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        Both animal data and human data indicates that vaccines alter the risk of developing diabetes. Immunization starting at birth is associated with a decreased risk of diabetes while immunization starting after 2 months is associated with an increased risk of diabetes. Vaccines probably affect the risk of diabetes by modulating the immune system. The data in humans shows a strong association between immunization and the risk of insulin dependent diabetes (IDDM) Type I diabetes, an autoimmune disease. At this time studies have not been performed to determine if Type II diabetes is also associated with vaccination. Based on the fact that many people diagnosed with Type II diabetes also have autoimmune destruction of there insulin secreting cells of the pancrease, it is reasonable to assume that immunization may be altering the risk of Type II diabetes as well. A review of Type I and Type II diabetes are included below. Data supporting a link between immunization and diabetes in humans and animals can be viewed on the corresponding linked pages.

 

Type I diabetes mellitus (IDDM)

        Type I diabetes mellitus, insulin dependent diabetes, is a chronic disease of humans with a primary onset occurring mainly in childhood and adolescence. The risk of developing type I diabetes varies significantly by country and race but not by sex. It is estimated that up to one in every 100 Caucasians may develop type I diabetes and that more than one million Americans are afflicted with the disease. The disease is a significant social and financial burden to most western nations. Its onset is often associate with an abrupt occurrence of polydipsia, polyuria, weight loss, fatigue, irritability and typically results in death if insulin therapy is not initiated. Serious chronic complications frequently afflict insulin treated diabetics later in life resulting in expensive hospitalization, loss of employment, and a decline in quality of life.

        Substantial evidence has existed for a while suggesting that type I diabetes is an autoimmune disease. This data has been extensively reviewed in several papers (Flier & Underhill, 1986; Barbosa & Bach, 1987; Zielasek, Jackson & Eisenbarth, 1989; Maclaren, 1992) so only some of the essential points will be discussed here. Findings suggesting an autoimmune etiology include the presence of insulitis in the pancreas of recently diagnosed type I diabetics along with the presence of islet cell antibodies in early diabetics and prediabetics. Glutamic acid decarboxylase reacts with sera from prediabetics and early diabetics in 70% or more of cases leading some believe that it may trigger the development of an anti-islet cell autoimmune response.

        Clinical trials and epidemiological studies have supported an immunological link to type I diabetes. Treatment of newly diagnosed type I diabetics with cyclosporine can reverse diabetes temporarily (Marks & Skyler, 1991; Martin, Schernthaner, Nerupet al.1991). Epidemiology has shown strong linkage of type I diabetes with the major histocompatability genes that control the development of immune responses. Approximately 95% of Caucasian type I diabetics express MHC class II alleles DR3 or DR4 while these alleles are expressed in only about 40% of the Caucasian population (Trucco & Dorman, 1989). Other studies suggest a protective effect of certain MHC alleles as demonstrated by an inverse correlation between the expression of the DR2 allele and the development of diabetes. Studies of type I diabetes in identical twins show that the concordance rate is only about 50%. This finding suggests that genes do not have absolute control on the development of diabetes and that environmental factors have a strong effect also.

        An extensive search has been underway to try to determine immunologic defects that could predispose individuals to develop type I diabetes but the findings are inconclusive. The difficulty in this endeavor is that it is hard to differentiate immunologic abnormalities that may cause diabetes from immunologic abnormalities caused by diabetes. This problem along with genetic heterogeneity and various environmental factors has led to often conflicting reports of immune disorders in diabetics. Autologous mixed lymphocyte reactions as well as responses to Concanavalin A and Phytohemagglutinin have been found to be decreased in newly diagnosed type I diabetics (Al-Kassab & Raziuddin, 1990; Knospe, Kohler, Rjasanowskiet al.1990) however studies focusing on long standing diabetics have failed to find any permanent defects (Pozzilli, Pagani, Arduiniet al.1987; Surcel, Karttunen, Ilonenet al.1987; Lorini, De Amici & Cortona, 1989). Some of the best evidence suggesting diabetics may have an immune disorder include papers showing an increased incidence of classic autoimmune diseases like thyroiditis in type I diabetics (Landin-Olsson, Karlsson, Dahlquistet al.1989a). That antithyroid antibodies are more common in females but islet cell antibodies and diabetes are equally common in males and females has raised questions on whether the disorders are casually related or are derived from common immunologic defects.

 

Type II diabetes mellitus

        Type II diabetes is a second and more common form of diabetes mellitus. The diseases typically occurs in patients over 35 years of age and affects 5% of the population in the U.S.A. Some of these patients suffer from low insulin sensitivity, while others have reduced insulin secretion. Diabetics have traditionally been classified as type II if their diabetes is controlled without insulin and if they failed to develop ketosis. Several recent studies have shown that many people classified as type II diabetics may actually suffer from a slowly progressing autoimmune destruction of the insulin secreting islet cells. These individuals may be better classified as having type I diabetes or both type I and type II diabetes (Groop, Bottazzo & Doniach, 1986; Landin-Olsson, Karlsson, Dahlquistet al.1989b; Niskanen, Karjalainen, Sarlundet al.1991; American Diabetes Association, 1993; Arnqvist, Littorin, Nystromet al.1993); (Temple, Luzio, Schneideret al.1989; King & Rewers, 1993) .

       Data suggests that 10% or more of patients diagnosed with type II diabetes suffer from low insulin production due to an autoimmune response against the pancreatic islet cells, as occurs in type I diabetes. Studies of Caucasians diagnosed with type II diabetes have revealed that between 14% and 32% develop autoantibodies to islet cell antigens within the first 5 years of diagnosis. These individuals represent a special subset of type II diabetics as seen by their deficiency of insulin secretion, elevated frequency of certain HLA genes, elevated frequency of thyroid or gastric autoantibodies and high risk for requiring insulin treatment. Twenty-nine percent of all diabetics in the USA use insulin. Assuming 10% of all diabetics are actually diagnosed as type I, insulin dependent diabetics, the remaining 19% of diabetics taking insulin are diagnosed as type II, non insulin dependent diabetics. Many of these 19% could be type I diabetics that were incorrectly diagnosed due to a slow progression of disease and inadequate laboratory testing (Turner, Stratton, Hortonet al.1997).