virus and central nervous system injury with once weekly natalizumab (sold under the brand name Tysabri) initiated on 28 days post-infection. After 3 weeks, the drug reversed the lesions present on the central nervous system. Additionally, the virus track to the brain was blocked in monocytes and macrophages. This was significant, the researchers explained, because those cells collect in “viral reserves” which are associated with comorbidities that HIV patients sometimes have. -

“We actually stopped all traffic and showed that if you physically block monocytes and macrophages, the virus does not enter the brain,” senior author Ken Williams, PhD said in a press release. “And even if full and major lesions of the central nervous system are present, application of the antibody can heal that damage and eliminate the virus, underscoring the necessity for continued traffic of cells to the central nervous system and the gut to maintain infection and lesions.”   The researchers also conducted a parallel trial over 3 weeks which measured the time of experimental infection. Natalizumab completed blocked the monocyte and macrophage traveling between the brain and the gut in animal models of HIV.

The researchers explained that this research confirmed the role that monocytes play in preparing the central nervous system with virus and leukocytes. Both of these are early warning signs of a myriad of potential comorbidities, the authors said.

 “So our question was if we can do that with HIV, does it stop virus replication in the brain, stop seeding and does it reverse injury?” continued Williams, who said that a “cure” for HIV or AIDS would essentially mean a destruction of these viral reservoirs. “The answer to each of those questions, we now know, is ‘yes’.”  

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Drug prices to treat multiple sclerosis soar, point to larger problem

04.24.15 - OREGON STATE UNIVERSITY

PORTLAND, Ore. - A new study released today found that drugs used to treat multiple sclerosis have soared in price in the past two decades, in some cases more than 700 percent, even though newer drugs have come to the market - a process that normally should have stabilized or reduced the cost of at least the older medications.
There are no multiple sclerosis drugs now available in the United States with a list price below $50,000 a year, which is two to three times more than the price in Canada, Australia or the United Kingdom. The group of drugs available to treat this disease is rising in price at five to seven times the normal rate of drug inflation in the U.S.
The findings of this research also point to a systemic problem in the U.S. pharmaceutical industry, with relevance to more than just drugs for multiple sclerosis, according to the authors of the study, which was supported by the Oregon State University College of Pharmacy.
Enormous, uncontrolled and rapidly increasing prices for some types of drugs, they say, may be linked to non-transparent drug pricing policies, a dysfunctional market and the lack of a national healthcare system to negotiate prices more aggressively and directly with pharmaceutical companies.
The end result, they say in the report, may be another industry "too big to fail."
This research was published today in Neurology, the medical journal of the American Academy of Neurology, by scientists at the Oregon State University/Oregon Health & Science University College of Pharmacy, the Oregon Health & Science University, and the Veterans Affairs Medical Center in Portland, Ore.
"The issue of astronomical drug costs, especially for newer drugs or rare conditions, is more and more common," said Daniel Hartung, lead author of the study and an associate professor in the Oregon State University/Oregon Health & Science University College of Pharmacy.
"There are often several drugs in a class available to treat a disease or condition, and 'economics 101' would suggest that competition should lower prices," Hartung said. "In the pharmaceutical industry we often don't see that. Many professionals now believe that it's time to push back, to say enough is enough."
Escalating costs for specialty pharmaceuticals, for conditions such as multiple sclerosis, cancer, and hepatitis C, have been a growing concern among many in the health care industry, the authors wrote in their study, raising questions about the ethics of our current approach, exorbitant pricing and increased burdens on "our already stressed healthcare system."
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Glimmers of Hope for Progressive MS: Human Stem Cell Trial, Biotin Study Both Show Efficacy

Posted: 26 Apr 2015 08:34 PM PDT
Progressive multiple sclerosis is a particularly horrendous and intractable illness. Unlike the relapsing remitting form of the disease, for which there are currently 12 approved treatment options (however imperfect these may be), there is tragically little available for progressive MS patients (one very flawed treatment option for SPMS and none for PPMS). At the recent American Academy of Neurology meetings, held last week in Washington DC, some rays of hope for progressive MS finally shone through, among them studies done on honest-to-goodness human progressive MS patients – as opposed to those done on mice or in test tubes – that show particular promise.

As I’ve written about extensively (click here ), the Tisch MS Research Center of New York is currently conducting the only FDA approved regenerative human stem cell trial on MS patients in the United States. Yes, this is the very same study that the National Multiple Sclerosis Society has repeatedly refused to fund (click here). Though this phase 1 trial is not yet complete, interim results were released at the AAN meeting, and they look impressive.

The Tisch Center utilizes a unique approach to using stem cells to treat MS, quite unlike the techniques used in previous regenerative stem cell trials or the stem cell treatments being offered by for-profit operations scattered around the world. Employing proprietary methodology developed in the Tisch Center’s research laboratories, raw mesenchymal stem cells – harvested from each patient’s bone marrow – are transformed into stem cells specific to the human nervous system, called neural progenitor cells. The 20 patients enrolled in this early stage trial will each receive three spinal (intrathecal) injections of neural progenitor cells, spaced three months apart. The interim results released last week report on the nine patients who have thus far begun treatment (click here).

Of these nine patients, seven displayed some form of disease improvement. Six of these seven patients suffer from SPMS, and one from PPMS. Based on neurologic exams, five of these seven patients displayed improved motor functions, including better balance, increase muscle strength, and improved ambulation. Six of the patients reported better bladder function. No significant adverse events were reported. Here’s a graphic detailing the Tisch Center stem cell trial results on a patient by patient basis, taken from the poster presented at the AAN meetings. To view the full poster, please (click here).

While exciting, it’s important to keep these results in perspective. We’re looking at a very small patient population taking part in an early phase 1 trial whose primary endpoint is establishing the safety of the treatment. That said, given the intractability of progressive MS, seeing any significant improvement is extremely encouraging, and these early results certainly validate the approach to regenerative stem cell therapy being taken by the Tisch Center.

Alarmingly, though, the Tisch Center is now facing a fund-raising crisis that threatens to impede the phase 2 extension of this study, as well as much of the other groundbreaking MS research currently underway in the Tisch laboratories. In previous posts I’ve expressed my extreme distress at the NMSS’s repeated refusals to fund research being done at the Tisch Center, and due to unforeseen circumstances the Center’s funding shortfall is now being felt quite acutely. The animal research laboratory used by Tisch Center scientists is being closed as a result of the sale of the hospital in which it’s located (only a block away from the Tisch MS Center), leaving the Center with no viable alternative other than constructing their own facility, which will require a massive fund-raising effort.

Since I’d rather this post concentrate on the research itself, I urge all readers to click here for more information regarding this fund-raising crunch, and to spread the word far and wide. While the Tisch Center is actively conducting the only current FDA approved MS stem cell trial on human beings, the NMSS funds preclinical stem cell experiments being done in test tubes and on mice that, even if spectacularly successful, won’t reach MS patients for more than a decade. Just saying…

(Full disclosure: I am a patient at the MS clinic directly associated with the Tisch MS Research Center of New York, and my MS as well as other physical ailments have been totally kicking my ass lately. So, yeah, I might take this crap just a wee bit personally.)

Another much-anticipated study presented at last week’s AAN conference provided yet more hope for progressive MS patients, though perhaps not as much as originally anticipated. The French pharmaceutical company MedDay released the results of a stage III clinical trial involving the use of massive doses of Biotin to treat patients with Primary Progressive Multiple Sclerosis (PPMS) and Secondary Progressive Multiple Sclerosis (SPMS).

Biotin (vitamin B7, also known As Vitamin H or Coenzyme R) has been used in much lower doses as an over-the-counter “nutraceutical” supplement to treat brittle hair and nails, some skin conditions, and neuropathy brought on by type II diabetes, among other applications (click here). Biotin is known to be necessary for cell growth, the production of fatty acids, and the metabolism of fats and amino acids (click here).

A small pilot study researching the use of high doses of Biotin to treat MS was conducted by MedDay starting in 2013. This initial study produced astounding results, with 91.3% of the 23 progressive MS patients involved displaying improvements in their neurologic condition (click here). This small, unblinded, non-placebo-controlled trial created much excitement, leaving patients and researchers awaiting the results of a much larger placebo-controlled phase 3 trial, which was completed in late 2014. The results of this phase 3 trial were presented at the AAN conferences on Friday, April 24, 2015.

In this late stage study, conducted at 19 centers around France, patients were given 300 mg of Biotin per day, which is the equivalent of approximately 10,000 times the maximum daily recommended dosage. The study involved 154 patients, 103 given Biotin and 51 given a placebo. The results of this study (click here), while positive, don’t appear to be nearly as compelling as had been anticipated based on the early pilot study results.

The results of MedDay’s late stage study revealed that after 12 months, 12.3% of the Biotin treated patients displayed a verified improvement in disability scores, as opposed to 0% of the placebo group. Secondarily, 4% of Biotin treated patients displayed disease progression after one year, versus 13% in the placebo group. Very few adverse events, all considered non-serious, were reported. While these numbers pale in comparison with those seen in the initial pilot study, they still represent a breakthrough of sorts in treating advanced progressive MS, which thus far has defied almost all attempts at treatment.

Looked at another way, about 1 in 8 patients treated with Biotin saw their disability scores improve, while 1 in 25 saw their disease progress. Interestingly, only 1 in 8 (I’m using ballpark figures here) untreated patients experienced disease progression. While these aren’t the kind of results many hoped for based on the early Biotin study results (9 in 10 patients experiencing neurologic improvement), they are still better than nothing, which is what mainstream medicine currently offers patients with advanced (non-relapsing) progressive MS.

Given these factors, many patients with progressive MS (myself included) have expressed great interest in giving Biotin a try, especially since the stuff is readily available in over-the-counter form. The highest dose capsules commercially available are 10 mg, meaning that a patient would need to take 30 capsules a day to replicate the doses used in MedDay’s trials, which administered 100 mg of biotin three times a day. There are a few serious problems with this approach, though, above and beyond the huge amount of capsules that would need to be ingested to replicate the doses used in MedDay’s trial.

First, the compound used in the MedDay trial is a highly concentrated and purified pharmaceutical grade form of Biotin called D-Biotin, a stereoisomer of Biotin that is extremely bioavailable (easily absorbed by the body) and contains active enzymes (click here). This type of Biotin is generally not available in over-the-counter capsules. Second, over-the-counter nutraceuticals are completely unregulated, and it’s almost impossible to know the purity of the compounds contained within the capsules or what other ingredients might also be present. One study found that a shocking one third of herbal supplements tested contained not a trace of primary ingredient the listed on the bottle (click here)! Additionally, some Biotin supplements contain calcium, which if taken in greater amounts can cause hypercalcemia, a potentially very serious medical condition (click here).

After consulting with a naturopathic physician, I'm looking into procuring ultra high grade, USP certified (click here) D-Biotin from a reputable wholesaler and having it put into properly dosed capsules through a compounding pharmacy (I'm doing this with my naturopath's help, of course, and will need a prescription in order to get the drug). While this approach is likely to be much more expensive than using over-the-counter product (probably about $300-$400/month), it will offer the best chance at replicating MedDay’s trials, and would certainly eliminate the vast uncertainties involved in consuming huge quantities of over-the-counter nutraceutical supplements.

So, there you have it, two clinical trials targeting progressive MS in very different ways, but coming up with encouraging results to one degree or another. While the Tisch Center stem cell therapy is still in early trials and is at least several years away from moving from the experimental stage to general clinical use, MedDay’s Biotin compound should be ready for FDA approval by the end of this year, and highly motivated patients might try to get a head start on things by taking matters into their own hands. Although the results of MedDay’s late stage phase 3 trial were a bit underwhelming, they do represent an important advance over the status quo, and many progressive MS patients are well past the “any port in a storm” stage.


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CME: Risk/Benefit Analysis of MS Therapies PLUS Clinical Decision Making in MS: Evaluating a Patient with Concerns about Symptoms and Therapeutic Efficacy

MS leaders e-mail logo header 

Dear MS-Leaders Registrant,

Can you correctly answer this question:

When evaluating JC virus antibody test results, what level of JC antibody index is considered to be a seropositive test?

A. Higher than 0.2
B. Higher than 0.4
C. Higher than 0.6
D. Higher than 0.8

Participate in our eCase Challenges to learn the answer to this and other questions related to MS therapy.

Earn Up to 1.0 Free CME or CNE Credit!

Below are links to 2 eCase Challenges focused on real-life MS cases. The University of Texas Southwestern Medical Center and Postgraduate Institute for Medicine, in cooperation with Medical Logix, LLC are pleased to offer these CME/CNE certified programs:




Acknowledgement of Commercial Support: 
Supported by independent educational grants from Genzyme, a Sanofi company and Novartis.

Intended Audience:
These activities are intended for healthcare professionals, specifically, neurologists, internists, family practice physicians, nurse practitioners, physician assistants, registered nurses and other providers involved in the care of patients with multiple sclerosis.

Accreditation Statement:
These activities have been planned and implemented in accordance with the Essential Areas and policies of the Accreditation Council for Continuing Medical Education through the joint sponsorship of The University of Texas Southwestern Medical Center and Medical Logix LLC. The University of Texas Southwestern Medical Center is accredited by the ACCME to provide continuing medical education for physicians.

Postgraduate Institute for Medicine is accredited as a provider of continuing nursing education by the American Nurses Credentialing Center's Commission on Accreditation.

Credit Designation Statement:
The University of Texas Southwestern Medical Center designates each of these enduring materials for a maximum of 0.50 AMA PRA Category 1 Credit(TM). Participants should claim only the credit commensurate with the extent of their participation in the activity.

Each of these educational activities for 0.5 contact hours is provided for nurses by Postgraduate Institute for Medicine.

Format and Method of Participation:
There are no fees for participating and receiving CME or CNE credit for these activities. During the accreditation period, participants must read the learning objectives and faculty disclosures and review each internet-based activity. To take the post-test, please click on the post-test button below the slide window of the player. Complete the post-test and evaluation and attest to the amount of time spent in each activity. Upon receiving a score of 70% or above, print your CME or CNE certificate(s).

Please keep in mind that you will need to login with your email address and password to access this program.  If you forgot your password, click on the 'Forgot Password' link in the top right corner of the site.
We hope you enjoy these informative educational programs! 

The MS-Leaders Team


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