Location and MS Risk in Canada

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Location and MS Risk in Canada

Postby Dunmann » Thu Oct 13, 2005 5:23 am

A study in Canada which shows MS risks based on province, with a speculative link to mercury (from coal-fired electrical generating plants).

The link.
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Postby dignan » Thu Oct 13, 2005 6:15 am

Interesting study. I'm most curious about the differences between Ontario and Quebec. Quebec has significantly lower incidence than Ontario, but on average, the population is further north and not at higher elevation. It makes me think that the difference would most likely be from dietary differences or genetic differences since Quebecois are more French and Ontarians more Anglo-saxon. If I remember correctly, France has lower incidence of MS than the UK...
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Postby bromley » Fri Oct 14, 2005 2:06 am

Dignan,

France and the UK have similar populations - around 60m

The number of MS sufferers in the UK is said to be 85,000 and the number in France 60,000.

The UK includes Scotland which has one of the highest MS rates in the world - and many Scots emigrated to Canada.

But the position is complicated in that the Normans (the French who invaded England in 1066) were from Scandinavian stock (and the theory is that MS originated in Sweden and was spread by the Vikings). So the French in Canada could have a mixture of genes - some with Viking genes some without.

For anoraks like me the MSIF site has a list of all countries with an estimate of the number of MS sufferers. I suspect that the real number is much higher and a neuro at the Institute of Neurology also thought so. The UK newspapers this week were talking about a diabetes epidemic. I suspect that MS is also going through a boom time - tracking the revenues of the CRAB manufacturers should give an indication of an increase.

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Postby Melody » Sun Oct 16, 2005 2:55 pm

I was raised in Quebec and every Quebecer I know takes a TBS of cod liver oil. We had to each morning before we got on the bus. Ontario doesn't use it like Quebec did. Quebec is also major into Dairy farms as well as pulp and paper but all in all a wholesome type of life. More smaller towns and still allot of home cooking. Ontario is faster and more fast foods. Not sure what this tells us though :lol:
John was diagnosed Jan 2005. On lipitor 20mg .On Copaxone since July 4,2005. Vitamin D3 2000iu-4000iu (depending on sunshine months)June 10 2005(RX::Dr. O'Connor) Omega 3 as well Turmeric since April 2005. Q10 60mg. 1500mg liquid Glucosamine Nov 2005.
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Postby Nick » Mon Oct 17, 2005 11:16 am

The one key environmental factor involved in MS that can
explain the anomalously high MS rate in Alberta is vitamin D
deficiency. Vitamin D deficiency is more common in Alberta than
other provinces, except perhaps Saskatchewan, because of the
high latitude of the populous areas. Half of the population of
Alberta resides at latitude greater than 53 degrees north.

This contrasts with the populations of Ontario and Quebec that
mainly reside south of latitude 50 degrees. The populations of
other provinces, with the exception of Saskatchewan, also reside
at significantly lower latitudes than the population of Alberta.

The CLO might also be a factor. The relatively low prevalence of MS in fish eating Newfoundland supports this element as being protective. By the same token, rates of MS in Newfoundland are 3 to 5 times as high as sun drenched Queensland, Australia.

Don't forget the huge drop (85%) in MS risk enjoyed by migrants from MS prevalent and sun deficient Great Britain to Queensland, either.

Ahoy dar matey, it's da vitamin D. That's the rub.

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Postby bromley » Mon Oct 17, 2005 12:41 pm

Nick,

The Vit D angle is extremely interesting and looks convincing i.e. vit D deficiency in susceptible people allows the disease to kick off. I'm surprised that there is not more robust research in this area. As already noted elsewhere, more men tend to have outside jobs which might explain the gender difference. The relatively recent skin cancer advice (cover up) might explain increases in MS - the Australian MS Society website says that MS is increasing by 8% per annum (I assume number of diagnoses).

But some simple tests might provide a clearer picture e.g. for men an analysis of jobs for those dx. One would expect those dx'd to be office workers rather than farmers / roofers etc. Another angle would be prisons where prisoners would only have limited exposure to the sun.

I would be grateful for any info on Vit D supplements. I eat plenty of oily fish and now get as much sun as possible. However, when I asked my health store they said 'calcium tablets' and did not have any Vit D tablets. What about sunbeds - do they provide Vit D? And will taking Vit D after dx make any difference?

At least global warning and the thinning ozone layer should be beneficial to future generations!

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Postby Melody » Tue Oct 18, 2005 8:30 am

You need vitamin D3 and Dr. O'Connor from St. Mikes the one heading that study prescribes between 2000iu and 4000iu. He is one of hubby's Doctor's. My hubby used to be a roofer and was outside all the time. He had no MS showing up at that time. Now about 10 years back our company took off well enough that hubby only oversees the roofer's and no longer spends much time on the roof. Feb 1998 was his first attack. I can't blame it on less vitamin D totally as we had a boat at the time and literally spent everyday in the summer on the water. Hubby is taking about 2300iu and 2500iu of Vitamin D3 per day and has improved greatly but so much has changed this year it is hard to say it was the vitamin D3. :D


Vitamin D3 (Vitamin 1,25(OH)2 D3) is a naturally occurring bodily substance that many believe to exert a protective effect in multiple sclerosis - both in the development of the disease and in limiting its progression. It is naturally produced in the skin in response to sunlight but is also present in certain foodstuffs (particularly oily fish). It is also available as a dietary supplement from health food stores.

Strictly speaking, because your body can produce it, Vitamin D3 isn't a vitamin. It's a type of steroid hormone and among other things, a powerful mediator of immune function.

D3 is best known for it's effects on calcium metabolism. Proper levels are necessary to maintain bone mineral density and serum (blood) calcium levels. This is especially true among the very young where it is used to treat rickets and in combination with vitamin A for the treatment of osteoporosis in the elderly, particularly post menopausal women who are often subject to fractures due to loss of bone density.

In studies, Vitamin D has been found helpful against autoimmunity for the down-regulation of Th1 and up-regulation of Th2 cells. It has also been shown to regulate the neurotrophins NGF (Nerve Growth Factor), NT-3 (NeuroTrophin 3) and NT-4. In addition, D3 has also been found to promote differentiation and cell death in neuroblastoma (brain tumour) cell lines as well as cancers in general making it a possible weapon against tumours.

D vitamin supplements available over the counter (cholecalciferol) and those included in foodstuffs like milk (D2) are precursors to transcriptionally active D3, actually to 1,25(OH)2 D3 the active form of vitamin D.

1,25(OH)2 D3 is created by your body in the following way.

UV or sunlight at between 290 and 315nm and heat on the skin results in the conversion of a molecule called 7-dehydrocholesterol (pro-vitamin D) into cholecalciferol.

The cholecalciferol or pre-vitamin then goes through two hydroxylations (additions of hydrated oxygen atoms -OH). The first usually happens in the mitochondria (a cytoplasmic organelle) of liver and kidney endothelial cells. This creates the relatively abundant 25OHD3. that's a weak form of Vitamin D3 which has a sterol or steroid "ring" structure. 25OHD3 then goes through another hydroxylation, mostly in the kidney's mitochondria, resulting in 1,25(OH)2 D3 which is really the subject here.

These hydroxylations are also performed by immune system cells under specific conditions. This "extrarenal" synthesis seems to have an "autocrine" role in certain types of cellular immune responses which mediate lymphoid cells (both B and T cells) as well as myeloid cells.

The process by which solar or U.V. light initiates VD3 synthesis is self limiting, so too much such exposure is unlikely to ever cause VD3 overdose.

As with all hormones and other messenger proteins, VD3 is only one part of the story. The communication requires a means of "hearing" and then acting on the message.

The active form of D3 has a particular molecular "tail" called a "side chain". That tail fits receptors in many cells in your body like a key into a lock. These receptors are called VDR or vitamin D receptors. Fitting themselves into these receptors, the VD3 molecules might be thought of as flipping switches that, depending on the cells in question, set any of several processes in motion by allowing the VDR to interact with a variety of VDRE (Vitamin D Response Elements).

In reality, a VDR (vitamin D receptor) usually forms a heterodimer with an RXR receptor. Thats "hetero" as in differing and "dimer" meaning a pair. So the VDR is almost always really an VDR-RXR joined pair of two different receptors. The RXR is a receptor that fits retinoic acid

There are many different VDRE. These "elements" signal sections of the host cell DNA that are "upstream" of the genetic region being activated. Keeping in mind that every nucleated cell in our bodies contains our complete genome, it becomes clear that we need a way to activate the specific sections of those genes pertinent to the tasks at hand.

These tasks include regulating serum (blood) calcium levels, stimulating cellular differentiation and subsequent apoptosis (cell death), as well as modulating the production of cytokines (messenger proteins) that pass signals within the immune and some other systems.

The role of Vitamin D3 in Multiple Sclerosis

Multiple Sclerosis is a neurodegenerative disease of the CNS (the Central Nervous System.) Both the myelin sheathing around nerve tissue and the axons or tissue themselves which conduct nerve impulses undergo an attack primarily mounted by the immune system. Over time this attack leaves scars called lesions which interfere with the transmission of signals to and from the brain. This immune attack against the "self" is called autoimmunity.

Epidemiologists have long observed a geographical north south gradient in MS occurrence. Moving further from earth's equator, there are more MS cases per capita. And among populations with similar genetics, those living at very high elevations are statistically less likely to contract MS than those below who live beneath a thicker layer of U.V. diminishing air.

Coastal populations where diets are rich in fish containing D3 are also less likely to have MS than inlanders in those same regions without fish in their diets.

These findings and our reliance on sunlight to produce VD3 coupled with its increasingly well documented immune system modulation have led many in the medical and research communities to suspect that a deficit of VD3 is involved in the development of multiple sclerosis.

It is beyond the scope of this article to fully describe the interactions of VD3 and immune system elements. If it were even currently possible, doing so would probably require several volumes. Of necessity, the following is only a few pertinent lines from a very long play.

Here's a snapshot of an immune system interaction.

An infectious agent like a virus or bacterium invades the body stimulating a response by the compliment system, killer T- cell and macrophage attack.

The infectious agent has molecules on it's surface that the body uses to identify it. These are called antigens. Macrophage actually engulf and dissolve invaders, they remove the antigen molecules from the invaders surface and act as APC (Antigen Presenting Cells) presenting examples of the antigen surface in order to recruit T and or B lymphocytes which produce receptors that fit the challenging antigens shape as a means of identifying it.

Next come the production of two types of cells, effectors and helpers. The helpers are those that "remember" the invading antigen by multiplying and generating more cells with surface receptors that fit it. These cells circulate throughout the body watching for the invaders return appearance. If it reappears, these cells stimulate the clonal production of both helper cells like themselves and effector cells which actually attack the challenging antigen.

Various stages of that process are controlled by messenger proteins called cytokines. There are over 100 different often structurally unrelated cytokines which fall into several families such as Interleukins (IL), Interferons (IFN) and Tumour Necrosis Factors TNF). Cytokines often work by controlling the direction of genetic transcription leading to immune cell production.

Most cytokines are very short lived, only working over short distances. Generally this short existence means that a cytokine acts only on the cell that produced it. It's called an "autocrine" effect. Those cytokines acting on other cells exhibit a "paracrine" effect. Usually that means other cells in the immediate area of the cell producing the cytokine. You'll often see that immediate area called a "micro-environment"

This is where VD3 enters. VD3 transcriptionally regulates cytokine production leading to differentiation (lineage maturation) and mitosis (multiplication) of these immune cells in subtle sometimes complex ways.

For example; 1,25(OH)/2D3 blocks animal models of (autoimmune) diabetes without generalized immuno-suppression. On the other hand VD3 actually increases the immune response by macrophage against bacteria. In some studies serum levels of 1,25(OH)/2D3 coincide with survival rates among those infected by HIV.

MS is typically characterized as presenting an elevated ratio of Th1 to Th2 cells. VD3 at least partially corrects that imbalance

VD3 influences ratios between these T-helpers reducing the over-proliferation of T and B leukocytes. this is partially caused at the hematopoietic level. that is at the point of blood cell creation in the bone marrow as well as at the point of leukocyte maturation in the thymus.

Vitamin D receptors have been found in both T and B lymphocytes maturing in the medulla of the thymus.

while glucocortical steroids limit maturation of many of these lymphocytes through apoptosis, some of those resistant to glucocorticoids may be stopped by VD3s ability to signal teir differentiation along a pathway leading to apoptosis rather than maturity as cytotoxic cells.

Vitamin d receptors are also found in cells of the lymph nodes and tonsils where VD3 down-regulates effector cell expression.

By these mechanisms VD3 actually has a biphasic effect on the immune system. Rather than a simple downregulation of immune response it blunts generalised over-proliferation of both lymphocytes and monocytes while sharpening the immune system attack on specific targets.

Copyright Ed Hill, 2002
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John was diagnosed Jan 2005. On lipitor 20mg .On Copaxone since July 4,2005. Vitamin D3 2000iu-4000iu (depending on sunshine months)June 10 2005(RX::Dr. O'Connor) Omega 3 as well Turmeric since April 2005. Q10 60mg. 1500mg liquid Glucosamine Nov 2005.
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Postby Nick » Tue Oct 18, 2005 12:10 pm

Mel

Thank you for your input.

If your history with hubby has occurred in Ontario then you will both experience a vitamin D winter for some portion of the year, unless one has supplemented or used a tanning bed. Since vitamin D has a half life of two months in ones body you need to either have adequate exposure to strong direct UVR or take appropriate supplements all year round.

Rather than accentuate the amount per day of UVR exposure or supplementation, the best determinant of ones serum vitamin D is to have it measured by blood analysis. For immunoregulation purposes, an internal concentration of 25 hydroxy>= 125 nmol/L is considered ideal.

You don't state the degree of symptoms your man has. Perhaps his history of sun exposure has determined the age of onset (as you have alluded to) or the extent of CNS impairment.

Although O'Connor downplays the dietary aspect of MS, he was a participant in the studies which demonstrated MS and Type 1 diabetes to share the same disease process and that a dairy protein (butriphyllin SP?) is a risk factor in MS.

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Postby Melody » Tue Oct 18, 2005 12:58 pm

When we saw Dr. O'Connor on June 10 2005 he pretty much felt hubby had PPMS. At that time hubby was blind in one eye no color nor shapes. He also limped noticeably and he had pins and needles as well as burning pain. He slept about 16 hours per day and I held the fort together. I realize when Dr. O'Connor saw hubby he had no improvement not from the attack in 1998 nor the one in Aug 2004. Since it was June 2005 Dr. O'Connor felt we were past the window where improvement would take place. He siad all he could offer us was the retuxin study as well as 2000iu -4000iu of D3.Now you will think I'm nuts but I had started different diet and exercise changes in Jan when we were diagnosed. When your system is running fine it actually smells different. You don't get odd odors when you pas gas nor do you get the best you check your drawers type of sounds. I believe at that time he suffered from leaky gut although never diagnosed. He also had restless leg as well as eczema. Loads of allergens being added through foods some intolerant some pretty much poison to him. We of course started with an allergist when diagnosed as well as balancing stomach flora with antibiotics 3 week course. All is well right now he no longer limps has pins and needles nor the burning type pain (I really don't understand this one as I've never had it)His eye now sees color and shapes although he is still clinically blind in it. He also sleeps about 8 hours per day no circles under his eyes and carrying his own weight once again. This is a big change for us as we were on a steady decline in his health since 1998 and at our last appointment in October the only sign left that he has MS is the eye. All other's are gone and the neurologist said without the eye he would be at an EDSS of 0 as he has no weakness in any limbs. Diet,vitamin D3, turmeric, Omega 3 as well as flax were started in the winter and spring of 2005. Lipitor was started in Aug 2004 and Copaxone was started July 4 2005. All the changes started in hubby around the end of June so Copaxone was not an initial factor. Like a giant gig saw puzzle I know buy hope this helps
John was diagnosed Jan 2005. On lipitor 20mg .On Copaxone since July 4,2005. Vitamin D3 2000iu-4000iu (depending on sunshine months)June 10 2005(RX::Dr. O'Connor) Omega 3 as well Turmeric since April 2005. Q10 60mg. 1500mg liquid Glucosamine Nov 2005.
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Postby Nick » Tue Oct 18, 2005 1:26 pm

bromley wrote:Nick,

The Vit D angle is extremely interesting and looks convincing i.e. vit D deficiency in susceptible people allows the disease to kick off. I'm surprised that there is not more robust research in this area. As already noted elsewhere, more men tend to have outside jobs which might explain the gender difference. The relatively recent skin cancer advice (cover up) might explain increases in MS - the Australian MS Society website says that MS is increasing by 8% per annum (I assume number of diagnoses).


Ironically this studyout of Australia found the correlation between MS and the inverse of ultra violet radiation levels to be stronger than that of skin cancer (melanoma) and ultra violet radiation levels.


bromley wrote:But some simple tests might provide a clearer picture e.g. for men an analysis of jobs for those dx. One would expect those dx'd to be office workers rather than farmers / roofers etc.


This study entitled Mortality from multiple sclerosis and exposure to residential and occupational solar radiation: a case-control study based on death certificates addressed the issue of vocation and MS.


bromley wrote:I would be grateful for any info on Vit D supplements. I eat plenty of oily fish and now get as much sun as possible. However, when I asked my health store they said 'calcium tablets' and did not have any Vit D tablets. What about sunbeds - do they provide Vit D? And will taking Vit D after dx make any difference?



You'll have to find this out on your own. Suffice to say I use vitamin D3 supps (made in Canada) from Jamieson that are in 1000 IU denomination pills.

Shame on you bromley, you really should read the information on out site prior to asking questions.

This paper documents the seasonal fluctuations between exacerbations and serum vitamin D content over the course of a year. The very close correlation suggests that vitamin D levels can positively affect the progress of MS.

Unfortunately there has not been much research which addresses the issue of vitamin D as an active therapy. Not surprising since there's no money to be made on this issue. As for prevention, the dataset indicates the effectiveness would be close to 100%, which doesn't necessarily benefit folks like you and I but rather its for people such as our offspring, assuming your are a parent.

Note the serum vitamin D levels on the chart are not above 80 nmolL for any of the partipants at any time of the year. We can only speculate on how effective vitamin D would be at entirely safe levels of 120 nmol/L.

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Postby Nick » Tue Oct 18, 2005 1:32 pm

Beautiful Melody. Thank you for sharing.
:D
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Postby JFH » Wed Oct 19, 2005 1:11 am

bromley wrote:I would be grateful for any info on Vit D supplements. I eat plenty of oily fish and now get as much sun as possible.

Straight Vit D tablets are available form Holland and Barrett.

dignan wrote:If I remember correctly, France has lower incidence of MS than the UK...

It is, of course, well known fact that MS is caused by .... Cricket :lol:
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