AI Disease, Response Starts Early, MS and Type 1 diabetes

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AI Disease, Response Starts Early, MS and Type 1 diabetes

Postby Nick » Mon Apr 17, 2006 11:27 am

Nick's foreword

I believe the following information is very important for a variety of reasons.


In Children with Autoimmune Disease, Response Starts Early

Newswise - Children with neurological autoimmune diseases develop immune reactions to other targets in their bodies and in food early in their disease, according to research that will be presented at the American Academy of Neurology 58th Annual Meeting in San Diego, Calif., April 1 - 8, 2006.

T cells are the body's regulators of the immune response. Increased T cell proliferation is a characteristic of autoimmune disease, in which the immune system attacks body tissues.
However, it wasn't known whether this increased proliferation occurred early, or as a result of chronic autoimmunity, said lead researcher Brenda Banwell, MD, from the Department of Pediatric Neurology at the Hospital for Sick Children in Ontario, Canada.

The researchers studied 166 children: 63 with an autoimmune demyelinating syndrome (either multiple sclerosis or an isolated event of central nervous system autoimmunity), 43 with type I diabetes (also an autoimmune disease), 31 with a non-autoimmune neurological condition, and 30 healthy controls. They examined blood samples for T cell proliferation in response to exposure to a variety of antigens (targets), including myelin protein from nerve cells, proteins in the pancreas, and proteins in milk.

As expected, more children with central nervous system autoimmunity had T cell proliferation after exposure to myelin than control children (50 percent versus 10 percent). About a quarter of these children also showed a response to proinsulin, a T-cell target in type I diabetes. Over sixty percent also responded to a protein in milk. Ninety percent of the children with type I diabetes responded to pancreatic antigens as expected, but almost as many (79 percent) responded to myelin, and 90 percent responded to milk protein.

Even at the onset of their disease, children with autoimmune diseases harbor T cells that will react against proteins within their tissues, Banwell said. The responses seen against milk proteins raise the possibility that substances in food may be associated with autoimmunity.

This study was supported by The Wadsworth Foundation.
The American Academy of Neurology, an association of more than 19,000 neurologists and neuroscience professionals, is dedicated to improving patient care through education and research. A neurologist is a doctor with specialized training in diagnosing, treating and managing disorders of the brain and nervous system such as Alzheimer disease, epilepsy, multiple sclerosis, Parkinson disease, and stroke.

For more information about the American Academy of Neurology, visit
Editor's Note: Dr. Banwell will present this research during a scientific platform session at 1:30 Thursday, April 6 in room 6AB of the San Diego Convention Center.


DIRECT-MS material


Direct-MS produces information booklets on various aspects of multiple sclerosis. These booklets are listed below and a PDF of each one can be opened and downloaded by clicking on the title.
Alternately we can mail you a hard copy of any of the booklets. Just write or email us and let us know which ones you would like sent to you. Don’t forget to include your mailing address. There is no charge for this service.

Booklet #1 Take Control of Multiple Sclerosis
This booklet discusses the main causal factors of MS and, with this information as a guide, it lays out our recommendations for nutritional strategies to help control MS.

Booklet #2 Protect Your Family from Multiple Sclerosis
This booklet emphasizes the high risk for contracting MS of first-degree relatives of persons with MS. It discusses the causal factors of MS with special emphasis on vitamin D deficiency as a primary cause. Finally it demonstrates that adequate vitamin D can likely prevent MS in most cases and provides a recommended supplementation regime.

Booklet # 3 Multiple Sclerosis: The Alberta Disadvantage
This booklet demonstrates that the province of Alberta, the home of DIRECT-MS, has by far the highest rates of MS in the world: Prevalence 340/1000,000; Incidence 20/100,000.
Data and arguments are provided to support the argument that the main reason for the MS Epidemic is that all the main causal factors are present in Alberta, with low vitamin D supply being especially problematic.


We have found that a Voiced PowerPoint presentation (‘Webcast’) is an effective way to communicate the science and the recommendations for nutritional strategies for controlling MS and preventing it in the first place.

The first presentation is Prospects for Vitamin D Nutrition. The discussion is narrated by Reinhold Vieth of the departments of Pathology and Laboratory Medicine, Mount Sinai Hospital and Laboratory Medicine and Pathobiology, University of Toronto.

Dr. Vieth addresses the topics of:
Vitamin D and Human Evolution
Clinical relevance of higher vitamin D intakes
Toxicology of Vitamin D

The second webcast is entitled Preventing Multiple Sclerosis and is the second in a series of web casts regarding nutrition and Multiple Sclerosis. The focus of the Prevention presentation is how MS can be easily, safely and inexpensively prevented by focusing on protective factors. This is a must see for those people with MS who have children.

Our first webcast, Nutritional Strategies for Controlling Multiple Sclerosis, addresses similar issues. It presents the probable causes of MS and how to effectively control those elements. A review of the protective factors and how to incorporate them into your lifestyle is also covered.
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Postby EricJohnson » Mon Apr 17, 2006 3:04 pm

Sometimes mice will be raised in germ-free housing to see how that affects various things.

This stupendous paper by Paul Plotz:

Plotz PH.
The autoantibody repertoire: searching for order.
Nat Rev Immunol. 2003 Jan;3(1):73-8. Review.
PMID: 12511877

cites a study in which genetically-autoimmune-prone mice were housed not only germ-free, but "macromolecule-free." They were fed a low-molecular-weight diet. So it contained all the vitamins and amino acids they needed, but no long peptides - perhaps no peptides at all. And they still developed the same autoantibody portfolio as they develop when they eat a normal proteinaceous diet.

Of course, those mice are inbred. Theres something wrong with them, probably something very specific. People with MS and diabetes-1 are outbred - and also have something wrong with them, but quite possibly its something very different than what is wrong with those mice. (Alas, that is the price of studying a model.)

Which I say just to emphasize that what I'm discussing is only a model and not necessarily a very natural one. Sometimes I wish more scientists would go down to the pound and get some dogs with arthritis, etc to study. Whatever got normal, outbred dogs sick is probably very similar to what gets us sick.
I dont have MS, but I study all diseases of immune activation. I had severe CFS and am 95% well, 1 yr into antimicrobial treatment.
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Postby mrhodes40 » Mon Apr 17, 2006 6:22 pm

The vitamin d presentation by Reigold Vieth is absolutely wonderful. You need a cable or high speed connection and it takes an hour but it is time well spent.
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Postby sojourner » Mon Apr 17, 2006 7:33 pm

All three of our kids get at least 800IU of Vit D per day from a combo of Cod Liver oil and a multi vit. This is a decision we made early on considering they have a Dad and Aunt with MS. Maybe a little less suncreen this summer, too.

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Postby Tiramisu » Sun Jun 11, 2006 7:14 pm

Wonderul info.
I am a T1 DIabetic and recently have been Dx w/ MS. How does the Vit. D react on somone that already had MS?
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D and MS

Postby jimmylegs » Mon Jun 12, 2006 4:14 am

in studies on mice, vitamin D supplementation prevented EAE and in mice that were given EAE and then vitamin D, the disease was halted. now whether EAE is an accurate representation of MS in humans is another issue. but there are studies that show sufficient D supplementation in MS patients has reduced anticipated relapse rates.
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Postby Nick » Fri Jun 16, 2006 11:30 am

Hi T

There really is a dearth of research regarding the effect vitamin D can have on active MS. Suffice to say that the medical community as a whole is in very early stages of recognizing the virtues of vitamin D.

Most of the research to date has been observational and that is why prevention and risk are usually accentuated. There is however novel research such as this paper suggests vitamin D, in high enough concentrations significantly influences disease progression, or a lack thereof.

There does exist quite a lot of research which demonstrates how the internal or hormone form of vitamin D influences the immune system with respect to autoimmune diseases. For these reasons I consider it prudent to maintain high enough internal concentrations of vitamin D.

One doesn’t require an official decree from an MS society to decide on whether to take vitamin D nor how much to take. The beauty of the Internet is the dissemination of information and the benefits of our intellect and freedoms are to use that information and employ it in a useful fashion. The articles I have linked to above provide well-referenced material and the selected information below also substantiates the properties that vitamin D possesses and how animal physiology uses it.

It stands to reason that the usefulness of vitamin D, be it for prevention or active therapy, use the same mechanisms. I speculate that the efficacy of vitamin D will be different for prevention and active therapy, both in how much is necessary and in the degree of down regulation. It could be that for active MS you will have to avoid the causal elements in addition to immunoregulation via vitamin D to best manage your MS.

For many years, it has been known that cells of the immune system, including T helper lymphocytes (the primary immune cell orchestrating MS immune dysfunction), possess receptors for vitamin D3 32. More recently, vitamin D3 has been shown to profoundly affect immune responses in cell culture, and in animal disease models mimicking multiple sclerosis32-35.

In vitro, vitamin D3 metabolites have been shown to be potent antiproliferative and immunosuppressive agents. Vitamin D3 metabolites can inhibit T lymphocyte proliferation, and significantly decrease the production of pro-inflammatory cytokines, including interleukin two (IL-2), interferon gamma (IFN-g) and tumour necrosis factor alpha (TNF-µ), all of which are prominently involved in disease immunopathogenesis33.

Vitamin D3 has been demonstrated to function as a physiologic regulator of T lymphocyte differentiation and development in vitro, suggesting important roles in immune regulation36. It has been hypothesized that vitamin D3 may act as a transcriptional regulator of T lymphocyte cytokine synthesis, and indeed, receptors for vitamin D3 can be found in the nuclei of immunocompetent cells, including T helper lymphocytes37-40. Vitamin D3 insufficiency has also been correlated to increasing levels of circulating matrix metalloproteinase 9 (MMP9)41, a molecule involved in the break down of the blood brain barrier, allowing for the transmigration of lymphocytes into the central nervous system, and the initiation of central nervous system inflammation.

The development of an animal model that mimics MS-like disease activity, called Experimental Allergic Encephalomyelitis (EAE), has helped to increase our understanding of the autoimmune processes that may be occurring in MS. In this animal model, T lymphocytes, (and more specifically, type-1 helper (Th1) cells), recognize central nervous system antigens of myelin basic protein and elicit an immune response resulting in the production of pro-inflammatory cytokines40. Conversely, type-2 helper (Th2) lymphocytes, which have anti-inflammatory functions, appear to be down-regulated.

Cantorna et al and Lemire et al have shown that vitamin D3 treatment (i.e. with the hormonal form of vitamin D3, 1,25(OH)2D) in mice with EAE results in the inhibition of pro-inflammatory Th1-driven responses, while increasing the proportion of anti-inflammatory Th-2 cell derived cytokines33, 40. Further, mice which are vitamin D3 deficient develop EAE more rapidly than mice which are vitamin D3 sufficient46.

Treatment of mice with 1,25(OH)2D prior to disease induction with myelin antigen immunization, can entirely prevent the development of EAE34,35. In addition, the injection of 1,25(OH)2D into mice with relapsing-remitting EAE at the first sign of neurological dysfunction results in the inhibition of further disease activity, suggesting that vitamin D3 treatment is also effective after disease onset in symptomatic animals34.

Finally, Cantorna et al have shown that combination treatment with 1,25(OH)2D and sub-therapeutic doses of cyclosporine A can suppress the progression of EAE in mice, while avoiding cyclosporine-induced toxicity, suggesting that vitamin D3 may also serve as an effective adjunct therapy to immunosuppressive treatment used in autoimmune disease46.

Overall, the evidence supports the hypothesis that vitamin D3 may be one factor shaping the development of the T cell repertoire, and therefore contributing to the development and progression of T cell mediated diseases such as multiple sclerosis.
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lab dish

Postby gwa » Fri Jun 16, 2006 1:05 pm


Everytime I read about MS and diabetes being indistinguishable in a petri dish, I wonder what is in the dish.

What "MS" and "diabete" thing is there? I could understand if there were a couple of viruses or bacterias, but for the life of me I have no idea what is being referred to in the dish.

It looks like if MS was in the dish that it would be easy to analyze it and find a cure.

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'identical' diseases

Postby jimmylegs » Fri Jun 16, 2006 2:01 pm

jeedub, i think they mean in both diseases, there is a self-reactive antibody 'in the dish'. in the case of diabetes, the victim selected = islets in the pancreas, in ms, the cns.

perhaps the victim cells are selected is based on genetic predisposition. this is too variable from person to person.

therefore, we might simplify, and address the tendency by the immune system to self-attack - not protection of the victim cells, which are different depending on individual genetic makeup.

this, i believe, is what makes the diseases 'identical' - the self attack tendency.

so. what regulates the tendency to attack? it has been found that calcitriol, the metabolically active hormone form of vitamin D, is very important in immune system regulation.

so, perhaps prevention has been found. and treatment. cure... i'll let you know how it goes. ;)
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go ahead

Postby gwa » Fri Jun 16, 2006 5:28 pm

I have been taking Vitamin D and calcium for many years and I still limp with one leg, can barely move the second leg and have the balance of a bonafied drunk.

The Vit D theory, in my opinion, is very simplistic and does not tell the whole story of the cause of MS.

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Postby jimmylegs » Fri Jun 16, 2006 7:41 pm

you could be right gwa! how much d do you take again? and did u always take lots prior to getting sick? or did u start supplementing after.
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Postby bromley » Sat Jun 17, 2006 12:54 am


The Vit D theory, in my opinion, is very simplistic and does not tell the whole story of the cause of MS.

We are on the same wavelength. This is a hugely complex disease, and Vit D may only play a small part. Genetic susceptibility is the key driver - but we can't change our genes (yet). Vit D may play a role in terms of prevention, but not sure how much it can influence the course of the disease once it kicks off.

I suppose Vit D supplements might give us the sense that we are trying to do all we can to improve our chances - which is good thing.

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genetics and environment

Postby jimmylegs » Sat Jun 17, 2006 6:34 am

i agree.

i think insufficient vitamin D status highlights genetic variability in individuals. you could supplement with vitamin D all your life at the current recommended daily intakes, and still be insufficient if you don't get enough sun or dietary source D. at this point i am firmly convinced that D status (and nutrient status in general) is strongly implicated as the environmental factor required in the ms equation. of course genetic susceptibility is the other factor.

the way i see it, why worry about genetic engineering solutions when you can eat right for prevention and treatment.

i am very early on in the progression here. we shall see how my approach pans out. i might be looking for answers in genetics in 20 more years too. or maybe my diagnosis will be reversed. who knows?
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