lc
Your hypothesis is interesting. Please continue in your postings as this kind of intellectual intercourse is one of my cherished reasons for frequenting these types of forums.
I quite like your focus on MS & type 1 diabetes. I am, however, a believer in the autoimmune disease process for both MS and type I diabetes. I believe their similarities result from certain common denominators, notably European heritage, genetic predisposition, causal food proteins and a deficiency in protective elements.
lyndacarol wrote:
Excess insulin production eventually burns out those insulin-producing beta cells in the pancreas, resulting in type-1 diabetes. Could this explain the common occurrence of diabetes with MS, if hyperinsulinemia (excess insulin) is involved with MS?
I think this would be the lay description for type 2 rather than type 1 diabetes. It has been well documented that in type 1 diabetes, the GAD protein in the pancreas is targeted and assailed by the immune system resulting in impaired islets and consequent insulin production impairment.
[Excerpt]The process of
molecular mimicry is deceivingly simple but entails a lot of understanding of the workings of the immune system. Basically molecular mimicry means that part of a molecule of a given protein closely resembles a part of another totally different protein. Proteins are made up of strings of amino acids and in molecular mimicry one series amino acids(eg~10) in one protein is very similar to a string of ten amino acids in another protein. Given that there are 20 different amino acids it is a rather rare occurrence to find such mimicking arrangements but many examples have been demonstrated.
The main types of proteins which came into play in autoimmune disease are:
1. self proteins which are part of the human body. An example of this would be myelin basic protein which is the most common protein in myelin and the GAD protein of the pancreas;
2. proteins of infectious agents such as viruses and bacteria;
3. food proteins. For example over 400 different proteins occur in cow's milk and most have over 150 amino acids.
To understand how molecular mimicry works in the induction of autoimmunity one must understand the basic mechanisms of an immune response to a foreign invader in the body. The immune system recognizes a part of the protein portion of the invader. It does this with T cells which have receptors which bind to short segments(~10 amino acids) of a foreign protein. A macrophage will engulf a foreign invader (e.g. a bacteria or food particle) and break it down into fragments.
A special molecule in the macrophage then carries a protein fragment(peptide) to the surface of the cell and "presents" it to the millions of circulating T cells. A T cell which has a matching receptor locks onto the presented protein fragment. The T cell then becomes activated and stimulates other portions of the immune system to begin an immune response against all proteins which contain a similar looking amino acid string. The details of what constitutes a similar looking string are beyond this summary but suffice to say it has been found that a variety of similar, yet somewhat different strings, can be recognized by the same T cell.
Thus, it is easy to understand how molecular mimicry can trigger an autoimmune reaction. If the protein fragment from a foreign invader which is presented to the T cell closely resembles part of a self protein then the activated immune system will not only attack all foreign invaders which have the same string of amino acids but will also attack a very similar string in a self protein. It has been shown that parts of proteins in various foods and infectious agents resemble parts of various self proteins. Sometimes a three way mimicry occurs with a protein fragment from a food closely resembling that of an infectious agent which in turn closely resembles part of a self protein.
In Celiac disease part of the gliadin molecule (found in various grains such as wheat and rye), part of adenovirus 12 and part of a gut protein all closely resemble each other and the result of such mimicry is an immune attack on the gut when food containing gliadin protein is eaten. A similar three way mimicry occurs between a cell wall protein in grains and legumes, part of the Epstein Barr virus and part of the collagen in joints. This leads to rheumatoid arthritis in genetically susceptible people. For type 1 diabetes parts of milk proteins and viral proteins mimic proteins in the insulin-producing beta cells of the pancreas.
For MS it has been established that numerous viruses and bacteria have amino acid strings which mimic parts of proteins in the myelin proteins of the central nervous system. Undoubtedly food proteins also contain such mimicking protein fragments and thus two and three way mimicry is a ready explanation for why the immune system attacks myelin and causes MS.
Below is my
post of April 18.
Nick's foreword
I believe the following information is very important for a variety of reasons.
Cheers
Nick
--------------
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
http://www.aan.com.
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.
----------------
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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.
Presentations
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
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Our first webcast,
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It allows me to speculate about all sorts of things about MS.
When I first had my hormone levels tested I had some estradiol but no progesterone. 
I also had a boatload of lesions. 
hehehe) but couldn't tell you if that's just regular old recovery from an attack.
