Tuesday, 28 June 2011

The autoimmune theory --doctors ask, "Have we got it horribly wrong?"

Another interesting research paper dug up by Joan Beal:

Have we got it horribly wrong? 
The following is the quote which begins a critical paper from 2002.

The fact that an opinion has been widely held is no evidence whatever that it is not utterly absurd; indeed in view of the silliness of the majority of mankind, a widespread belief is more likely to be foolish than sensible.
Bertrand Russell*

The Pathogenesis of MS revisted.  
The Full paper available here (this is one to print out and share...)

Here is a breakdown of the paper in an issue of the New Scientist from 2002
New Scientist vol 176 issue 2369 - 16 November 2002, page 12 

It's not surprising there's no cure for multiple sclerosis. Researchers have been studying the wrong disease for over a century, argue a few rebels.

THE century-old assumption that multiple sclerosis is an autoimmune disease is under attack. Treatments based on the autoimmune theory have failed so miserably, say a group of doctors, that it is time to look for other explanations.

In a lengthy review to be published next week in The Journal of the Royal College of Physicians of Edinburgh, the three neurologists dispute the received wisdom that the disease wreaks its havoc when immune cells attack and destroy myelin protein, which insulates nerves and helps them conduct signals. Instead, they back an emerging theory that MS is caused when support cells called astrocytes malfunction, perhaps as a result of genetic and environmental triggers.
 (NOTE from Joan:  One well-documented environmental cause of astrocyte malfunctioning is hypoxia, or low oxygen in the brain)

Many mainstream MS researchers contacted by New Scientist have poured scorn on the review. But a few agree it's time for a rethink.

Peter Behan and Abhijit Chaudhuri at the University of Glasgow and Bart Roep of the Leiden University Medical Centre pull no punches in their attempts to demolish the prevailing theory. They begin by attacking the animal experiments that have underpinned the autoimmune theory since the late 19th century.
Back then, researchers discovered that if they injected nerve or brain tissue into an animal, its immune system would attack the nervous system. They called this experimental allergic encephalomyelitis, and before long adopted EAE as the "animal model" of multiple sclerosis.

This, say the heretics, was a big mistake. In their view, EAE is completely different from MS. "There are huge differences, and they've been skipped over," Behan told New Scientist.

For instance, EAE either kills animals or leaves them with permanent disabilities. "It doesn't come and go like MS," he says. Animals with EAE also suffer severe nerve inflammation, whereas in MS inflammation is usually mild, if present at all.

Despite this, virtually all treatments for MS have been tested on EAE. Little wonder then, says Behan, that the treatments do not work for people. "Not a single human has been cured using these approaches," he says.

However, steroids and other immunosuppressants do work for a brain disease called acute disseminated encephalomyelitis, a rare result of infections. Behan thinks ADEM, not MS, is the human equivalent of EAE.
He also argues that the fact that traces of white blood cells are found at some sites of nerve and brain damage in MS patients does not prove they caused the damage. The same traces are found after strokes and neurodegenerative diseases.

 Israel Steiner, a neurologist at the Hadassah University Hospital in Jerusalem, agrees that EAE has blocked "effective progress" for decades. He thinks alternative theories should be put to the test. "I definitely believe it's high time to reconsider the entire field. It has not led us into understanding the disease or to a better therapy for patients," he says. "Many people in the community who do not have a vested interest in the autoimmune hypothesis share my views, but I'm not sure they would like to step out."

Almost 10 years since this review was written, and EAE is still used to create pharmaceuticals for MS.  When will this insanity end?

Tuesday, 7 June 2011

Information comes to light

I haven't posted in a while, as it seems hard to keep saying, yep I'm still feeling good. But that's the way it is.

Some days it is hard to remember what it was like to live with MS before my operation.

I still keep up with all the stuff that appears on the web, though, and thought it would be good to share information that appeared on Joan Beale's excellent Facebook page.

Research from the 1970s on spinal venous hypertension and myelopathies

by CCSVI in Multiple Sclerosis on Saturday, 04 June 2011 at 06:09
Thanks to  Mylène Therrien for the following info on research from the 1970s on myelopathy of the spine due to venous hypertension and malformations in the veins surrounding the spine.  The 80 patients tested and treated in these studies had paraplegia and injury of the spine due to venous malformations.  They were treated for venous stenosis in the 1970s.  Dr. Zamboni has referenced this research in his publications, but I hadn't seen these abstracts or understood the history.
Here are the abstracts and links I found from the info given in her posting:

Acta Radiol Suppl. 1976;347:395-401.
[Intraspinal venous hypertension due to multiple anomalies in the caval system. A major cause of myelopathies].
[Article in French]
Aboulker J, Aubin ML, Leriche H, Guiraudon G, Ancri D, Metzger J.
Increased venous intraspinal pressure is described as a venous system disease, resulting in numerous unexplained paraplegias and tetraplegias. The chronic venous stasis in the intraspinal plexuses, into which the circulation of the spinal cord is drained, is due to the association of multiple abnormalities (stenoses, compressions, thromboses) on the major pathways of the caval and azygos system. The abnormalities, most of which are not known, are demonstrated by a special procedure, the cavo-spinal phlebography, and some of them are subjected to surgery.
 207125 [PubMed - indexed for MEDLINE]

 Acta Radiol Suppl. 1976;347:415-7.
[Cavo-spinal phlebography in myelopathies. Stenoses of internal jugular and azygos veins, venous compressions and thromboses].
[Article in French]
Leriche H, Aubin ML, Aboulker J.
Increased intraspinal venous pressure, resulting according to ABOULKER in numerous spastic paraplegias and quadriplegias is due to multiple venous abnormalities demonstrated by cavo-spinal phlebography. The most frequent are stenoses of the internal jugular veins, the left renal, the left iliac veins, the azygos veins and compressions of the innominate venous trunks. These abnormalities cause a permanent stasis in the intraspinal plexuses through excessive supply or insufficient drainage. Out of 80 patients, 60 per cent had at least 2 abnormalities, 38 per cent at least 3 abnormalities.
 207127 [PubMed - indexed for MEDLINE]

Acta Radiol Suppl. 1976;347:403-13.
[Cavo-spinal phlebography in myelopathies of venous origin. Application of the method in 115 cases].
[Article in French]
Aubin ML, Leriche H, Aboulker J, Ernest C, Ecoiffier J, Metzger J.
The intraspinal venous stasis, described by ABOULKER as the cause of numerous myelopathies, is due to the addition of multiple venous abnormalities, demonstrated by cavospinal phlebography. The venae cavae and their major affluents and the prespinal system (lumbar and ascending lumbar veins, azygos, hemi-azygos, right superior intercostal and vertebral veins) are explored by catheterization. Cavo-spinal phlebography reveals multiple obstacles and the resulting stasis in the intraspinal plexus.


The following quote is Mylene writing about her conversation with Dr. Garel, the IR who performed these procedures, and her translations from the research, originally written in French.

I spent 45 minutes on the phone with Dr.Garel from St-Justine Hosptial who was the IR who did the catheterization under Dr.Aboulker's study in the 70's. Interestingly enough. the results and the outcome of that experiemental treatment were exactly what Zamboni is finding. Here is a part of his work, translated from French to English from me. Note that : First : You should know that I do not know when to use the word " stenoses " vs " stenosis" 

The basis for surgical indication : To whom was surgery proposed ? 

Any patients who had a major cause of spinal cord problems of unknown origin resulting in progressive disabilities for whom no other therapeutic alternatives were available to them and whose cavo-spinal phlebography examination revealed multiple abnormalities of the major pathways of the caval and azygous system.

Note that it was a new and an experimental procedure proposed and well-explained to the patients at the time ( in the 1970's). Only those whose paraplegia were progressing and regularly worsening were offered the surgery.

Aboulker and al., were investigating the multiple abnormalities ( stenosis-compression-thrombosis) which reduce or block the circulation in the large veins of the caval system, resulting in spinal venous stasis as a result of excessive supply and inadequate drainage. That would result in impairment in function of the cord, just like any organ when return circulation is chronically impaired. 

HERE ARE THE RESULTS of the cavo-spinal phlebography done on 80 patients who experienced unexplained spastic paraplegias and quadraplegias. 

Out of the 80 patients, only 21 patients had the left renal vein investigated. 

INTERESTINGLY ENOUGH, ABNORMALITIES WERE FOUND AT ALL LEVELS OF THE VENOUS SYSTEM. The left primitive iliac vein was found to be among the most frequent abnormalities observed. The other ones were stenoses of the IJVs, the left renal vein, the azygous veins and the compressions of the innominate venous trunks.

Out of the 80 patients, 60% had at least 2 abnormalities and 38% had at least 3.



- left primitive iliac vein showed recanalized old thrombus in 5% of the patients.
 - 48% of the patients showed a stenosis of the left primitive iliac vein. 
(Note that an upstream stasis were always found with those obstructions.) 
 - 34% of the patients had an abnormality of the intraspinal dorsal and lumbar plexuses and an abnormality of the azygous system as well.. 

 RENAL VEIN: - Note that only 21 patients out of 80 patients had their left renal vein investigated. 
 -47,6% of those 21 patients had a compression of their left renal vein. 
-30% of the 21 patients had an abnormality in the intraspinal dorsal and lumbar plexuses and in the azygous system


-12% of the patients had either a stenosis or a compression of the arch of the azygous ( " crosse de l'azygos ") and hemiazygous. Those abnormalities resulted in all those cases in a distal stasis in the intraspinal plexus. 


-A venous abnormality at the cervical level was found in 77% of the 80 patients. 
 - 65% of the 80 patients had a stenosis of the IJV ( again here , don't know when to use stenosis or stenose) 
( 16% = bilateral stenosis ; 49% = unilateral stenosis where 33% were mainly found on the left side whereas 16% were found on the right side). 
 -12% were found to have a bone or arterial compression of the innominate venous trunks. 



Out of the 80 patients :

-15% had a normal venous cavo-spinal phlebography.
-25% had one abnormality
-21% had 2 abnormalities
-26% had 3 abnormalities
-12% had 4 and more abnormalities.

Note that those percentages are lower (less important ) than reality because the roots (" les racines") of the azygous were seen only 41 times out of 80 and because the left renal vein was investigated in only 21 patients out of 80 patients. So when the roots of the azygous and the renal vein were investigated, abnormalities were found in 50% of the cases ( one time out of two).



- Out of 80 patients, 60% had at least 2 abnormalities whereas 38% had at least 3 abnormalities.

thanks, Mylène .  I'm floored.  This is not new...
The researcher, Jose Aboulker (1920-2009) was a pioneer of neurosurgery and neurology in France and a renowned anti-Nazi partisan.

Dr. Laurent Garel is a research and interventional radiologist in Montreal (he must have been a student in the 1970s!)


Thursday, 31 March 2011

Amazing video

I saw this clip on a friend's blog, Enjoying the Ride, (see links below at the side) and thought it was worth sharing with you:


Tuesday, 29 March 2011

Downside to treatment?

I guess this is a downside, but one I'll happily live with for all the gains I've had.

My hay fever is back. Every spring, when the daffodils began to flower, I would get snuffly and snotty. Then MS bit, and the hayfever went away. Suppose my immune system had bigger fish to fry. But this spring, lo and behold the hayfever is back along with the daffodils.

Perhaps my immune system has given up on attacking my nerves for a while.

This does sit well with some of the more recent research done, and if more widely experienced, could perhaps be another piece in the jigsaw that is MS. I'm not going to quote all the references in here - there are plenty in the side pages, and it would take too long, but if someone needs some guidance where to look, leave me a question in the comments, and I'll help you out.

Basically, the immune activity kicks in after the lesions have started to form, as a result of hypoperfusion, iron deposition and cell death in the CNS. This in turn is triggered by the blockages in the veins draining the brain and spinal chord. Remove the blockages and the hypoperfusion goes away, inflammation and immune activity in those new areas of damage also cease.

So while treating CCSVI does not remyelinate pre-existing areas of damage, and does not remove long term symptoms experienced by PWMS, it does holt damage being done now, which may not show up as full blown lesions on MRI, and so those with active disease and in the relatively early stages should get the most relief.

Is hayfever a downside then? Or a sign that , at least for now, the damage in my brain has stopped?

I would love to know.

Wednesday, 23 March 2011

how fragile is confidence

It is now six months since I had my procedure, and life is pretty good. MS still reminds me that is has not given up on me; I have TN (trigeminal neuralgia) unless I take my meds regularly, and my left hand and foot occasionally play up.

But overall, the difference is still incredible. From considering wheelchairs to being able to walk without a cane. Getting psyched up to never being able to work again, to coping with a 25 hour week.

So it was a bit of a shock to the system when I had a fall at the weekend. Not as a direct consequence of MS, but I caught my feet in a cable on the floor as I turned, and hit the deck like someone poleaxed.

 So now my body is bruised and battered, but not as much as my confidence. Even now waves of misery and uncertainty pass over me, as I fear that I have lost all that I have gained. Logically, I know that this was the type of fall anyone could have had, but what has logic ever got to do with the fears that lurk in the soul?

Monday, 14 March 2011

When people I know go for the procedure

Holding my breath again this week and crossing every toe and finger as another person I know goes for venoplasty. It seems about two thirds see improvement, sometimes dramatic, as I did, and can be seen in the many YouTube videos across the net.

But what about the other third? I must say I am struck with a form of guilt when I hear their stories. Here I am, so much better than before, and they get nothing. I hope at least that this information will finally crack the enigma that we call MS.

Maybe this is not just one disease, with one set of causes, but a number of different ones, that result in similar signs and symptoms. Getting a diagnosis of MS can be a long and drawn out process for some, as all the alternatives are checked and discarded. For others it seems swift and relatively straight forward. For some, the diagnosis is never clear or straightforward.

So each time I hear of someone I know undergoing CCSVI investigation and treatment, I hope they have the same form of MS as me and all those other responders out there. But sometimes it doesn't work, and all they are left with is hope.

Monday, 7 March 2011

Upset and disappointed

Back in November I took part in a recording for a BBC Radio programme about CCSVI. It was never broadcast. I was annoyed, but ce la vie. I felt it was a shame because there were some doctors interviewed to give a balanced and scientific basis to both sides of the argument.

Today I find out why. On the BBC News website is an announcement of a forthcoming programme about CCSVI labelled Concerns about Controversial MS Treatment. 

It is obviously not intended to be balanced, as is clear from the language used. Doctors "not licenced to practice medicine", another " reported to the doctors' watchdog, the General Medical Council".

Stents are described as little metal tubes and any improvements are "apparent" or "placebo". An "undercover reporter" is scanned and is diagnosed with CCSVI. This is intended to discredit, but shows lack of reasearch by the programme's staff, as nowhere is it claimed that CCSVI is only  found in MS patients, rather that it is found at a signifiantly higher percentage than in the rest of the population.

Meanwhile Biogen report 10 more cases of PML and four more deaths from the approved drug Tysabri, between January 7th and February 2nd.

I had hoped for better from the BBC. This is tabloid journalism, poorly researched and out for a juicy headline.

Friday, 25 February 2011

That wonderful word, normal.

What a wonderfully diverse disease MS is. Just when you think you have a handle on what is going on with your particular brand, it throws you another surprise into the mix.

That is why I am so grateful for, and in some ways scared  by, what my CCSVI treatment has done for me.

What brought this to a head was a combination of entering my plus five months data on CCSVI Tracking   and emails from the clinic in Poland asking about my six month follow up with the doctors there. I sometimes wonder where the time has gone, and then realise it has gone in both living a normal life (wonderful word that, normal) and in waiting for the other shoe to drop.

I am back at work, although not full time. I drive myself about. I can walk to the local shop and back without needing to sleep for 6 hours to recover. I am exercising at a gym, under the watchful eye of my wonderful personal trainer. I feel like I have my life back.

But I still have those dratted holes in my brain, and some intentional tremor in my left hand and leg. Enough to remind me that the MonSter may not have released its grip on me entirely. And I still do the MS person's check on waking - which bits are/are not working today.

To be given a gift , like I have, is to live with the fear that tomorrow may be the day it is all taken away again. It is not placebo, the effects have lasted too long for that. But it may just be the longest and best remission of my life. Amazing how many other people experience remission, starting on that particular operating table.

So tomorrow morning, I will wake up and face the day. All the more thankful for what I have, because I know what it is to lose it.

Monday, 21 February 2011

Women and MS

Currently the diagnosis rate for women with MS is about twice that of men, although 100 years ago it was about even. So why this change?

One factor is the rapid decline in maternal mortality. Researchers estimated the number of women dying around the world in ,2008, during or shortly after pregnancy, to be 342,900, down from 526,300 in 1980. The historical level was about 1 in 100 births.

As MS tends to be diagnosed later in life, how many women died before their disease became apparent?

For those of us interested in CCSVI, it is interesting to note that the rate of  Chronic Venous Disease (CVD) is also twice as high in women as in men.

Here is Dr. Ferlini's genetic study, where she found CCSVI and MS share copy number variations on the same HLA locus region that is associated with MS.

Maybe someone will join up the dots one day............................

Wednesday, 16 February 2011

Dietary Supplements and MS

With thanks to some very well informed MS friends here is an extensive list of supplements used to help patients with MS. It includes references to clinical studies, so that you can follow up with your own research.
Even though these supplements are available over-the-counter, please consult with your doctor before taking any of them, or starting any form of  restricted diet.
Low-Fat Diet

The Swank Diet: Between 1949 and 1984, 150 MS patients were directed to consume low-fat diets. Their intake of proteins, fats, and oils was documented, and subsequent disabilities and deaths were noted. The research team found that people who consumed a low-fat diet had less disease progression and increased survival than their counterparts who ate a higher-fat diet (Swank, 1991).

The Best Bet Diet: Ashton Embury in his various esays , booklets and on-line presentations details a form of diet, which, along with suitable supplements, has become known as the Best Bet diet. For more detailed information see the Multiple Sclerosis Resource Centre.

The link between MS and the types and amount of dietary fats consumed has also been established through epidemiological analysis. A high or increased intake of saturated fats, animal fats, and dairy products (another source of saturated fats, except in the case of low-fat dairy products) is associated with an increased risk of developing MS (Agranoff, 1974; Lauer, 1997; Schwarz, 2005; van Meeteren, 2005).

Vitamin D

The incidence of MS increases the farther one lives from the equator, where exposure to ultraviolet light is at its greatest. Growing evidence linking vitamin D and the risk of MS may begin to explain this latitude phenomenon. Studies show that higher sun exposure during childhood and early adolescence is associated with a reduced risk of MS.

A 2004 study found that women who took vitamin D supplements were 40% less likely to develop MS than women who did not take supplements. (However, this study did not provide enough data to conclude that vitamin D has a beneficial influence on ongoing MS.) (Munger, 2004.)

A 2006 study analyzed blood serum stored from military personnel during their service, and found that those with higher levels of vitamin D were at lower risk for later developing MS. This study adds to growing evidence that vitamin D may help protect against the development of MS. (Munger, 2006)

In June 2007, the Canadian Cancer Society said that based on current research, adults should consider increasing their daily dosage of vitamin D. The society said Canadians should now consume 1,000 IU of vitamin D daily during the fall and winter months, in consultation with a health-care provider.

In a small 2009 study, 25 people with relapsing-remitting multiple sclerosis were given a high dose of vitamin D (14,000 international units, IU, each day for a year) and were compared to 24 people who took a lower dose of vitamin D (1,000 IU a day for a year). In the high-dose group, 16% of the people had a relapse, compared to 40% in the low-dose group. As a bonus, the high dose group reported no side effects from the vitamin D supplement.

• Do not take vitamin D if you have hypercalcemia.
• Consult your doctor before taking vitamin D if you are taking digoxin or any cardiac glycoside.
• Only take large doses of vitamin D (2000 international units or 50 micrograms or more daily) if prescribed by your doctor.
• See your doctor frequently if you take vitamin D and thiazides or if you take large doses of vitamin D. You may develop hypercalcemia.
• Chronic large doses (95 micrograms or 3800 international units or more daily) of vitamin D can cause hypercalcemia.


There is considerable statistical evidence that the incidence of MS varies in countries where the diet differs.

Evidence shows that a higher consumption of polyunsaturated fatty acids, especially omega-3 fatty acids, is associated with a decreased risk of MS and slower disease progression in people who have milder forms of the disease (Agnello E et al 2004; Bates D 1990; Swank RL et al 1990; Swank RL 1991; Zhang SM et al 2000). Increased consumption of omega-3 fatty acids may moderate the course of the disease. (Agnello, 2004; Ferrucci, 2005; Nordvik, 2000; Shapiro, 2003).

A 1989 study looked at the long-term effects of omega-3 fatty acids in the treatment of MS, and concluded that there were improvements in the treated group when compared to the control group in terms of duration, frequency and severity of relapses, and the number of patients who either improved or remained unchanged. (Bates, 1989.)

A 2005 study investigated the effects of dietary fat consumption on the course of disease in patients with RRMS. Researchers found that a low-fat diet supplemented with omega-3 fatty acids had moderate benefits in terms of physical components of health status and quality of life. Patients also experienced lower relapse rates while on the supplemented diet than they did in the preceding year (Weinstock-Guttman, 2005).

There are three major types of omega-3 fatty acids that are ingested in foods and used by the body; they are also available as over-the-counter dietary aids:

-- alpha-linolenic acid (ALA), an organic compound found in many vegetable oils, seed oils, nuts and green vegetables;

-- eicosapentaenoic acid (EPA), is obtained by eating oily fish or fish oil—cod liver, herring, mackerel, salmon, menhaden and sardines;

-- docosahexaenoic acid (DHA), is obtained from fish oils; DHA is actively promoted by manufacturers as a food additive. There is less DHA available in the average diet than formerly, due to cattle being taken off grass and fed grain before butchering; likewise, there is less in eggs due to factory farming.

• Consult your doctor before taking EPA/DHA if you take warfarin . Taking EPA/DHA with warfarin may increase the risk of bleeding.
• Discontinue using EPA/DHA 2 weeks before any surgical procedure.


Omega-6 fatty acids are a family of polyunsaturated fatty acids. Blood tests have revealed that MS patients have lower levels of omega-6 fatty acids than people without MS.

-- Linoleic acid is an essential omega-6 fatty acid, found in high concentration in sunflower and safflower oil as well as in lower concentrations in most other vegetable oils; also available as a dietary supplement.

Studies, beginning in the early 1970s, suggest that diets high in linoleic acid can be helpful for MS patients. Patients who supplemented their diet with linoleic acid had longer remissions and reduced the severity of their attacks. A 1984 study reported that some MS patients have abnormally low levels of linoleic acid. (Homa, 1984.)

In another 1984 study, the results of several clinical trials of linolenic acid supplementation for the treatment of MS were evaluated by meta-analysis. The conditions of 87 patients with MS and 85 normal control subjects were assessed for neurological changes over 2.5 years. Patients with low levels of disability at the beginning of the study had a smaller increase in disability over the study period than did the control subjects. In addition, linoleic acid was found to reduce the severity and duration of MS episodes in patients at all levels of the disease (Dworkin, 1984).

The best natural sources for linoleic acid include black currant seed oil and borage oil, both available as dietary supplements. Sunflower seed oil is also rich in linoleic acid and can be used in cooking.

-- Gamma-linolenic acid (GLA) – Another omega-6 fatty acid. Ordinarily, the body makes all the GLA it needs from linoleic acid. But this conversion is occasionally interrupted or inhibited, especially in inflammatory diseases. (Horrobin, 1997, 2000; Jamal, 1994; Kidd, 2001.) Defects in conversion may have a genetic basis, which is thought to predispose some people to inflammatory conditions (Horrobin, 2000).

GLA quells inflammation by competing with pro-inflammatory arachidonic acid. In animals with MS, GLA-fed animals fared significantly better than did control animals (Harbige, 2000).

GLA is available directly from evening primrose oil, black currant seed oil, and borage oil. Most of these oils also contain some linoleic acid.

• GLA should be taken with food.
• Individuals undergoing treatment for cancer should not take GLA (or any other supplement) except under physician supervision.
• Consult your doctor before taking GLA if you take warfarin. Taking GLA with warfarin may increase the risk of bleeding.
• Discontinue using GLA 2 weeks before any surgical procedure.
• GLA can cause gastrointestinal symptoms such as nausea and diarrhoea.


Antioxidants neutralize naturally-occurring but harmful chemicals known as free radicals. MS patients tend to have abnormally low levels of certain key antioxidants. (Mai,1990; Mazzella, 1983; van Meeteren, 2005).

Supplemental antioxidants support cellular antioxidant defenses by scavenging free radicals; reducing inflammatory cell responses by interfering with gene transcription, protein expression, and enzyme activity; and by chelation of metals. Antioxidant therapy in animals with MS has yielded decreases in clinical signs of the disease (van Meeteren, 2005).

-- Selenium, Vitamin C and Vitamin E:

In a small 1990 study, patients with MS were given an antioxidant mixture containing 6 mg of sodium selenite (equivalent to 2740 micrograms of elemental selenium), 2 grams of vitamin C, and 480 mg of vitamin E, once a day for 5 weeks. Although glutathione peroxidase levels were initially lower in patients with MS than in normal control subjects, after 5 weeks of antioxidant therapy, levels of this antioxidant increased 5-fold; side effects were minimal (Mai J et al 1990).

Selenium is available as a dietary supplement, but the best source of natural selenium is Brazil nuts.

N acetyl cysteine (NAC)

NAC is a potent antioxidant. NAC can increase glutathione levels, which increases antioxidant capacity.

MS patients tend to have abnormally low levels of certain key antioxidants, such as glutathione peroxidase (Mai, 1990; Mazzella, 1983; van Meeteren, 2005). Glutathione is available in supplement form, but it is poorly absorbed. A better strategy for increasing the body's supply of glutathione is taking NAC. (Arfsten, 2004; Kidd, 2001).

In animals with MS, NAC has been shown to reduce nitric oxide production in brain-supporting tissues and reduce clinical symptoms and microscopic evidence of brain cell injury and inflammation (de Bustos, 2000; Gilgun-Sherki, 2005; Syburra , 1999).

• NAC clearance is reduced in people who have chronic liver disease.
• Do not take NAC if you have a history of kidney stones (particularly cystine stones).
• NAC can produce a false-positive result in the nitroprusside test for ketone bodies used to detect diabetes.
• Consult your doctor before taking NAC if you have a history of peptic ulcer disease. Mucolytic agents may disrupt the gastric mucosal barrier.
• NAC can cause headache (especially when used along with nitrates) and gastrointestinal symptoms such as nausea and diarrhoea.

Coenzyme q10

Coenzyme Q10 (CoQ10) is another antioxidant of potential usefulness in treating MS and, while there is some debate, its levels may be low in patients with MS (Syburra, 1999). Although CoQ10 has not been investigated specifically for the treatment of MS, it is generally recognized as safe, well tolerated, and potentially useful in the treatment of neurodegenerative disorders.

CoQ10 is a naturally occurring, lipid-soluble antioxidant that serves as a co-factor in the mitochondrial respiratory chain. As an added bonus, CoQ10 is capable of regenerating the antioxidant capacity of spent vitamin E in the body. Decreased levels of CoQ10 are associated with many disease states, including heart disease, cancer, and neurodegenerative diseases (Bonakdar, 2005; Siemieniuk, 2005).

DOSAGE: “I would not feel comfortable recommending to my patients to take more than 50 mg or maximum 100 mg of CoQ10 a day, unless for the temporary treatment of a medical condition.”

“The daily dosage of CoQ10 in healthy individuals is generally in the 15-30 mg range and is taken for general well-being. In patients with heart disease or other chronic conditions, a minimum of 100 mg a day has been used in numerous clinical trials. A dosage in the range of 600-1200 mg is being used in the on-going study on Huntington’s disease, supported by the National Institutes of Health.”

“If on a statin drug, 60 to 90mg per day is suggested.”

Cautions: See your doctor and monitor your blood glucose level frequently if you take CoQ10 and have diabetes. Several clinical reports suggest that taking CoQ10 may improve glycemic control and the function of beta cells in people who have type 2 diabetes.

Lipoic Acid

Lipoic acid, also known as alpha-lipoic acid, is a sulfur-containing fatty acid. It is found inside every cell of the body, where it helps generate the energy that keeps us alive and functioning. Lipoic acid is a key part of the metabolic machinery that turns glucose (blood sugar) into energy for the body's needs.

Lipoic acid is an antioxidant, but unlike other antioxidants, which work only in water or fatty tissues, lipoic acid is unusual in that it functions in both water and fat. By comparison, vitamin E works only in fat and vitamin C works only in water. This gives lipoic acid an unusually broad spectrum of antioxidant action.

Lipoic acid has been studied specifically in MS. Known to cross the blood-brain barrier and to penetrate cellular mitochondria, lipoic acid decreases the activity of intercellular adhesion molecule-1, a small molecule that plays a role in the genesis of MS. It is believed that ICAM-1 and other adhesion molecules are responsible for allowing certain pro-inflammatory immune system cells, namely T-lymphocytes, to cross the blood-brain barrier, paving the way for induction or exacerbation of damage to neurons (Biernacki, 2004; Cournu-Rebeix, 2003; Dedrick, 2003).

In experiments on rodents with MS, lipoic acid produced significant reduction of demyelination and reduced the infiltration of inflammatory T-cells across the blood-brain barrier (Marracci, 2002, 2004; Morini, 2004).

In 2005, in a small clinical trial of lipoic acid in the treatment of patients with MS, thirty-seven patients with MS were randomly assigned to receive various doses of lipoic acid (up to 2400 mg/day) or placebo. Lipoic acid was generally well tolerated and reduced ICAM-1 levels, as well as interfered with T-cell migration into the central nervous system (Yadav, 2005).

There are two types of Lipoic acid: the synthetic S form, and the natural R form. R-Lipoic acid is much more potent (2 times on average) than commonly sold synthetic lipoic acid which contains both the R and S forms of lipoic acid. The S form is chemically the mirror image of the R form of lipoic acid and cannot be used by the body, hence it is useless. Make sure you buy the R form. Fifty mg of R-Lipoic Acid is equivalent to 100 mg of synthetic lipoic acid.


• Lipoic acid may lower blood glucose levels. Consult your doctor before taking lipoic acid if you have diabetes and glucose intolerance; monitor your blood glucose level frequently.

Acetyl L-carnitine (ALCAR)

ALCAR is a derivative of amino acids, naturally produced by the human body. Meat, poultry, fish, and dairy products are the richest sources of L-carnitine. Commercially, it is often marketed as a "life extension" supplement.

A 2004 study showed that acetyl L-carnitine was more effective than amantadine (a prescription drug) for the treatment of fatigue in MS (Thomassini 2004). (Dosage for this trial was 1g twice daily.)

However, the percentage of LCAR that is absorbed when taken via oral supplementation is much lower than that from food sources. In one study, it was shown that approximately 20% of orally supplemented L-carnitine is absorbed, with a bioavailability of roughly 15%, as compared to a bioavailability of between 60% and 75% when absorbed from food.
Vitamin B12

Vitamin B-12 is naturally found in foods of animal origin including meat (especially liver and shellfish) and milk products.

When a patient is B-12 deficient, injection is sometimes used if digestive absorption is impaired. There is evidence that injection may not necessary with modern high potency oral supplements (such as 500 to 1000 mcg or more).

Vitamin B-12 is important for the normal functioning of the brain and nervous system and for the formation of blood. Vitamin B12 plays a key role in the generation of myelin. MS and vitamin B12 deficiency share remarkably similar characteristics, occasionally rendering correct diagnosis difficult (Miller, 2005). Some physicians prescribe vitamin B12 supplements for MS patients.

A 1992 study showed that MS patients often have abnormally low levels of vitamin B12 in their cerebrospinal fluid and/or blood serum (Reynolds, 1992).

In a 2001 study, MS patients who received vitamin B12 supplements reportedly experienced consistent clinical improvements in their symptoms (Kidd, 2001).

In a 2002 study, researchers investigated the effects of 6 months of vitamin B12 injections (1 mg/week) on 138 MS patients. Researchers concluded that the patients improved after starting vitamin B12 injections (Wade, 2002).


Glucosamine, an over-the-counter natural product that has been shown to help with arthritis, may also provide some relief to MS patients.

In a 2005 study, neurologists at Jefferson Medical College, using the mouse model of MS, found that doses of glucosamine similar to those taken for osteoarthritis dramatically delayed the onset of symptoms, and improved the animals' ability to move and walk. The animals’ spinal cords and found less inflammation and “demyelination” in those that were given glucosamine. (Rostami, 2005.)

N-acetylglucosamine (GlcNAc, or NAG)

Previous studies which suggested that glucosamine has some value in the treatment of MS (see above), led Michael Demetriou and colleagues at the University of California, Irvine, to investigate a similar but more potent compound called N-acetylglucosamine (GlcNAc).

In a 2007 study using the mouse model of MS, NAG inhibited the growth and function of abnormal T-cells that incorrectly direct the immune system to attack specific tissues in the body, such as brain myelin in MS.

Defects on cell-surface sugars may promote the short-term inflammation and long-term neurodegeneration that occurs in the central nervous system of MS patients.

Demetriou found that the dietary supplement N-acetylglucosamine (GlcNAc), which is similar but more effective than the widely available glucosamine, corrected defects in protein glycosylation in cells and inhibited inflammatory demyelination in mice. The new study opens the possibility that metabolic therapy with GlcNAc may also prevent neurodegeneration.

The findings suggest that NAG may be useful as an oral therapy to correct neurodegenerational defects and to treat both short-term and long-term symptoms of MS. (Demetriou, 2007.)


People who get gout almost never get MS. A 1998 study showed that MS and gout are almost always mutually exclusive; people almost never have both diseases. In a review of 20 million Medicare and Medicaid patient records, researchers discovered almost no overlap between multiple sclerosis and gout. (Hooper, 1998.) This may have something to do with uric acid.

Uric acid is a chemical created when the body breaks down substances called purines. Purines are found in some foods and drinks, such as liver, anchovies, mackerel, dried beans and peas, beer, and wine. Most uric acid dissolves in blood and travels to the kidneys, where it passes out in urine.

If the body produces too much uric acid or doesn't remove enough if it, disease results. Abnormally high levels of uric acid in the body result in a number of disorders including hypertension, cardiovascular disease, renal disease, and gout. A number of studies have shown that MS patients have been shown to have abnormally low levels of uric acid (Peng, 2007 and others).

MS exacerbations are often treated with intravenous methylprednisolone. A 2002 study showed that methylprednisolone therapy increases serum uric acid levels, suggesting that increasing the uric acid concentration may represent one of the mechanisms of action of methylprednisolone in MS patients. (Toncev, 2002.)

Another 2002 study showed that uric acid levels in MS patients correlate with activity of disease and blood-brain barrier dysfunction. (Toncev, 2002.)

A 2008 study noted that “a reduced uric acid concentration has been linked to multiple sclerosis, Parkinson's disease, Alzheimer's disease, and optic neuritis. Historically, uric acid has been considered a marker of these disease states. Recent studies, however, have provided evidence that uric acid may actually play a role in the development or progression of such diseases.” (Kutzing, 2008.)

Uric acid can't be administered orally, because it is degraded by the gastric process before it reaches the bloodstream. However, uric acid levels can be raised by the oral administration of inosine, an over-the-counter supplement.

Two different mechanisms of action have been proposed. First, inosine produces uric acid after ingestion, which is a natural antioxidant; second, it has been shown to induce axonal rewiring in laboratory animals with stroke and spinal cord injury

In a 2006 study, MS patients treated with inosine were found to have a lower relapse rate than non-treated MS patients. (Toncev, 2006.)

Another 2006 study suggests that therapeutic strategies aimed at raising serum uric acid levels may have a neuroprotective effect on MS patients. (Koch 2006.)

In a 2009 study, oral administration of inosine was used to raise serum levels of the natural peroxynitrite scavenger UA in 16 patients with RRMS during a 1-year randomized, double-blind trial. Results showed that increased serum UA levels correlated with a significant decrease in the number of gadolinium-enhanced lesions and improved EDSS.

The only side-effect correlated with inosine treatment was kidney stone formation in 4/16 subjects.

Monday, 14 February 2011

MS and the sense of self

One of the most common phrases I hear from people who have had the CCSVI treatment is "I have my life back". This, along with the sensation of gaining some control back.

This made me begin to think about what MS does to us. MRIs give a picture of lesions in our brains and spinal chords, while functional testing by neurologists and others can measure what is happening to our physicality, but what about "US".

The betrayal by our bodies, which cease to obey even the most basic commands, leaves us uncomfortable in our own skins.

But it is not just this that causes our loss of self. Cognitive failure of varying degrees of severity also chips away at our sense of who we are. The fog that fills our brains displaces all but the most rudimentary thoughts.

It can be deeply distressing for a journalist to lose the grasp of language, to struggle to find an appropriate word. The struggle of a former professor to organise his or  her thoughts, to apply lessons learned, to come up wth alternate solutons to problems. To be unable to read a simple story, because each sentence disappears as soon as it is fnished. The parent who can no longer help their child wth the simplest of homework.

With that loss of function comes a decided feeling of loss of self., wth all the distress that entails.

This, the hardest thing to quantify, may be one of the most distressing effects of this disease.

Tuesday, 25 January 2011

I survived the gym

Despite last minute trepidation and a strong desire not to go, I made it through my first gym session today. I started by using an MS knowledgeable trainer, to make sure I did things properly and got the most out of it

The trainer was worth every penny, as he took me through the exercise machines and stretches, working out what was best for me. Although it wasn't  a full workout, I was getting tired by the end. But we have set out  a detailed plan for me, including stretches to do at home, in between gym sessions. Having someone there , as well as helping me do things correctly,  helped keep me going rather than giving up and going home.

Once I had showered and dressed, I did feel quite energised, although I think I'll sleep well tonight. This seeems to fit in with current findings. Read more here.

Although in the past it was thought that exercise was not suitable for MS  patients, because of the fear that it might bring on an exacerbation.

But latest information is that exercise may actually help protect our brains, reducing inflammation and loss of white matter. Which also fits with the CCSVI hypothesis, as exercise will improve circulation in the brain.

So roll on Friday and my next session.

Monday, 24 January 2011

4 month update

Still feeling the benefit, so I guess no re-stenosis, and no placebo effect.

It has been a while since I posted because I have been caught up in ordinary life. Yes, folks, you did read ordinary. Such a plain word, but so magical for a person with MS. How many times have we uttered the cry "I just want to be normal", only to find ourselves adapting to our new normal. Which is not what most people would consider normal at all.

Christmas and New Year have come and gone, along with the snow and really severe frosts. Although Winter may still have some surprises up her sleeve. But the first snowdrops are poking their heads out of the ground. Spring can't be that far away.

We were looking at some photos of being out in the snow last night. Last years ones were obvious - they were the ones where I was using a stick.

I am logging my status on CCSVI tracking and looking forward to my six month check-up in Poland. One thing that friends have commented on is that the tracking site tends to show a big initial improvement, then a gradual decrease as time goes by. I wonder though if this is a genuine deterioration, or others like myself find it harder and harder to remember what their pre-operation state was like.

The act of recording makes you focus on every little thing, and what would have been ignored in the general scheme of things assumes an overly great significance. It is not always MS.

But I have still come so far. I work 20-25 hours a week. I can read and comprehend something first time through. I have signed up at a gym with a personal trainer who knows about MS. No stick. My bladder functions like it belongs to an adult not a toddler. I get tired and sleep normally. I don't need medication just to get through a day.

Thank you Dr Zamboni.