A study has reported that Viagra given to mice with the animal model of MS showed  staggering results in 50% of the animals.

Daily treatment with Sildenafil (Viagra) rapidy reduced MS-like symptoms so that after 8 days there was an almost complete recovery.

For the first time it was shown how the drug reduced the infiltration of inflammatory cells into the white mattter of the spinal chord. This threrfore reduced the damage to the axons making myelin repair easier for the myelin-making cells.

Recent studies had already pointed to the fact that as well as vasodilation this drug seems to have neroprotective actions so can be used in MS, stroke and Alzheimers.

Researcher are confident that clinical trails in humas will soon be carried out.

Already a study , in the USA , has shown that bloodflow to the brain can be increased in both men and women who have MS using Viagra.

Have you used Viagra and did you find any change in your MS symptoms

Why not visit A Voice For MS Facebook Page

Cinnamon is Native to Ceylon (Sri Lanka), true cinnamon, Cinnamomum zeylanicum, dates back in Chinese writings to 2800 B.C., and is still known as kwai in the Chinese language today. Ceylon cinnamon is largely used in the uk, Europe, and Asia but  there is another form of cinnamon “Cassia” which is mainly used in the US.

Due to the presence of a moderately toxic component called coumarin, European health agencies have recently warned against consuming large amounts of cassia. This is contained in much lower dosages in Ceylon cinnamon due to its low essential oil content. Coumarin is known to cause liver and kidney damage in high concentrations. Ceylon cinnamon has negligible amounts of coumarin

Ceylon cinnamon sticks (or quills) have many thin layers and can easily be made into powder using a coffee or spice grinder, whereas cassia sticks are much harder. These are impossible to break by hand so this is one way to tell if you have the right cinnamon.

Regularly drinking tea made from the bark of Sri Lanka cinnamon could be beneficial to oxidative stress related illness in humans, as the plant part contains significant antioxidant potential.

Most “cinnamon” on grocery store shelves is actually cassia if you are in the US and even in some stores in the UK.

Apart from the recent belief that cinnamon may slow down MS, here are 10 Health Benefits of Cinnamon

1. Studies have shown that just 1/2 teaspoon of cinnamon per day can lower  LDL cholesterol. So good for heart health.

2. Several studies suggest that cinnamon may have a regulatory effect on blood sugar, making it especially beneficial for people with Type 2 diabetes.

3. In some studies, cinnamon has shown an amazing ability to stop medication-resistant yeast infections.

4. In a study published by researchers at the U.S. Department of Agriculture in Maryland, cinnamon reduced the proliferation of leukemia and lymphoma cancer cells.

5. It has an anti-clotting effect on the blood.

6. In a study at Copenhagen University, patients given half a teaspoon of cinnamon powder combined with one tablespoon of honey every morning before breakfast had significant relief from arthritis pain after one week and could walk without pain within one month.

7. When added to food, it inhibits bacterial growth and food spoilage, making it a natural food preservative .

8. One study found that smelling cinnamon boosts cognitive function and memory.

9. Researchers at Kansas State University found that cinnamon fights the E. coli bacteria in unpasteurized juices.

10. It is a great source of manganese, fiber, iron, and calcium.

So that seems like a lot of reasons to eat, the right, cinnamon.

A friend of mine Steven Tate has recently made a video about cinnamon.

Steve is a musician a film maker and has PPMS. While this is not a scientifically valid study it is hugely fascinating and a very interesting subject for film making. Keep us up to date Steven.

Please cheer him on by liking this post or better still leave a comment.

By Julie  Stachowiak, Ph.D.,

Just recently, I ran into a “situation” after giving myself an injection of Copaxone, which I have been taking now for about 5 years. It was scary, but I think I am past the worst of it.

Once again I am turning to you, my readers and fellow people with multiple sclerosis (MS) to answer questions that have come up in my own experiences with this disease that I cannot answer by looking in the medical literature or talking to “experts.” I figure if it has happened to me, it has happened to some of you. I also figure that if I am frustrated by the lack of information out there, then gathering our voices together can only help one another.

Here is what happened:

When I gave myself the injection in my left hip, it felt odd. Not extremely painful, just “hot” going in. It actually bled a little (more than a drop) when I withdrew the needle. The warm feeling seemed to intensify, and the site began to itch.

When I positioned myself to look at the area in a mirror, I was a little shocked to see what looked like a huge, splotchy bruise across the site – measuring about 6 inches across – accompanied by tiny hive-like bumps.

I tried to distract myself for about 30 minutes. When I looked at it again, the bruise-like discoloration was gone, and the small bumps seemed to have joined into a gigantic hive. I had a big glass of wine and went to bed. The next morning, it looked fairly normal, but was just sensitive.

Three days later, the bruise was back. Two days after that, a patch of skin about 1.5 inches in diameter peeled off. To make a long story short(er), I have kept the area covered with a dressing and antibiotic ointment, and it seems to be shrinking (but healing much more slowly than a normal scrape or cut would).

Shared Solutions told me to monitor the area. I am out of town, so cannot visit my neurologist. I am trying to research this – I have been searching under “injection site skin necrosis,” although I am not sure that is an accurate description – but have found that it is considered “extremely rare” (like many things that we all seem to experience) and there is little in the medical literature about it. I am hoping that some of you can fill in the blanks.

Has this ever happened to you? What did you do? What did your doctor say? How long did it take to heal? Did it ever happen again? Please leave your story or any information that you may have in the comments section below. I thank you from the bottom of my heart.

Good bacteria, also known as ‘Probiotics’ are known for their favourable effects in maintaining gastrointestinal health, but can they encourage psychological health too?

New research conducted at the Texas Tech University Health Sciences Center has explored the new world of neurological probiotics and the scientists have put forward novel ideas on how neurochemicals enforce their beneficial effects in maintaining a healthy gut and even psychological well-being when delivered directly to the gut, via probiotic intestinal microbiota. The study was led by Professor Mark Lyte and has been published recently in BioEssays.

The researchers have proposed that neuroactive compounds if delivered via neurochemical-producing probiotics could help improve a host’s gastrointestinal and psychological health. These probiotics could be prepared for delivery of the compound using a unifying process of microbial endocrinology.

“This paper proposes a new field of microbial endocrinology, where microbiology meets neuroscience,” said Lyte.

“There is already evidence to suggest that the connection between gut microbes and the nervous system represents a viable route for influencing neurological function. A recent study in mice, for example, showed that the presence of neurochemicals such a serotonin in the bloodstream was due to direct uptake from the gut.”

Neurochemicals generated in the gut by ‘good bacteria’ such as lactobacilli and bifidobacteria are actively absorbed by the intestines and circulated through a patient’s bloodstream. According to Dr. Lyte, this is the hypothesis of the pathway for probiotics to exert extra-intestinal effects including changes in behavior.

Commenting on some of the potential clinical implications of this research, Professor Gregor Reid, from the University of Western Ontario, in the same issue of BioEssays stated,

“Until recently the idea that probiotic bacteria administered to the intestine could influence the brain seemed almost surreal. Yet in Lyte’s paper the concept is supported by studies showing that microbes can produce and respond to neurochemicals, which can induce neurological and immunological effects on the host.”

Professor Reid concluded, “The research presents an idea for selecting probiotic strains with neurological applications and linking this with immune-modulatory effects, while highlighting the fact that microbial strains already being widely ingested in fermented food can produce neurochemicals,” “Could this mean that adjunct treatment for people suffering from certain types of mental health problems is a fecal transplant? Food for thought.”

“Probiotics function mechanistically as delivery vehicles for neuroactive compounds: Microbial Endocrinology in the design and use of probiotics”
Lyte. M,
BioEssays, Wiley-Blackwell, July 2011, DOI: 10.1002/bies.201100024

“Neuroactive probiotics”
Reid. G
BioEssays, Wiley-Blackwell July 2011, DOI: 10.1002/ bies.201100074

Source: Medical News Today © MediLexicon International Ltd 2004-2011 (07/07/11)

Stem Cells

The study, published in Nature Neuroscience, was carried out by scientists at the University of California San Francisco and the University of Cambridge, and funded by the MS societies of the US and UK.

Robin Franklin, Professor of Neuroscience at Cambridge and co-author of the study, said: “There are currently no treatments that repair damage to myelin caused by MS, which is a missing link in the treatment of the condition.

“This discovery means we now have even more credible opportunities to promote myelin repair, which is a really promising step forward. Our efforts will now be focused on translating these findings into treatments for people with MS.”

Dr Doug Brown, Head of Biomedical Research at the MS Society said: “Myelin repair holds real potential to prevent or even reverse the devastating effects of MS.

“We’ve made a significant investment in myelin repair research in recent years and are delighted to see this investment starting to pay dividends.

“We are excited to see this work moving towards clinical trials and are hopeful that this will lead to a new form of treatment for people with MS within the next ten-15 years.”

MS affects about 100,000 people in the UK, about 10,500 of them in Scotland

Starting interferon-beta-1a (Rebif New Formulation) immediately upon an episode of a clinically isolated syndrome delayed progression to full-blown multiple sclerosis, but once-weekly treatment was less effective than the standard dosing interval, a researcher said here.

A randomized, placebo-controlled trial called REFLEX showed that 62% and 76% of patients assigned to 44 mcg of interferon subcutaneously three times or once weekly, respectively, met 2005 McDonald criteria for MS after two years – the study’s primary endpoint – compared with 86% of patients treated with placebo, said Mark Freedman, MD, of the University of Ottawa.

The differences between the two interferon dosing schedules, and between the interferon schedules and placebo, were all statistically significant (P<0.01), he told attendees at the annual meeting of the Consortium of Multiple Sclerosis Centers (CMSC).

On the other hand, there was no difference between interferon regimens in the percentage of patients diagnosed with “clinically definite multiple sclerosis,” standards for which were set in 1983 with endpoints somewhat different from the 2005 McDonald criteria.

This “main secondary endpoint” was met by 21% and 22% of the three times and once weekly groups, respectively, versus 38% of the placebo group, Freedman reported.

Also similar between the two interferon regimens was the annualized relapse rate: 0.118 and 0.115, respectively, compared with 0.22 with placebo.

Overall, the REFLEX results were similar to those seen in an earlier study called BENEFIT, reported in 2006, which tested the three times weekly dosage – then as now the standard of care for MS treatment – against placebo in patients diagnosed with clinically isolated syndrome.

This condition is essentially the first definite disease event in MS, but under the current diagnostic framework, it is not sufficient for a diagnosis of MS until either symptoms worsen, or MRI scans confirm lesions characteristic of MS.

The purpose of the REFLEX study was to determine if a lower dosage and reduced injection frequency would be as effective as the standard schedule in delaying progression.

The study enrolled 517 patients who were assigned in nearly equal numbers to the three treatment regimens. To maintain the trial’s double-blinding, all patients received three injections weekly, such that those assigned to once weekly interferon had two injections of placebo each week.

In addition to the clinical endpoints, the trial also evaluated lesion burden as determined from MRI scans. As with the primary clinical endpoint, the three times weekly regimen appeared more effective than the once weekly schedule, although both were markedly more effective than placebo.

Mean counts of combined, unique active lesions at the two-year evaluation were 2.70 with placebo, 1.23 with once weekly interferon dosing, and 0.60 with the standard schedule, Freedman said, with all two-way comparisons significant at P=0.002 or less.

Tolerability was another area where the once weekly regimen fell short of the standard schedule, he said, in particular with respect to the flu-like symptoms often seen with interferons.

These were reported by 71% of the once weekly group versus 54% of those on the standard regimen and 20% of the placebo group, according to Freedman.

He said the once weekly dosing itself was likely responsible.

“Once weekly patients never really get to tolerate the flu-like symptoms,” he said.

An audience member, Paul O’Connor, MD, of the University of Toronto, countered during the question-and-answer session that neutralizing antibodies are often credited with being responsible for the tolerance effect, by reducing the amount of interferon actually in circulation.

However, neutralizing antibody titers were measured in the trial and did not differ between the two regimens.

Freedman said he did not believe that neutralizing antibodies are the source of tolerance to flu-like effects, but rather the immune system’s responsiveness to interferon. With the three times weekly dosing, those elements responsible for the flu-like symptoms become less responsive over time.

But with once weekly dosing, they are able to rebound fully and therefore tolerance does not develop, he said.

Limitations to the study included the use of 2005 McDonald criteria, which were revised last year in ways that would have increased the number of participants receiving an MS diagnosis, Freedman said.

He also noted that the interferon-beta-1a formulation used in the study is not yet approved in the US. This formulation, unlike the current FDA-approved version, is free of fetal bovine serum and human serum albumin.

Rush University Medical Center has received a grant from the National Institutes of Health (NIH) to evaluate whether cinnamon, a common food spice and flavoring material, may stop the destructive process of multiple sclerosis (MS).

The two-year, $750,000 NIH grant will fund research that will analyze the effects of cinnamon on the disease process in mice.

“Since medieval times, physicians have used cinnamon to treat a variety of disorders including arthritis, coughing and sore throats,” said Kalipada Pahan, PhD., who is the Floyd A. Davis professor of neurology at Rush and principal investigator of the study. “Our initial findings in mice indicate that cinnamon may also help those suffering from MS.”

MS is an autoimmune disease that attacks the central nervous system, which consists of the brain, spinal cord and optic nerves. The disease is caused by damage to the myelin sheath, which is a fatty tissue that surrounds and protects the nerve cells. When myelin or the nerve fiber is damaged or destroyed, the nerve impulses are slowed down and the electrical impulses to and from the brain are disrupted. This disruption causes the symptoms of MS, which include numbness in the limbs, paralysis and loss of vision.

The progress, severity and specific symptoms of MS are unpredictable and vary from one person to another. Episodes can last for days, weeks or months. These episodes alternate with periods of reduced or no symptoms. Because nerves in any part of the brain or spinal cord may be damaged, patients with MS can have symptoms in many parts of the body including muscles, bowel and bladder, eyes, speech, and swallowing.

Researchers are not sure what triggers the disease. The most common theories point to a virus or genetic defect, or a combination of both. Geographic studies indicate there may be an environmental factor involved.

Glial cell activation in the brain has been implicated in the pathogenesis of a variety of neurodegenerative diseases such as Alzheimer’s disease, Parkinson’s disease and MS. Activated glial cells accumulate and secrete different neurotoxin factors that cause various autoimmune responses that lead to brain injury.

“These autoimmune reactions in the brain ultimately kill oligodendrocytes, which are a certain type of brain cell that protects the nerve cells and myelin sheath,” said Pahan. “However, cinnamon has an anti-inflammatory property to counteract and inhibit the glial activation that causes brain cell death.”

What makes this chemical unique is that at the same time, it stimulates the body to produce interferon-beta, an anti-inflammatory molecule, that is commonly given to patients as an injected drug to treat MS.

Together, these effects cause significant reduction in the severity of an animal model of MS. The researchers have also discovered that cells of the immune system obtained from the blood of people with MS are more sensitive to the effects of this drug than those obtained from people who do not have MS.

Dr Gran said: “Under laboratory conditions we have found a way of encouraging the body to produce its own Interferon-beta. When other experimental substances have been tested in the laboratory to achieve this effect, they usually cause the immune system to produce a mixture of anti-inflammatory as well as pro-inflammatory molecules, typically reducing the overall efficacy. In the case of the compound tested in this study (a synthetic cannabinoid known as R(+)WIN55,212-2), the predominantly anti-inflammatory effects appear promising for further pre-clinical, and hopefully clinical, testing.”

With no available cure MS is the focus of intense study for the hundreds of scientists across the world who are working on new treatments for this disabling disease. MS is more common in temperate climates. With around 100,000 people suffering from MS in the UK the country has one of the highest rates of the disease in the world.

Until 20 years ago there was little progress in the search for treatments.

After their first approval in 1993 Beta Interferons still represent one of the first line treatments for relapsing-remitting multiple sclerosis. These drugs are not a cure but they can reduce the number and severity of relapses. Despite this, more effective, well tolerated therapeutic strategies are needed.

Dr Gran’s research continues a line of investigation which his laboratory has carried out for a number of years on the role of endogenous type I interferons in regulating multiple sclerosis inflammation in the central nervous system.

The cause of MS is still something of a mystery. Numerous factors are thought to contribute, including genetic susceptibility and environmental factors. The latter are thought to include certain viral infections and low levels of vitamin D, linked to poor sun exposure.

These latest findings highlight a new selective mechanism that may be open to exploitation in the development of new therapeutics for the treatment of MS.

Source: Medial Xpress © Medical Xpress 2011 (21/06/11)

This article was taken from the MSRC news service

Brain Volume 133, Issue6

Introduction

 
Multiple sclerosis presents in various ways and subsequently shows variable disease courses. If we knew early on what the disease course for Multiple Sclerosis would be then we could better target the medication in each individual case. To date it has been unpredictable right from disease onset but , knowing the disease course is of crucial importance in guiding treatment.

Now “The Department of Neurosciences” at Cardiff University has recently been looking into factor H as a biomarker for multiple sclerosis and the findings are promising
Effective and accessible biomarkers are needed in order to stratify ( separate into groups) patients and inform treatment. The team at Cardiff University decided to look into factor H as such a marker. Regulator factor H, has recently been implicated as a biomarker in other chronic inflammatory central nervous system conditions. Could it identify or predict specific pathological processes and outcomes in multiple sclerosis?

Method
They measured factor H in blood serum from 350 patients with multiple sclerosis classified according to disease course and relapse status. Controls were found for variables including disease duration, age, gender, disability and treatment. I have decided not to go into the full method in this document as the details will be somewhat turgid to the average reader. However, the findings are fairly clear and very encouraging.

Results
1) Factor H levels were significantly higher in progressive disease compared to controls and relapsing patients. Thus factor H levels were capable of distinguishing secondary progressive from relapsing remitting disease (excluding patients in clinical relapse)
2) Acute relapse was also associated with temporarily increased factor H levels compared to stable relapsing disease.
3) In clinically stable patients, factor H levels remained constant over 1 year but in patients in transition from relapsing to progressive disease, factor H levels significantly increased over a period of 2 years . This is a crucial point as the transition between relapsing and progressive signals the need for therapy change.

Conclusion
Serum factor H could be an effective indicator of progression and a practical and accessible tool to split patients into groups and to predict disease course, Once we have this information we have objective evidence which can help guide therapeutic decisions. As we have known for some time, the earlier you can pick up a disease pattern the better chance of success you have with the treatment.

Doctors don’t have a complete answer yet. In theory, it makes sense that if you limit damage from inflammation, the disease will progress more slowly. Some researchers have even tried using periodic treatments with corticosteroids in hopes of delaying the progression of MS. But so far, there’s little evidence that the approach offers any benefit.

“In general, I believe that steroids hasten recovery and may reduce the risk of future relapses for a time,” neurologist Elliot Frohman, MD, an MS researcher at the University of Texas Southwestern Medical Center, wrote in an email to WebMD. 

But one recent study, called the Optic Neuritis Treatment Trial, found that treating relapses may have little if any effect on the long-term course of MS. Researchers looked at acute relapses that caused optic neuritis. Some patients were given oral prednisone. Others received no treatment at all. Patients in the high-dose prednisone group recovered more quickly from optic neuritis. But a year later, researchers found no difference between the treated and untreated groups in terms of disease progression.

To Treat or Not to Treat

Even when they are untreated, however, acute relapses of MS typically resolve on their own over a matter of days or weeks. For that reason, and because corticosteroids are powerful drugs with some unwanted side effects, doctors may recommend using them only for relapses that significantly affect a patient’s function. Adverse side effects of corticosteroids can include fluid retention, weight gain, elevated blood pressure, and mood swings.

Personally I have found oral steroids to be little or no use as they take so long to take effect that it is impossible to tell if the remission was spontaneous or caused by the steroids. What is you experience of treating a relapse ?