Listed below are supporting and opposing articles that vaccinations could be connected to Type 1 Diabetes. I have the opinion (which could be wrong) that vaccinations can affect certain people who are not immune to Type 1 Diabetes, and can cause that person to become Diabetic. I feel that certain people are born immune to the disease and would never get it, no matter what vaccinations they were given at whatever age. I feel that some people may carry the disease and it may lay dormant in their body until something triggers it. In conclusion, I believe that certain vaccinations that we are required to get at a young age can trigger Type 1 Diabetes in those who are not immune to it. Feel free to read some of the supporting information listed below, the links are provided as well, and share your opinion, either against or in agreement with mine.
Vaccinations & Being Diagnosed with Type 1 Diabetes
Another theory put forward is that childhood vaccinations could increase the chances of developing type 1 diabetes. One researcher, Dr J B Classen has investigated incidences of type 1 diabetes in the human population as well as in animals. Dr Classen’s research indicates there could be a link between type 1 diabetes and childhood vaccinations such as smallpox, tuberculosis and Hib vaccines.
The Pertussis Vaccine
The vaccine for pertussis, or whooping cough, is part of the DPT shot (diphtheria, pertussis, tetanus) given to all children. The pertussis vaccine includes “pertussis toxin,” a toxin secreted by the microbe which causes whooping cough (the Bordetella pertussis). This toxin, which has been described as one of the most virulent poisons known to science, has several names and has a variety of effects on the body.
Pertussis Toxin Affects Pancreas
One of the names for pertussis toxin has traditionally been “islet-activating protein,” signifying that this substance acts specifically and directly on the “islets of Langerhans,” which are the insulin-secreting parts of the pancreas.
At least since the 1970s, pertussis vaccine has been known in animal experiments to stimulate over-production of insulin by the pancreas followed by exhaustion and destruction of the “islets” with consequent under-production of insulin; in the first case the outcome is hypoglycemia, and in the latter it is diabetes.
Physicians as early as 1949 called attention to low blood glucose in children who had severe reactions to the pertussis vaccine. In 1970, Margaret Pittman wrote: “the infant whose blood sugar level is influenced by food intake may be especially vulnerable to vaccine-induced hypoglycemia…the vaccine induces hypoglycemia in mice and rabbits.”
Gordon Stewart wrote in 1977: “more than any other vaccine in common use, pertussis vaccine is known pharmacologically to provoke…hypoglycemia due to increase production of insulin.” Two Dutch researchers, Hannik and Cohen, observed in 1978: “infants who show serious reactions following pertussis vaccination suffer from a failure to maintain glucose homeostasis.” And two German researchers, Hennessen and Quast, found in 1979 that 59 out of 149 children who manifested adverse reactions to the pertussis vaccine developed symptoms of hypoglycemia.
The next logical step – deciding that the whooping cough vaccine could be responsible for the presently observed increase in the incidence of hypoglycemia and diabetes – has been inhibited by the federal government’s pro-vaccination policy, but enough researchers have spoken out in favor of a diabetes connection to suggest that this is a very real possibility deserving of further investigation.
Haemophilus Influenzae B and Hib Vaccine
A study of haemophilus influenzae B (Hib) vaccine in 114,000 Finnish children found that those who received 4 doses of the vaccine had a higher incidence of Type-I diabetes than those who received only one dose.
Mumps and Mumps Vaccine: Mumps Infection Can Cause Diabetes
There is copious evidence of a causal relationship between clinical mumps and subsequent development of diabetes. This evidence consists of: data linking mumps with pancreatitis; individual case reports of Type-I diabetes following clinical mumps infection; clusters of Type-I diabetes cases after mumps epidemics; and large epidemiological studies demonstrating parallel curves between outbreaks of mumps and new cases of Type-I diabetes (with a lag of 2-3 years).
Furthermore, mumps virus can infect human pancreatic beta cells in vitro and destroy them.
These and similar reports are noted and described in Adverse Events Associated with Childhood Vaccines: Evidence Bearing on Causality (Washington, D.C: National Academy of Sciences, Institute of Medicine, 1993). This compendium was prepared by the Vaccine Safety Committee appointed as part of the overall effort of the federal government to evaluate vaccination risks and benefits as charged by the National Childhood Vaccine Injury Act of 1986 (100 Stat. 3780, 3781). The IOM Committee concluded:
“There is evidence suggesting that mumps virus infection can trigger the onset of Type-I diabetes in some individuals. Biologic plausibility data implicating the mumps virus in the pathogenesis of Type-I diabetes include: the association between viral infections, including mumps, and Type-I diabetes in humans; the detection of circulating autoantibodies against pancreatic antigens, particularly islet cells, during convalescence from mumps infection as well as early in the course of Type-I diabetes; and in vitro studies demonstrating that the wild-type mumps virus can infect human pancreatic beta cells.
The question to be answered is whether the mumps vaccine can have the same effect as the clinical infection with mumps.
Diabetes Reported Following Mumps Vaccination
There are many reports in the literature of Type-I diabetes emerging after mumps vaccination. In 1997, Sinaiotis and colleagues reported the onset of Type-I diabetes one month after receipt of mumps vaccine in a 6.5 year old boy. In 1991, Pawlowski and Gries described an 11-year old body who had mumps disease at age 16 months and then received measles-mumps vaccine 5 months prior to the emergence of Type-I diabetes; he had severe abdominal pain and fever one week after vaccination.
In 1984, Otten and colleagues reported three cases of Type-I diabetes with onset in one case 10 days and, in other cases, 3 weeks after mumps vaccination in children 3,2 and 16 years of age. In 1986, Helmke and colleagues reported seven children who developed Type-I diabetes in the second to fourth week following mumps or measles-mumps vaccination.
In 1979, Quast and colleagues noted that in the first two years after mumps and measles-mumps vaccines were introduced into Germany, two cases of Type-I diabetes following immunization with measles-mumps and mumps vaccines respectively were reported to the manufacturer.
But, oddly enough, despite this finding and despite the series of case studies already noted, the Vaccine Safety Committee concluded that there was insufficient evidence either to accept or reject a causal relation between mumps vaccine and Type-I diabetes. This contradicted its own assertion in the Preface that: “In reaching conclusions favoring acceptance of a causal relation…the committee most commonly relied on case series and individual case reports.”
Rubella and the Rubella Vaccine
Of the three vaccines making up the MMR shot, the rubella component is the major suspect because rubella (German measles) itself, like mumps, is known to be a cause of diabetes and the action of the vaccine resembles that of the disease. If the disease can cause diabetes, so can the vaccine.
Rubella Virus Causes Diabetes
In 1978 Margaret Menser wrote: “Since 1968 there has been increasing interest in the possibility that viral infection may play a part in the etiology of diabetes mellitus in man…[but] only one virus consistently produces diabetes in man – the congenitally acquired rubella virus.”
“Congenital rubella syndrome” is the name given to the group of impairments and disabilities often seen in babies whose mothers become infected with rubella during pregnancy. These impairments include: heart disease, mental retardation, deafness, and blindness. E.J. Rayfield and colleagues wrote in 1986: “The congenital rubella syndrome provides the best documentation in humans that a viral infection is associated with the subsequent development of insulin-dependent [Type-I} diabetes mellitus.”
In the 1960’s and 1970’s, researchers came to realize that the effect of the rubella virus does not end at the moment of birth, but that it remains in the organism of the baby and continues to exert its influence for many years thereafter. Especially to be noted is the fact that up to 20 percent of these individuals later come down with Type-I diabetes. This may take from 5 to 20 years to develop, indicating that the rubella virus remains active in the organism for all that time.
This virus acts by forming “rubella-specific immune complexes” (an immune complex” is a mixture of the rubella virus and the antibody to it). P.K. Coyle and colleagues showed in 1982 that such immune complexes are found in individuals with congenital rubella and also in persons vaccinated against rubella. They were not found in persons who had never been infected with rubella nor in those who had had the disease naturally and recovered from it. These immune complexes can and do act on the pancreas.
In 1989, Numazaki and colleagues infected laboratory cultures of human pancreatic islet cells with rubella virus. They found that these infected cells produced much lower levels of insulin and concluded: these results suggest that rubella virus can infect human pancreatic islet cells and that such infection may lead to significant reductions in levels of secreted insulin.”
Thus, rubella itself has been demonstrated to be a causal agent in Type-I diabetes.
Rubella Vaccine Virus Persists In Body
P.K. Coyle and colleagues demonstrated in 1982 that “rubella-specific immune complex formation is frequent after vaccination and could be demonstrated in two-thirds of an unselected group of vaccinates for as long as eight months after vaccination.” In fact, the virus has been found to persist in the body of the vaccinated person for as long as seven years after vaccination.
This is not surprising, given that in congenital rubella syndrome the virus can persist for at least 20 years and, probably, for a lifetime.
Thus, there is no reason to make a distinction between rubella virus entering the organism as part of the disease process and the same virus entering via a vaccination. It is known, for instance, that “vacines sometimes develop mild rubella, including rash, lymphadenopathy, fever, sore throat and headache.” In adult women this occurs in about half the vacines.
In both cases, immune complexes are formed and persist in the host organism for lengthy periods. Immune complexes from a vaccination can attack the pancreas just as easily as if they were from congenital rubella syndrome.
The actual mechanism of such an attack on the pancreas is probably multifactorial. Aside from the possibility that the immune complexes attack the islet cells of the pancreas directly, there is also the likelihood that they generate an allergic (anaphylactic, hypersensitive) or autoimmune state with subsequent autoimmune destruction of the pancreas. Margaret Menser wrote:
“Clinically it is not possible to show whether the pathogenesis of the diabetes initiated by the rubella virus is due solely to direct viral invasion of the beta-cells of the islets of Langerhans, or whether the virus induces an immunologic reaction in the islet cells, which then leads to the development of diabetes.”
E.J. Mayfield and colleagues wrote in the same connection:
“The mechanism of virus-induced diabetes is not known. Viruses associated with diabetes in animals may cause disease by directly lysing [i.e., dissolving] the beta-cells; triggering an autoimmune response; or specifically impairing the secretory process of beta-cells through a persistent infection.”
He concluded that option was the most probable one: the generation of an autoimmune state in which the body, as it were, becomes allergic to itself or to a part of itself.
The reasonableness of this explanation is enhanced by the observation that the rubella vaccine can cause an allergic reaction. A Canadian survey in 1987 found “allergic reactions” in 30 children who reacted adversely to the MMR vaccine. Indeed, the possibility of an anaphylactic reaction from the MMR vaccine is specifically recognized by the Vaccine Injury Table in Title 21 of the Public Health Service Act (this table was developed as a guideline for compensating victims of vaccination under the National Childhood Vaccine Injury Act of 1986, Public Law 99-660).
Diabetes after a rubella vaccination probably represents a combined effect: the virus attacks the islet cells of the pancreas in an organism which has already been weakened by an autoimmune reaction to the same virus.
Link opposing this view that Vaccinations could cause Type 1 Diabetes or be related in anyway.