"The doctor of the future will give no medicine, but will interest his patients in the care of the human frame, in diet and in the cause and prevention of disease."
- Thomas Edison
Rich Murray: notmilk.com: Cohen: Dosch & O'Connor:
dairy causes MS & diabetes 3.27.1 rmforall
Subject: NOTMILK -MULTIPLE SCLEROSIS AND MILK
Date: Tue, 27 Mar 2001 06:04:33 -0500
From: Robert Cohen <email@example.com>
Multiple Sclerosis (MS) is a common neurological disease, affecting approximately 300,000 Americans. Two-thirds of those diagnosed with MS are women.
Most researchers believe that MS is an auto immune disease. Auto means "self." The body's reaction to a foreign protein is to destroy that antigen-like invader with an antibody. The antibody then turn upon one's own cells. That is an auto-immune response. In the case of MS, the body's response is to attack the outer membrane-protecting nerve cells, or the myelin sheath.
Symptoms of MS include tingling or numbness of the limbs, paralyses, and vision problems. Sometimes MS patients experience slurred speech accompanied by chronic pain.
MS costs approximately $2.5 billion each year in America. MS is found in milk-drinking populations. It is interesting to note that Eskimos and Bantus (50 million living in East Africa) rarely get MS. Neither do those native North and South American Indian or Asian populations that consume no dairy products.
Many physicians have noted a dairy link to MS. Many little clues have been reinforced by one very large clue, just published. Each clue provides a piece of the puzzle.
Norway has the highest rates of milk and dairy consumption in the world. Dr. Ashton F. Embry analyzed geographical regions, and provides this dairy clue:
"...In Norway MS is up to five times more common in the inland farming areas than in the relatively nearby coastal fishing areas."
John McDougall, M.D., cites the British medical journal Lancet in pointing out that a diet filled with dairy products has been closely linked to the development of MS. (The Lancet 1974;2:1061)
Dr. Luther Lindner is involved in clinical MS experiments at Texas A & M University College of Medicine. Lindner, a pathologist, writes on his website:
"It might be prudent to limit the intake of milk and milk products..."
A worldwide study published in the journal Neuroepidemiology revealed an association between eating dairy foods (cow's milk, butter, and cream) and an increased prevalence of MS. (Neuroepidemiology 1992;11:304-12.)
The April 1, 2001 issue of the Journal of Immunology will contain a study linking MS to milk consumption. It has long been established that early exposure to bovine proteins is a trigger for insulin dependent diabetes mellitus. Researchers have made that same milk consumption connection to MS.
The July 30, 1992 issue of the New England Journal of Medicine first reported the diabetes auto immune response milk connection:
"Patients with insulin dependent diabetes mellitus produce antibodies to cow milk proteins that participate in the development of islet dysfunction... Taken as a whole, our findings suggest that an active response in patients with IDDM (to the bovine protein) is a feature of the auto immune response."
In October of 1996, The Lancet reported:
"Antibodies to bovine beta-casein are present in over a third of IDDM patients and relatively non-existent in healthy individuals."
Two months later (December 14, 1996), The Lancet revealed:
"Cow's milk proteins are unique in one respect: in industrialized countries they are the first foreign proteins entering the infant gut, since most formulations for babies are cow milk-based. The first pilot stage of our IDD prevention study found that oral exposure to dairy milk proteins in infancy resulted in both cellular and immune response...this suggests the possible importance of the gut immune system to the pathogenesis of IDD."
THE MULTIPLE SCLEROSIS/MILK CONNECTION
H. Michael Dosch, M.D., and his team of researchers have determined that multiple sclerosis and type I (juvenile) diabetes mellitus are far more closely linked than previously thought. Dosch attributes exposure to cow milk protein as a risk factor in the development of both diseases for people who are genetically susceptible. According to Dosch:
"We found that immunologically, type I diabetes and multiple sclerosis are almost the same - in a test tube you can barely tell the two diseases apart. We found that the autoimmunity was not specific to the organ system affected by the disease. Previously it was thought that in MS autoimmunity would develop in the central nervous system, and in diabetes it would only be found in the pancreas. We found that both tissues are targeted in each disease." (Journal of Immunology, April, 2001)
Robert Cohen http://www.notmilk.com
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Source: The Hospital For Sick Children (http://www.sickkids.on.ca/)
Date: Posted 3/22/2001
Researchers Determine That MS And Diabetes Are Closely Linked Diseases
Toronto, March 20, 2001 - A team of researchers led by Hospital for Sick
Children (HSC) senior scientist H. Michael Dosch has determined that multiple sclerosis and type I (juvenile) diabetes mellitus are far more closely linked than previously thought, including the role cow milk protein plays as a risk factor in the development of both diseases for people who are genetically susceptible. This research is published in recent issues of The Journal of Immunology
(April 1 and February 15, 2001).
Multiple sclerosis (MS) and type I diabetes mellitus are autoimmune disorders, where the body's immune system attacks its own tissue. The diseases are entirely different clinically, but have nearly identical ethnic and geographic distribution, genetic similarities, and, as is now known, shared environmental risk factors.
In a collaboration between The Hospital For Sick Children, St. Michael's Hospital and the Pittsburgh Children's Hospital, Dr. Dosch's laboratory discovered a high degree of similarity in the autoimmunity of MS and diabetes patients, and that a widely used mouse model for diabetes could also develop an MS-like disease.
"Much to our surprise, we found that immunologically, type I diabetes and multiple sclerosis are almost the same -- in a test tube you can barely tell the two diseases apart," said Dr. Dosch, the study's principal investigator, a senior scientist in the HSC Research Institute, and a professor of Paediatrics and Immunology at the University of Toronto (U of T). "We found that the autoimmunity was not specific to the organ system affected by the disease. Previously it was thought that in MS autoimmunity would develop in the central nervous system, and in diabetes it would only be found in the pancreas. We found that both tissues are targeted in each disease."
In diabetes and MS, there is a long, drawn-out period of silent disease years before the appearance of symptoms and diagnosis of the disease. In diabetes, it is this "pre-diabetes" phase that is targeted by interventions to stop the development of the full-blown disease. Similar efforts are planned for individuals at high risk for MS.
"We are planning a large international study with centres in Canada and the US to test the possibility of interventions during the pre-MS phase," added Dr. Dosch.
One of the major environmental risk factors for diabetes is exposure to cow milk protein. Based on the role of cow milk protein as a risk factor in the development of type I diabetes, an international global diabetes prevention trial called TRIGR-- Trial to Reduce Insulin-dependent diabetes in the Genetically at Risk - is expected to begin later this year, with Dr. Dosch as the trial's basic science chair. In the first step to test just how far the similarities between MS and diabetes go, the study's researchers looked for signs of abnormal immunity to cow milk in MS patients. Such abnormalities were indeed found in most patients, suggesting that similar processes may contribute to both diseases. If confirmed in a larger and prospective family study, it may become possible to design dietary means to influence the course of MS as well as diabetes.
"The similarities found between MS and type I diabetes will open new avenues of research. Our next focus will be to study MS family members for signs of early MS," said Dr. Paul W. O'Connor, head of the MS clinic at St. Michael's Hospital, a co-author of the study and Associate Professor of Neurology at U of T.
Other collaborators on this research were: Shawn Winer, Igor Astsaturov, Roy K. Cheung, Lakshman Gunaratnam, Denise D. Wood and Professor Mario Moscarello, all from the HSC Research Institute; Colin McKerlie, Sunnybrook and Women's Health Sciences Centre and the University of Toronto; and Professor Dorothy J. Becker, Children's Hospital of Pittsburgh and the University of Pittsburgh.
Funding for this research was provided by the Canadian Institutes of Health Research, the Juvenile Diabetes Foundation, the Canadian Diabetes Association, the US National Institutes of Health and the Renziehausen Fund.
J Immunol 2001 Apr 1;166(7):4751-4756
T Cells of Multiple Sclerosis Patients Target a Common Environmental Peptide that Causes Encephalitis in Mice. Winer S, Astsaturov I, Cheung RK, Schrade K, Gunaratnam L, Wood DD, Moscarello MA, O'Connor PW, McKerlie C, Becker DJ, Dosch HM
The Hospital For Sick Children, Research Institute,
Division of Neurology, St. Michael's
Hospital, and Division of Laboratory Animal Services,
Sunnybrook Hospital, and Departments of
Paediatrics and Medicine, University of Toronto
Toronto, Ontario, Canada. Department of
Pediatrics, Division of Endocrinology
Children's Hospital of Pittsburgh
University of Pittsburgh, Pittsburgh, PA 15260.
Multiple sclerosis (MS) is a chronic autoimmune disease triggered by unknown environmental factors in genetically susceptible hosts. MS risk was linked to high rates of cow milk protein (CMP) consumption, reminiscent of a similar association in autoimmune diabetes. A recent rodent study showed that immune responses to the CMP, butyrophilin, can lead to encephalitis through antigenic mimicry with myelin oligodendrocyte glycoprotein. In this study, we show abnormal T cell immunity to several other CMPs in MS patients comparable to that in diabetics. Limited epitope mapping with the milk protein BSA identified one specific epitope, BSA(193), which was targeted by most MS but not diabetes patients. BSA(193) was encephalitogenic in SJL/J mice subjected to a standard protocol for the induction of experimental autoimmune encephalitis. These data extend the possible, immunological basis for the association of MS risk, CMP, and CNS autoimmunity. To pinpoint the same peptide, BSA(193), in encephalitis-prone humans and rodents may imply a common endogenous ligand, targeted through antigenic mimicry.
J Immunol 2001 Feb 15;166(4):2831-41
Type I diabetes and multiple sclerosis patients target Islet plus central nervous system autoantigens; nonimmunized nonobese diabetic mice can develop autoimmune encephalitis.
Winer S, Astsaturov I, Cheung R, Gunaratnam L, Kubiak V, Cortez MA,
Moscarello M, O'Connor PW, McKerlie C, Becker DJ, Dosch HM
The Hospital For Sick Children, St. Michael's Hospital
University of Toronto, Sunnybrook and
Women's College Health Sciences Center
University of Toronto, Ontario, Canada.
Type I diabetes and multiple sclerosis (MS) are distinct autoimmune diseases where T cells target either islet or CNS self-proteins. Unexpectedly, we found that autoreactive T cells in diabetic patients, relatives with high diabetes risk, nonobese diabetic (NOD) mice, and MS patients routinely target classical islet as well as CNS autoantigens. The pathogenic potential of CNS autoreactivity was testable in NOD mice. Pertussis holotoxin, without additional Ags or adjuvants, allowed development of an NOD mouse-specific, autoimmune encephalitis with variable primary-progressive, monophasic, and relapsing-remitting courses. T cells from diabetic donors transferred CNS disease to pertussis toxin-pretreated NOD.scid mice, with accumulation of CD3/IFN-gamma transcripts in the brain. Diabetes and MS appear more closely related than previously perceived. NOD mouse-specific, autoimmune encephalitis provides a new MS model to identify factors that determine alternative disease outcomes in hosts with similar autoreactive T cell repertoires. PMID: 11160351