Vaccines Cause Diabetes-- Centers for Disease Control and Prevention (CDC)
Tagged: * Diabetes (SEE THE BOLD PART ABOUT THE CDC MANIPULATING DATA) ARE WE SURPRISED???
TORONTO, Sept. 20 PRNewswire - The US Centers for Disease Control (CDC) yesterday presented data at the Interscience Conference on Antimicrobial Agents and Chemotherapy (ICAAC) that supports data presented earlier by Dr. Bart Classen, an immunologist at Classen Immunotherapies, proving vaccines cause insulin dependent diabetes.
Earlier this month, Dr. Bart Classen presented data at the International Public Conference on Vaccination which proved vaccines are the largest cause of insulin dependent diabetes in children. This data included data from a prospective randomized clinical trial in Finland showing vaccinated groups had a statistically significant, 17%, increased risk of diabetes after 10 years follow up. Further analysis of people receiving newer, more potent, hemophilus vaccine indicated that these hemophilus vaccines increased the risk of diabetes by about 25%. The CDC's study indicated that 247 of 260 diabetics received the hemophilus vaccine compared to 733 of 780 controls. This indicates the hemophilus vaccines associated with an odds ratio of 1.22 or an approximately 22% increased risk of
diabetes, almost identical to what Classen found.
Dr. Classen has published both animal and human data with several different vaccines that immunization starting in the first month of life was associated with an decreased risk of diabetes while immunization starting after the second month of life is associated with an increased risk of diabetes. Classen has published data from both New Zealand and Italy that the Hepatitis B vaccine, when given after 2 months of life, is associated with an approximately 50% increased risk of diabetes. The CDC only published part of their data on the hepatitis B vaccine. The CDC found the hepatitis B vaccine was associated with an overall decreased risk of diabetes (relative risk 0.92) which is consistent with an large per cent of those vaccinated receiving the vaccine at birth. The CDC however found that those immunized starting after 2 months of life were at a 60% increased risk of developing diabetes than those immunized starting in the first month of
life (.88/.52). The CDC's hepatitis B vaccine data is thus also consistent with Classen's finding.
The CDC's study and analysis suffered from some obvious limitations and flaws. The CDC studied only 260 diabetics and 780 controls while Dr. Classen's studies typically have involved 100,000 people or more. The CDC's study did not compensate for the interaction between the two different vaccines since people received both the hepatitis B vaccine and the hemophilus vaccine while Classen studied these vaccines separately. The CDC study was also limited because over 94% of controls were vaccinated with the hemophilus vaccine while Classen performed studies where almost none of the controls were vaccinated. The net effect is the CDC's study did not have the power of Classen's studies. More importantly the CDC's analysis was flawed because the results were altered, after they were calculated, to compensate for a family history of diabetes. This practice that is considered unorthodox in part because the CDC has many different "fudge" factors by which it can manipulate the results. Last year the CDC presented data from the same data HMO data source but manipulated their results using a different variable to compensate for breast feeding. In 1997 the CDC also presented an analysis on the hepatitis B vaccine, also from the same HMO data source, but did not use either "fudge" factor. In this study the hepatitis B vaccine, when given after 8 weeks of life, was associated with a
90% increased risk of diabetes. The fact that the CDC manipulates similar data in different years using different "fudge" factors has raised suspicion that their analysis is severely flawed and their interpretations of the data
should be viewed with caution.
Dr. Bart Classen presented data at the International Public Conference on Vaccination on September 10 that vaccines cause approximately 80% of cases of insulin dependent diabetes in children who have received multiple vaccines starting after 2 months of life. Children receive 10 or more vaccines and many of these are associated with an increased risk of diabetes. Classen's data and other published data indicates the following vaccines are associated with an increased risk of diabetes (increased risk): hepatitis B (50%), hemophilus (25%), tetanus (20%), diphtheria (9%), pertussis (25%), mumps- rubella (23%). These findings are supported by a case control study performed in Europe. The cumulative effect of all these vaccines on diabetes is tremendous. Highly immunized sailors in the US navy have been found to develop insulin dependent diabetes at a rate of 5.5 times that of controls even though their rate of diabetes on entering the navy was equal to that of controls.
The US and other governments provide compensation for vaccine induced injuries however there is a statute of limitations. Insulin dependent diabetes cost the patient about $1 million over their lifetime. Many diabetics have contacted Dr. Classen about receiving compensation from the US government. Information on this subject can be found on the Vaccine Safety Website (http://vaccines.net).
FDA Told Pneumococcal Vaccine Likely to Cause Epidemic of Diabetes
BALTIMORE, Nov. 8 /PRNewswire/ -- At last Friday's meeting of the FDA's Vaccines and Related Biological Products Advisory Committee meeting the committee heard testimony that the conjugated 7-valent pneumococcal vaccine was likely to cause a large epidemic of diabetes. The committee was meeting to discuss whether to recommend approval of a new conjugated pneumococcal vaccine intended for preventing meningitis and other infections in children. The vaccine is similar in structure to conjugated vaccines to prevent hemophilus meningitis which have been widely used for 10 years and have been linked to large rises in insulin dependent diabetes. The difference is the 7-valent vaccine is composed of 7 different vaccines, each to a separate strain of pneumococcus, so its toxicity may be 7 times as great as the currently marketed hemophilus vaccines.
Dr. J. Bart Classen, an immunologist at Classen Immunotherapies, presented to the committee his recently published data in the British Medical Journal (BMJ 1999;319:1133) supporting a causal relationship between the hemophilus vaccine and the development of insulin dependent diabetes. The BMJ study looked at the rate of diabetes in children receiving 4 or 1 dose of a weak, early generation, hemophilus vaccine and compared this to the rate in children who received no vaccine. The children were followed for 10 years. In the group receiving 4 doses of vaccine the rate of diabetes was elevated by 26% after 7 years compared to children receiving 0 doses. There were an extra 58 cases of insulin dependent diabetes per 100,000 children immunized in the group receiving 4 doses of vaccine compared to children receiving 0 doses. The data is particularly disturbing because it indicates the potential risks of the vaccine exceeds the potential benefit. Immunization against hemophilus is expected to prevent 7 deaths and 7 to 26 cases of severe disability per 100,000 children immunized in Finland.
Committee members were told that based on the rates of diabetes seen in Finland following the hemophilus vaccine that the pneumococcal vaccine could cause a major epidemic of diabetes. Taking into account both the rate of rise of diabetes in Finland and the larger population in the US, the early hemophilus vaccine would be expected to cause 2,300 cases of diabetes a year in the US. However, the newer more potent hemophilus vaccines are expected to cause up to 4,000 cases of diabetes in the US. Since the 7-valent pneumococcal vaccine contains 7 separate vaccines each similar to the hemophilus vaccine the pneumococcal vaccine may cause 28,000 cases of insulin dependent
diabetes in the US each year. As with the hemophilus vaccine the risks with the conjugated pneumococcal vaccine are expected to exceed the benefit.
The FDA was also told that they should delay approval of the vaccine until methods were developed to give the vaccine without inducing diabetes. One such method being considered is early immunization. Several studies have indicated that starting immunization in the first month of life may have the opposite effect and may actually prevent diabetes. Classen's work published in this month's Diabetes Care (Diabetes Care 22 (10): 1760, 1999) explains how early immunization may prevent diabetes.
Dr. Classen's research has been published in numerous journals and featured in national news reports. For the latest information on the effects of vaccines on insulin dependent diabetes and other autoimmune diseases visit the Vaccine Safety Website (http://vaccines.net).
Classen Immunotherapies, Inc.
6517 Montrose Avenue
Baltimore, MD 21212 U.S.A.
Tel: (410) 377-4549
Fax: (410) 377-8526
Classen@vaccines.net
http://vaccines.net
SOURCE: Classen Immunotherapies, Inc.
Childhood Vaccinations and Juvenile-Onset (Type-1) Diabetes
by Harris Coulter, Ph.D.
President, Center for Empirical Medicine Testimony before the Congress of the United States, House of Representatives, Committee on Appropriations, subcommittee on Labor, Health and Human Services, Education, and Related Agencies April 16, 1997
Diabetes, both juvenile-onset (Type I) and adult-onset (Type II), is a major health problem in the United States, and the number of diabetics is increasing every year. In 1947, there were an estimated 600,000 cases of diabetes in the United States.(1)
Thirty years later, in 1976, Henry Bearn wrote: It is perhaps not generally appreciated that in the United States diabetes, or at least the recognition of the disease, has increased about 300 percent over the last fifteen years. It is the second leading cause of blindness, and the third cause of death. In 1950 there were 1.2 million diabetics in the United States; the estimation now is that there are over 10 million, yet the population has increased by only 50 percent.(2)
Today the Metropolitan Life Insurance Co.'s quarterly Statistical Bulletin estimates that diabetics make up 5 percent of the US population, or 13 million persons.(3) Of these, 85-90 percent are adult onset, which is more or less controlled by diet and exercise; the other 10-15 percent require daily injections of insulin. So, while the US population has approximately doubled since the 1940's, the number of diabetics has risen more than 20 times. While the statistical data, like any medical statistics, are based to some degree on estimates, there has clearly been a huge increase in the number of diabetics in the United States. Billions Spent to Help Diabetics - Furthermore, diabetics consumer about 15 percent of all health care costs, again according to Metropolitan Life.
People not only die from diabetes (160,000 cases in 1994) but the disease leads to cardiovascular complications, stroke, gangrene of the extremities requiring amputation, kidney failure, and blindness. With an estimated total health bill in the United States of about $1 trillion per year at the end of the 20th century, the annual bill for the care and treatment of diabetics will shortly amount to $100-$150 billion unless steps are taken to prevent this. If the Medicare and Medicaid expenditures for treatment of diabetics could be reduced by half, it would be a major savings.
African Americans At Risk - Of particular concern is the heightened prevalence of diabetes in the American black population. In 1991 the death rate from diabetes in American white males was 11.5/100,000 (resident population), for white females it was 9.6; for black males it was 24.6 and for black females it was 25.7. In other words, the death rate for blacks is 2-3 times as high as for whites (4).
This is an especially serious problem in the armed services. The expected incidence of Type-I (insulin-dependent) diabetes for persons aged 17-34 is 4/100,000 for whites and 90/100,000 for black sailors in the 17-34 age group. (5) The authors of this study admit ignorance about the reason why the diabetes incidence should be higher in black naval personnel. Especially worrisome in this connection, is the ignorance of scientists about the reasons for the steep rise in diabetes. It may be due, in part, to earlier diagnosis or better treatment of the disease, thus preventing or postponing death and/or the development of stroke, kidney failure, and blindness. But this factor cannot account for the tremendous increase in cases since the 1940s. Genetic and Environmental Factors - In any case, the very origin of diabetes is still a mystery. Since the late 19th century, diabetes has been known to be related to the pancreas and, in 1922, Canadians Frederick Banting and Charles H. Best, discovered that the missing factor was insulin - an internal secretion of the pancreas. But why does the pancreas stop, or fail to start, secreting insulin? Or, more specifically, why do the beta-cells of the pancreas cease to perform their functions? The consensus on the causation of diabetes was expressed in 1976 in a paper by Alexander Bearn: "Diabetes appears to be one of those diseases in which susceptibility may be inherited but where environmental factors may lead to the onset of disease and illness." (6) One environmental factor - viral infection - has been recognized; the other factor of significance for diabetes is the presence of an autoimmune process. (7) But the cause or causes of the epidemic of autoimmune disease in the United States, which commenced in the 1950's, are themselves mysterious. (8) Since the incidence and prevalence of diabetes continues to rise at a rather rapid rate in the United States and the other industrialized countries, every possible causal or environmental factor is worth examining. On such factor which has hardly been investigated at all is the relationship with childhood vaccinations.
The purpose of my appearance here today is to draw the Committee's attention to this connection. No Investigation of the Vaccine Connection - As we will see, while there is much circumstantial and "anecdotal" evidence (meaning case histories) in favor of a diabetes/vaccination connection, this has never been officially investigated. The fact that the federal medical establishment - which would be the major source of funds for such an epidemiologic investigation - is itself highly committed to the childhood vaccination program, goes far to explain the absence of any official interest in this connection. This is a major disadvantage of all research on damage from the childhood vaccination program. In fact, several of the vaccines administered for the disease of childhood have been implicated in the causation of diabetes.
1. 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. (9) 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. (10) Physicians as early as 1949 called attention to low blood glucose in children who had severe reactions to the pertussis vaccine. (11) In 1970, Margaret Pittman wrote: "the infant whose blood sugar level is influenced by food intake may be especially vulnerable to vaccine-induced hypglycemia...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. (12) 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.
II. The Measles-Mumps-Rubella Vaccine
The MMR (measles, mumps, rubella) vaccine, especially its mumps and rubella components, has been especially implicated in the causation of Type-I diabetes.
A. 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. Let us first look at the disease.
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." (13) "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." (14)
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. (15)
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. (16)
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." (17)
Thus, rubella itself has been demonstrated to be a causal agent in Type-I diabetes. How about the vaccine?
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." (18) In fact, the virus has been found to persist in the body of the vaccinated person for as long as seven years after vaccination. (19) This is not surprising, given that in congenital rubella syndrome the virus can persist for at least 20 years and, probably, for a lifetime. (20)
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 "vaccinees sometimes develop mild rubella, including rash, lymphadenopathy, fever, sore throat and headache." (21) In adult women this occurs in about half the vaccinees. (22) 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." (23)
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 (1) directly lysing [i.e., dissolving] the beta-cells; (2) triggering an autoimmune response; or (3) specifically impairing the secretory process of beta-cells through a persistent infection." He concluded that option (2) 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. (24)
The reasonableness of this explanation is enhanced by the observation that the rubella vaccine can cause an allergic reaction. (25) A Canadian survey in 1987 found "allergic reactions" in 30 children who reacted adversely to the MMR vaccine. (26) 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.
B. Mumps and the 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). (27) Furthermore, mumps virus can infect human pancreatic beta cells in vitro and destroy them. (28)
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: (1) the association between viral infections, including mumps, and Type-I diabetes in humans; (2) 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 (3) in vitro studies demonstrating that the wild-type mumps virus can infect human pancreatic beta cells. (29)
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. (30)
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." (31)
C. Measles and Measles Vaccine
There is little convincing evidence of an association between measles as a clinical disease and diabetes; thus there is no reason to suspect the measles component of the MMR vaccine of any causal relationship to diabetes. (32)
III. 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. (33)
IV. Hepatitis B and Hep-B Vaccine
According to J. Barthelow Classen, M.D., a hepatitis B vaccination program in New Zealand, which commenced in 1988, led to a 60 percent increase in Type-I diabetes in the recipients. In the under-20 age group, the incidence of Type-I diabetes prior to the vaccination campaign (i.e. from 1982-1991) was 18.2/100,000 person years. Classen's data have led the National Institute of Allergy and Infectious Diseases to request the Swedish health authorities to investigate the possible connection between the pertussis vaccine and Type-I diabetes. Results are expected to be available in several months. In Classen's view, the Hepatitis B vaccine and other vaccines can induce Type-I diabetes through the release of interferons, since interferons have already been implicated as causing autoimmunity, including Type-I diabetes. Classen also observes that the package inserts for the various hepatitis B vaccines on the market notes that they cause several autoimmune diseases, and the FDA itself has recognized that they can cause alopecia (baldness) of autoimmune origin. (34)
V. Conclusion
The vaccines discussed above are not an exhaustive list of those suspected of causing Type-I diabetes. Apparently in all cases, factors relating to autoimmunity are involved in the causal chain between vaccination and the emergence of Type-I diabetes. Any vaccine capable of giving rise to the autoimmune state is thus a candidate. Little Research Exists on Vaccination and Autoimmunity - A 1996 article on vaccination and autoimmunity by researchers at Tel Aviv University in Israel throws additional light on this question. (35) The authors note that "in recent decades, although it has been suggested in case reports that some vaccines might trigger autoimmune disorders, the subject has received comparatively little attention in clinical and laboratory studies."
Such vaccines as influenza, hepatitis A, hepatitis B, rabies, MMR, tetanus and oral polio have all been linked with autoimmune diseases such as reactive arthritis, thrombocytopenia purpura and lupus. Also, the authors note, "it seems that vaccines have a predilection to affect the nervous system: neuritis, demyelination, myasthenia gravis, and Guillain-Barre syndrome have been described." Furthermore, the incidence of vaccine-induced autoimmunity is twice as high as high in females as in males. The authors conclude: "The subject of the vaccine autoimmunity relationship is still obscure; reports have been rare, not laboratory experimentation on this topic has been undertaken, and there are few animal models. For the time being no conclusions can be drawn."
Since this is still virgin territory, we may expect far more data in support of the vaccine-autoimmunity connection as work progresses and, specifically, on the connection with Type-I diabetes. Military and African American Populations Need Study - Further evidence of a possible vaccination link is found in the data on diabetes in US Navy enlisted personnel mentioned above. These are individuals in whom Type-I diabetes has appeared after the age of enlistment (since diabetes is a bar to enlistment). Frequent vaccinations seems to be a fact of life in the US armed forces. In the absence of any suggestion as to other possible causative factors which could transform a healthy sailor into a diabetic, the vaccinations which these men and women receive at regular intervals during their naval service must be considered as prime suspects. (36) The greater incidence of diabetes in the US African American population can readily be explained in terms of enhanced susceptibility to vaccine damage. The genetic background of this population may differ in significant respects from that of white populations sufficiently to account for a greater likelihood of vaccine damage.
Public Health Agencies Ignore Diabetes-Vaccine Connection - A striking feature of this whole diabetes/vaccination picture is the division or bifurcation of medical opinion. While researchers are well aware of the significance of vaccinations as etiological agents in the production of diabetes, the Public Health Service and related agencies promoting vaccination programs deny or ignore this relationship or are simply unaware of it. At any rate, the public is not yet being informed of this additional and very real risk from the vaccines which they are compelled to administer to their children.
The seriousness of Type-I diabetes is perhaps not appreciated by the public at large. While not quite a death sentence, it is close to it. Panzram wrote in 1984: "Type-I diabetes, particularly at a young age, must be considered as a rather serious disease, with a 5 to 10-fold higher excess in mortality in comparison with the general population." (37) Diabetes is the seventh leading cause of death in the United States. Type-I, especially, means a shortened life with many disagreeable features such as stroke, kidney failure, cardiovascular complications, blindness and the need to amputate gangrenous limbs. The bill for treating these conditions is, as already noted earlier, in the neighborhood of $100-$150 billion every year.
VI. Suggestions for Action
As noted throughout this paper, the Public Health Service and other federal health agencies promote vaccination programs and do not readily criticize them. Even the scanty information we have today about vaccine damage would not have been available if the Congress had not adopted the National Childhood Vaccine Injury Act of 1986 (over a presidential veto), compelling these agencies to investigate areas they would have preferred to ignore. The following action items are suggested as ways to prevail on these agencies to pursue further research on these matters and thus increase our knowledge of the vaccination-diabetes connection.
Study Military Personnel - An effort should be made to contact former armed services personnel who contracted Type-I diabetes while on active service. Since diabetes is a bar to military service, one can be relatively certain that these individuals were diabetes-free at the time of enlistment. It would be interesting to ascertain the chronological relationship between one or another of the many vaccinations received by servicemen and women and the date of onset of the first symptoms of diabetes (the testimony of one who did contract diabetes in this way is given in the Appendix).
Study Modification of Vaccination Schedules - Alternative scheduling of childhood vaccinations as a way of minimizing the incidence of Type-I diabetes should be studied. Conduct Cost-Benefit Analyses - Cost-benefit analyses of various childhood vaccines should be prepared based on the assumption that they contribute to the incidence of Type-I diabetes.
Alert Doctors - Physicians should be alerted to Type-I diabetes as a possible consequence of rubella, pertussis and other childhood vaccinations; if that were done, the reporting of Type-I diabetes would be intensified.
Add Type-I Diabetes to Vaccine Injury Compensation Table - Consideration should be given to including Type-I diabetes in the Vaccine Injury Table of the national vaccine injury compensation program created under PL99-660.
NOTES
1. Henry A. Christian, The Principles and Practice of Medicine. Sixteenth Edition. New York: D. Appleton-Century, 1947, 582.
2. Alexander G. Bearn, "Structural Determinants of Disease and Their Contribution to Clinical and Scientific Progress." SIBA Foundation Symposiums 44 (1976), 25-40, at 28.
3. Washington Post. Health. April 1, 1997.
4. USDHHS, Health United States 1993. Washington, D.C: GPO, 1994-93.
5. Edward D. Gorham, Frank G. Garland, Elizabeth Barrett-Connor, Cedric F. Garland, Deborah L. Wingard and William M. Pugh, "Incidence of Insulin-dependent Diabetes Mellitus in Young Adults: Experience of 1,587,630 US Navy Enlisted Personnel." A.J. Epidemiology 138:11 (1993), 984-987.
6. Alexander Bearn, op cit, 36-37.
7. Daniel P. Stites, John D. Stobo, H. Hugh Fudenberg and J. Vivian Wells, Basic and Clinical Immunology. Fifth Edition. Los Altos, California: Lange, 1984, 152ff.
8. Ibid., 153.
9. H.L. Coulter and Barbara Loe Fisher, DPT: A Shot in the Dark, Garden City Park, N.Y.: Avery Publishers, 1991, 49-50. 10. Ronald D. Sekura, Joel Moss and Martha Vaughan, Pertussis Toxin. New York and London: Academic Press, 1985, 19-43; J.J. Munoz and R.K. Bergman, Bordetella Pertussis. New York and Basel: Marcel Dekker, 1977, 160ff.; B.L. Furman, A.C. Wardlaw and L.Q. Stevenson, "Bordetella Pertussis-Induced Hyperinsulinemia Without Marked Hypoglycemia: A Paradox Explained." British Journal of Experimental Pathology 62 (1981), 504-511.
11. Cited in C.S.F. Easmon and J. Jeljaszewicz, Medical Microbiology, Volume 2. Immunization Against Bacterial Diseases. London and New York: Academic Press, 1983, 246.
12. Cited in H.L Coulter and Barbara Loe Fisher, op. cit., 49-50.
13. Margaret Menser et al., "Rubella Infection and Diabetes Mellitus." Lancet (January 14, 1978), 57-60, at 57.
14. E.J. Rayfield et al, "Rubella Virus-Induced Diabetes in the Hamster." Diabetes 35 (December, 1986), 1278-1281, at 1278. 15. Ibid., 1280. Daniel H. Gold and T.A. Weingeist, The Eye in Systemic Disease. Philadelphia: Lippincott, 1990, 270.
16. P.K. Coyle et al., "Rubella-Specific Immune Complexes After Congenital Infection and Vaccination." Infection and Immunity 36:2 (May, 1982), 498-503, at 501.
17. Kei Numazaki et al. "Infection of Cultured Human Fetal Pancreatic Islet Cells by Rubella Virus." A.J. Clinical Pathology 91 (1989), 446-451.
18. P.K. Coyle et al, op. cit., 501.
19. Ibid, 502. Wolfgang Ehrengut, "Central Nervous System Sequelae of Immunization Against Measles, Mumps, Rubella and Poliomyelitis." Acta Paediatrica Japonica 32 (1990), 8-11, at 10; Aubrey J. Tingle et al., "Postpartum Rubella Immunization: Association with Development of Prolonged Arthritis, Neurological Sequelae, and Chronic Rubella Viremia." J. Infectious Diseases 152:3 (September, 1985), 606-612, at 607.
20. E.J. Rayfield et al., op. cit., 1281.
21. Stanley A. Plotkin and Edward Mortimer, Jr., Vaccines. Philadelphia: W.B. Saunders Co., 1988, 248.
22. M. Poyner et al., "The Reactogenicity of Rubella Vaccine in a Population of United Kingdom Schoolgirls." B.J. Clinical Practice 40:11 (November, 1986), 468-471, at 470.
23. Margaret Menser et al., op. cit, 59.
24. E.J. Rayfield et al., op. cit., 1278, 1280.
25. T.M. Pollock and Jean Morris, "A 7-Year Survey of Disorders Attributed to Vaccination in North West Thames Region." Lancet (April 2, 1983), 753-757, at 754.
26. Sasson Lavi et al., "Administration of Measles, Mumps and Rubella Vaccine (Live) to Egg-Allergic Children." Journal of the AMA 263:2 (January 12, 1990), 269-271.
27. Kathleen R. Stratton et al, editors, Adverse Events Associated with Childhood Vaccines: Evidence Bearing on Causality, Washington, D.C.: National Academy Press, 1993, 153-154.
28. Ibid, 156.
29. Ibid, 158-159.
30. Ibid, 154.
31. Ibid, vi.
32. Kathleen R. Stratton, et al., opc. cit., 154, 158.
34. J. Barthelow Classen, "Childhood Immunisation and Diabetes Mellitus." New Zealand M.J., 109 (May 24, 1996), 195.
35. Arnon Dov Cohen and Yehuda Shoenfeld, "Vaccine-Induced Autoimmunity." J. Autoimmunity 9 (1996), 699-703.
36. Edward D. Gotham et al, op. cit.
37. G. Panzram, "Epidemiologic Data on Excess Mortality and Life Expectancy in Insulin-Dependent Diabetes Mellitus - Critical Review." Exp. Clin. Endocrinol. 83: 1(1984), 93-100, at 93.
Tagged: * Diabetes (SEE THE BOLD PART ABOUT THE CDC MANIPULATING DATA) ARE WE SURPRISED???
TORONTO, Sept. 20 PRNewswire - The US Centers for Disease Control (CDC) yesterday presented data at the Interscience Conference on Antimicrobial Agents and Chemotherapy (ICAAC) that supports data presented earlier by Dr. Bart Classen, an immunologist at Classen Immunotherapies, proving vaccines cause insulin dependent diabetes.
Earlier this month, Dr. Bart Classen presented data at the International Public Conference on Vaccination which proved vaccines are the largest cause of insulin dependent diabetes in children. This data included data from a prospective randomized clinical trial in Finland showing vaccinated groups had a statistically significant, 17%, increased risk of diabetes after 10 years follow up. Further analysis of people receiving newer, more potent, hemophilus vaccine indicated that these hemophilus vaccines increased the risk of diabetes by about 25%. The CDC's study indicated that 247 of 260 diabetics received the hemophilus vaccine compared to 733 of 780 controls. This indicates the hemophilus vaccines associated with an odds ratio of 1.22 or an approximately 22% increased risk of
diabetes, almost identical to what Classen found.
Dr. Classen has published both animal and human data with several different vaccines that immunization starting in the first month of life was associated with an decreased risk of diabetes while immunization starting after the second month of life is associated with an increased risk of diabetes. Classen has published data from both New Zealand and Italy that the Hepatitis B vaccine, when given after 2 months of life, is associated with an approximately 50% increased risk of diabetes. The CDC only published part of their data on the hepatitis B vaccine. The CDC found the hepatitis B vaccine was associated with an overall decreased risk of diabetes (relative risk 0.92) which is consistent with an large per cent of those vaccinated receiving the vaccine at birth. The CDC however found that those immunized starting after 2 months of life were at a 60% increased risk of developing diabetes than those immunized starting in the first month of
life (.88/.52). The CDC's hepatitis B vaccine data is thus also consistent with Classen's finding.
The CDC's study and analysis suffered from some obvious limitations and flaws. The CDC studied only 260 diabetics and 780 controls while Dr. Classen's studies typically have involved 100,000 people or more. The CDC's study did not compensate for the interaction between the two different vaccines since people received both the hepatitis B vaccine and the hemophilus vaccine while Classen studied these vaccines separately. The CDC study was also limited because over 94% of controls were vaccinated with the hemophilus vaccine while Classen performed studies where almost none of the controls were vaccinated. The net effect is the CDC's study did not have the power of Classen's studies. More importantly the CDC's analysis was flawed because the results were altered, after they were calculated, to compensate for a family history of diabetes. This practice that is considered unorthodox in part because the CDC has many different "fudge" factors by which it can manipulate the results. Last year the CDC presented data from the same data HMO data source but manipulated their results using a different variable to compensate for breast feeding. In 1997 the CDC also presented an analysis on the hepatitis B vaccine, also from the same HMO data source, but did not use either "fudge" factor. In this study the hepatitis B vaccine, when given after 8 weeks of life, was associated with a
90% increased risk of diabetes. The fact that the CDC manipulates similar data in different years using different "fudge" factors has raised suspicion that their analysis is severely flawed and their interpretations of the data
should be viewed with caution.
Dr. Bart Classen presented data at the International Public Conference on Vaccination on September 10 that vaccines cause approximately 80% of cases of insulin dependent diabetes in children who have received multiple vaccines starting after 2 months of life. Children receive 10 or more vaccines and many of these are associated with an increased risk of diabetes. Classen's data and other published data indicates the following vaccines are associated with an increased risk of diabetes (increased risk): hepatitis B (50%), hemophilus (25%), tetanus (20%), diphtheria (9%), pertussis (25%), mumps- rubella (23%). These findings are supported by a case control study performed in Europe. The cumulative effect of all these vaccines on diabetes is tremendous. Highly immunized sailors in the US navy have been found to develop insulin dependent diabetes at a rate of 5.5 times that of controls even though their rate of diabetes on entering the navy was equal to that of controls.
The US and other governments provide compensation for vaccine induced injuries however there is a statute of limitations. Insulin dependent diabetes cost the patient about $1 million over their lifetime. Many diabetics have contacted Dr. Classen about receiving compensation from the US government. Information on this subject can be found on the Vaccine Safety Website (http://vaccines.net).
FDA Told Pneumococcal Vaccine Likely to Cause Epidemic of Diabetes
BALTIMORE, Nov. 8 /PRNewswire/ -- At last Friday's meeting of the FDA's Vaccines and Related Biological Products Advisory Committee meeting the committee heard testimony that the conjugated 7-valent pneumococcal vaccine was likely to cause a large epidemic of diabetes. The committee was meeting to discuss whether to recommend approval of a new conjugated pneumococcal vaccine intended for preventing meningitis and other infections in children. The vaccine is similar in structure to conjugated vaccines to prevent hemophilus meningitis which have been widely used for 10 years and have been linked to large rises in insulin dependent diabetes. The difference is the 7-valent vaccine is composed of 7 different vaccines, each to a separate strain of pneumococcus, so its toxicity may be 7 times as great as the currently marketed hemophilus vaccines.
Dr. J. Bart Classen, an immunologist at Classen Immunotherapies, presented to the committee his recently published data in the British Medical Journal (BMJ 1999;319:1133) supporting a causal relationship between the hemophilus vaccine and the development of insulin dependent diabetes. The BMJ study looked at the rate of diabetes in children receiving 4 or 1 dose of a weak, early generation, hemophilus vaccine and compared this to the rate in children who received no vaccine. The children were followed for 10 years. In the group receiving 4 doses of vaccine the rate of diabetes was elevated by 26% after 7 years compared to children receiving 0 doses. There were an extra 58 cases of insulin dependent diabetes per 100,000 children immunized in the group receiving 4 doses of vaccine compared to children receiving 0 doses. The data is particularly disturbing because it indicates the potential risks of the vaccine exceeds the potential benefit. Immunization against hemophilus is expected to prevent 7 deaths and 7 to 26 cases of severe disability per 100,000 children immunized in Finland.
Committee members were told that based on the rates of diabetes seen in Finland following the hemophilus vaccine that the pneumococcal vaccine could cause a major epidemic of diabetes. Taking into account both the rate of rise of diabetes in Finland and the larger population in the US, the early hemophilus vaccine would be expected to cause 2,300 cases of diabetes a year in the US. However, the newer more potent hemophilus vaccines are expected to cause up to 4,000 cases of diabetes in the US. Since the 7-valent pneumococcal vaccine contains 7 separate vaccines each similar to the hemophilus vaccine the pneumococcal vaccine may cause 28,000 cases of insulin dependent
diabetes in the US each year. As with the hemophilus vaccine the risks with the conjugated pneumococcal vaccine are expected to exceed the benefit.
The FDA was also told that they should delay approval of the vaccine until methods were developed to give the vaccine without inducing diabetes. One such method being considered is early immunization. Several studies have indicated that starting immunization in the first month of life may have the opposite effect and may actually prevent diabetes. Classen's work published in this month's Diabetes Care (Diabetes Care 22 (10): 1760, 1999) explains how early immunization may prevent diabetes.
Dr. Classen's research has been published in numerous journals and featured in national news reports. For the latest information on the effects of vaccines on insulin dependent diabetes and other autoimmune diseases visit the Vaccine Safety Website (http://vaccines.net).
Classen Immunotherapies, Inc.
6517 Montrose Avenue
Baltimore, MD 21212 U.S.A.
Tel: (410) 377-4549
Fax: (410) 377-8526
Classen@vaccines.net
http://vaccines.net
SOURCE: Classen Immunotherapies, Inc.
Childhood Vaccinations and Juvenile-Onset (Type-1) Diabetes
by Harris Coulter, Ph.D.
President, Center for Empirical Medicine Testimony before the Congress of the United States, House of Representatives, Committee on Appropriations, subcommittee on Labor, Health and Human Services, Education, and Related Agencies April 16, 1997
Diabetes, both juvenile-onset (Type I) and adult-onset (Type II), is a major health problem in the United States, and the number of diabetics is increasing every year. In 1947, there were an estimated 600,000 cases of diabetes in the United States.(1)
Thirty years later, in 1976, Henry Bearn wrote: It is perhaps not generally appreciated that in the United States diabetes, or at least the recognition of the disease, has increased about 300 percent over the last fifteen years. It is the second leading cause of blindness, and the third cause of death. In 1950 there were 1.2 million diabetics in the United States; the estimation now is that there are over 10 million, yet the population has increased by only 50 percent.(2)
Today the Metropolitan Life Insurance Co.'s quarterly Statistical Bulletin estimates that diabetics make up 5 percent of the US population, or 13 million persons.(3) Of these, 85-90 percent are adult onset, which is more or less controlled by diet and exercise; the other 10-15 percent require daily injections of insulin. So, while the US population has approximately doubled since the 1940's, the number of diabetics has risen more than 20 times. While the statistical data, like any medical statistics, are based to some degree on estimates, there has clearly been a huge increase in the number of diabetics in the United States. Billions Spent to Help Diabetics - Furthermore, diabetics consumer about 15 percent of all health care costs, again according to Metropolitan Life.
People not only die from diabetes (160,000 cases in 1994) but the disease leads to cardiovascular complications, stroke, gangrene of the extremities requiring amputation, kidney failure, and blindness. With an estimated total health bill in the United States of about $1 trillion per year at the end of the 20th century, the annual bill for the care and treatment of diabetics will shortly amount to $100-$150 billion unless steps are taken to prevent this. If the Medicare and Medicaid expenditures for treatment of diabetics could be reduced by half, it would be a major savings.
African Americans At Risk - Of particular concern is the heightened prevalence of diabetes in the American black population. In 1991 the death rate from diabetes in American white males was 11.5/100,000 (resident population), for white females it was 9.6; for black males it was 24.6 and for black females it was 25.7. In other words, the death rate for blacks is 2-3 times as high as for whites (4).
This is an especially serious problem in the armed services. The expected incidence of Type-I (insulin-dependent) diabetes for persons aged 17-34 is 4/100,000 for whites and 90/100,000 for black sailors in the 17-34 age group. (5) The authors of this study admit ignorance about the reason why the diabetes incidence should be higher in black naval personnel. Especially worrisome in this connection, is the ignorance of scientists about the reasons for the steep rise in diabetes. It may be due, in part, to earlier diagnosis or better treatment of the disease, thus preventing or postponing death and/or the development of stroke, kidney failure, and blindness. But this factor cannot account for the tremendous increase in cases since the 1940s. Genetic and Environmental Factors - In any case, the very origin of diabetes is still a mystery. Since the late 19th century, diabetes has been known to be related to the pancreas and, in 1922, Canadians Frederick Banting and Charles H. Best, discovered that the missing factor was insulin - an internal secretion of the pancreas. But why does the pancreas stop, or fail to start, secreting insulin? Or, more specifically, why do the beta-cells of the pancreas cease to perform their functions? The consensus on the causation of diabetes was expressed in 1976 in a paper by Alexander Bearn: "Diabetes appears to be one of those diseases in which susceptibility may be inherited but where environmental factors may lead to the onset of disease and illness." (6) One environmental factor - viral infection - has been recognized; the other factor of significance for diabetes is the presence of an autoimmune process. (7) But the cause or causes of the epidemic of autoimmune disease in the United States, which commenced in the 1950's, are themselves mysterious. (8) Since the incidence and prevalence of diabetes continues to rise at a rather rapid rate in the United States and the other industrialized countries, every possible causal or environmental factor is worth examining. On such factor which has hardly been investigated at all is the relationship with childhood vaccinations.
The purpose of my appearance here today is to draw the Committee's attention to this connection. No Investigation of the Vaccine Connection - As we will see, while there is much circumstantial and "anecdotal" evidence (meaning case histories) in favor of a diabetes/vaccination connection, this has never been officially investigated. The fact that the federal medical establishment - which would be the major source of funds for such an epidemiologic investigation - is itself highly committed to the childhood vaccination program, goes far to explain the absence of any official interest in this connection. This is a major disadvantage of all research on damage from the childhood vaccination program. In fact, several of the vaccines administered for the disease of childhood have been implicated in the causation of diabetes.
1. 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. (9) 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. (10) Physicians as early as 1949 called attention to low blood glucose in children who had severe reactions to the pertussis vaccine. (11) In 1970, Margaret Pittman wrote: "the infant whose blood sugar level is influenced by food intake may be especially vulnerable to vaccine-induced hypglycemia...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. (12) 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.
II. The Measles-Mumps-Rubella Vaccine
The MMR (measles, mumps, rubella) vaccine, especially its mumps and rubella components, has been especially implicated in the causation of Type-I diabetes.
A. 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. Let us first look at the disease.
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." (13) "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." (14)
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. (15)
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. (16)
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." (17)
Thus, rubella itself has been demonstrated to be a causal agent in Type-I diabetes. How about the vaccine?
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." (18) In fact, the virus has been found to persist in the body of the vaccinated person for as long as seven years after vaccination. (19) This is not surprising, given that in congenital rubella syndrome the virus can persist for at least 20 years and, probably, for a lifetime. (20)
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 "vaccinees sometimes develop mild rubella, including rash, lymphadenopathy, fever, sore throat and headache." (21) In adult women this occurs in about half the vaccinees. (22) 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." (23)
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 (1) directly lysing [i.e., dissolving] the beta-cells; (2) triggering an autoimmune response; or (3) specifically impairing the secretory process of beta-cells through a persistent infection." He concluded that option (2) 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. (24)
The reasonableness of this explanation is enhanced by the observation that the rubella vaccine can cause an allergic reaction. (25) A Canadian survey in 1987 found "allergic reactions" in 30 children who reacted adversely to the MMR vaccine. (26) 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.
B. Mumps and the 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). (27) Furthermore, mumps virus can infect human pancreatic beta cells in vitro and destroy them. (28)
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: (1) the association between viral infections, including mumps, and Type-I diabetes in humans; (2) 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 (3) in vitro studies demonstrating that the wild-type mumps virus can infect human pancreatic beta cells. (29)
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. (30)
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." (31)
C. Measles and Measles Vaccine
There is little convincing evidence of an association between measles as a clinical disease and diabetes; thus there is no reason to suspect the measles component of the MMR vaccine of any causal relationship to diabetes. (32)
III. 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. (33)
IV. Hepatitis B and Hep-B Vaccine
According to J. Barthelow Classen, M.D., a hepatitis B vaccination program in New Zealand, which commenced in 1988, led to a 60 percent increase in Type-I diabetes in the recipients. In the under-20 age group, the incidence of Type-I diabetes prior to the vaccination campaign (i.e. from 1982-1991) was 18.2/100,000 person years. Classen's data have led the National Institute of Allergy and Infectious Diseases to request the Swedish health authorities to investigate the possible connection between the pertussis vaccine and Type-I diabetes. Results are expected to be available in several months. In Classen's view, the Hepatitis B vaccine and other vaccines can induce Type-I diabetes through the release of interferons, since interferons have already been implicated as causing autoimmunity, including Type-I diabetes. Classen also observes that the package inserts for the various hepatitis B vaccines on the market notes that they cause several autoimmune diseases, and the FDA itself has recognized that they can cause alopecia (baldness) of autoimmune origin. (34)
V. Conclusion
The vaccines discussed above are not an exhaustive list of those suspected of causing Type-I diabetes. Apparently in all cases, factors relating to autoimmunity are involved in the causal chain between vaccination and the emergence of Type-I diabetes. Any vaccine capable of giving rise to the autoimmune state is thus a candidate. Little Research Exists on Vaccination and Autoimmunity - A 1996 article on vaccination and autoimmunity by researchers at Tel Aviv University in Israel throws additional light on this question. (35) The authors note that "in recent decades, although it has been suggested in case reports that some vaccines might trigger autoimmune disorders, the subject has received comparatively little attention in clinical and laboratory studies."
Such vaccines as influenza, hepatitis A, hepatitis B, rabies, MMR, tetanus and oral polio have all been linked with autoimmune diseases such as reactive arthritis, thrombocytopenia purpura and lupus. Also, the authors note, "it seems that vaccines have a predilection to affect the nervous system: neuritis, demyelination, myasthenia gravis, and Guillain-Barre syndrome have been described." Furthermore, the incidence of vaccine-induced autoimmunity is twice as high as high in females as in males. The authors conclude: "The subject of the vaccine autoimmunity relationship is still obscure; reports have been rare, not laboratory experimentation on this topic has been undertaken, and there are few animal models. For the time being no conclusions can be drawn."
Since this is still virgin territory, we may expect far more data in support of the vaccine-autoimmunity connection as work progresses and, specifically, on the connection with Type-I diabetes. Military and African American Populations Need Study - Further evidence of a possible vaccination link is found in the data on diabetes in US Navy enlisted personnel mentioned above. These are individuals in whom Type-I diabetes has appeared after the age of enlistment (since diabetes is a bar to enlistment). Frequent vaccinations seems to be a fact of life in the US armed forces. In the absence of any suggestion as to other possible causative factors which could transform a healthy sailor into a diabetic, the vaccinations which these men and women receive at regular intervals during their naval service must be considered as prime suspects. (36) The greater incidence of diabetes in the US African American population can readily be explained in terms of enhanced susceptibility to vaccine damage. The genetic background of this population may differ in significant respects from that of white populations sufficiently to account for a greater likelihood of vaccine damage.
Public Health Agencies Ignore Diabetes-Vaccine Connection - A striking feature of this whole diabetes/vaccination picture is the division or bifurcation of medical opinion. While researchers are well aware of the significance of vaccinations as etiological agents in the production of diabetes, the Public Health Service and related agencies promoting vaccination programs deny or ignore this relationship or are simply unaware of it. At any rate, the public is not yet being informed of this additional and very real risk from the vaccines which they are compelled to administer to their children.
The seriousness of Type-I diabetes is perhaps not appreciated by the public at large. While not quite a death sentence, it is close to it. Panzram wrote in 1984: "Type-I diabetes, particularly at a young age, must be considered as a rather serious disease, with a 5 to 10-fold higher excess in mortality in comparison with the general population." (37) Diabetes is the seventh leading cause of death in the United States. Type-I, especially, means a shortened life with many disagreeable features such as stroke, kidney failure, cardiovascular complications, blindness and the need to amputate gangrenous limbs. The bill for treating these conditions is, as already noted earlier, in the neighborhood of $100-$150 billion every year.
VI. Suggestions for Action
As noted throughout this paper, the Public Health Service and other federal health agencies promote vaccination programs and do not readily criticize them. Even the scanty information we have today about vaccine damage would not have been available if the Congress had not adopted the National Childhood Vaccine Injury Act of 1986 (over a presidential veto), compelling these agencies to investigate areas they would have preferred to ignore. The following action items are suggested as ways to prevail on these agencies to pursue further research on these matters and thus increase our knowledge of the vaccination-diabetes connection.
Study Military Personnel - An effort should be made to contact former armed services personnel who contracted Type-I diabetes while on active service. Since diabetes is a bar to military service, one can be relatively certain that these individuals were diabetes-free at the time of enlistment. It would be interesting to ascertain the chronological relationship between one or another of the many vaccinations received by servicemen and women and the date of onset of the first symptoms of diabetes (the testimony of one who did contract diabetes in this way is given in the Appendix).
Study Modification of Vaccination Schedules - Alternative scheduling of childhood vaccinations as a way of minimizing the incidence of Type-I diabetes should be studied. Conduct Cost-Benefit Analyses - Cost-benefit analyses of various childhood vaccines should be prepared based on the assumption that they contribute to the incidence of Type-I diabetes.
Alert Doctors - Physicians should be alerted to Type-I diabetes as a possible consequence of rubella, pertussis and other childhood vaccinations; if that were done, the reporting of Type-I diabetes would be intensified.
Add Type-I Diabetes to Vaccine Injury Compensation Table - Consideration should be given to including Type-I diabetes in the Vaccine Injury Table of the national vaccine injury compensation program created under PL99-660.
NOTES
1. Henry A. Christian, The Principles and Practice of Medicine. Sixteenth Edition. New York: D. Appleton-Century, 1947, 582.
2. Alexander G. Bearn, "Structural Determinants of Disease and Their Contribution to Clinical and Scientific Progress." SIBA Foundation Symposiums 44 (1976), 25-40, at 28.
3. Washington Post. Health. April 1, 1997.
4. USDHHS, Health United States 1993. Washington, D.C: GPO, 1994-93.
5. Edward D. Gorham, Frank G. Garland, Elizabeth Barrett-Connor, Cedric F. Garland, Deborah L. Wingard and William M. Pugh, "Incidence of Insulin-dependent Diabetes Mellitus in Young Adults: Experience of 1,587,630 US Navy Enlisted Personnel." A.J. Epidemiology 138:11 (1993), 984-987.
6. Alexander Bearn, op cit, 36-37.
7. Daniel P. Stites, John D. Stobo, H. Hugh Fudenberg and J. Vivian Wells, Basic and Clinical Immunology. Fifth Edition. Los Altos, California: Lange, 1984, 152ff.
8. Ibid., 153.
9. H.L. Coulter and Barbara Loe Fisher, DPT: A Shot in the Dark, Garden City Park, N.Y.: Avery Publishers, 1991, 49-50. 10. Ronald D. Sekura, Joel Moss and Martha Vaughan, Pertussis Toxin. New York and London: Academic Press, 1985, 19-43; J.J. Munoz and R.K. Bergman, Bordetella Pertussis. New York and Basel: Marcel Dekker, 1977, 160ff.; B.L. Furman, A.C. Wardlaw and L.Q. Stevenson, "Bordetella Pertussis-Induced Hyperinsulinemia Without Marked Hypoglycemia: A Paradox Explained." British Journal of Experimental Pathology 62 (1981), 504-511.
11. Cited in C.S.F. Easmon and J. Jeljaszewicz, Medical Microbiology, Volume 2. Immunization Against Bacterial Diseases. London and New York: Academic Press, 1983, 246.
12. Cited in H.L Coulter and Barbara Loe Fisher, op. cit., 49-50.
13. Margaret Menser et al., "Rubella Infection and Diabetes Mellitus." Lancet (January 14, 1978), 57-60, at 57.
14. E.J. Rayfield et al, "Rubella Virus-Induced Diabetes in the Hamster." Diabetes 35 (December, 1986), 1278-1281, at 1278. 15. Ibid., 1280. Daniel H. Gold and T.A. Weingeist, The Eye in Systemic Disease. Philadelphia: Lippincott, 1990, 270.
16. P.K. Coyle et al., "Rubella-Specific Immune Complexes After Congenital Infection and Vaccination." Infection and Immunity 36:2 (May, 1982), 498-503, at 501.
17. Kei Numazaki et al. "Infection of Cultured Human Fetal Pancreatic Islet Cells by Rubella Virus." A.J. Clinical Pathology 91 (1989), 446-451.
18. P.K. Coyle et al, op. cit., 501.
19. Ibid, 502. Wolfgang Ehrengut, "Central Nervous System Sequelae of Immunization Against Measles, Mumps, Rubella and Poliomyelitis." Acta Paediatrica Japonica 32 (1990), 8-11, at 10; Aubrey J. Tingle et al., "Postpartum Rubella Immunization: Association with Development of Prolonged Arthritis, Neurological Sequelae, and Chronic Rubella Viremia." J. Infectious Diseases 152:3 (September, 1985), 606-612, at 607.
20. E.J. Rayfield et al., op. cit., 1281.
21. Stanley A. Plotkin and Edward Mortimer, Jr., Vaccines. Philadelphia: W.B. Saunders Co., 1988, 248.
22. M. Poyner et al., "The Reactogenicity of Rubella Vaccine in a Population of United Kingdom Schoolgirls." B.J. Clinical Practice 40:11 (November, 1986), 468-471, at 470.
23. Margaret Menser et al., op. cit, 59.
24. E.J. Rayfield et al., op. cit., 1278, 1280.
25. T.M. Pollock and Jean Morris, "A 7-Year Survey of Disorders Attributed to Vaccination in North West Thames Region." Lancet (April 2, 1983), 753-757, at 754.
26. Sasson Lavi et al., "Administration of Measles, Mumps and Rubella Vaccine (Live) to Egg-Allergic Children." Journal of the AMA 263:2 (January 12, 1990), 269-271.
27. Kathleen R. Stratton et al, editors, Adverse Events Associated with Childhood Vaccines: Evidence Bearing on Causality, Washington, D.C.: National Academy Press, 1993, 153-154.
28. Ibid, 156.
29. Ibid, 158-159.
30. Ibid, 154.
31. Ibid, vi.
32. Kathleen R. Stratton, et al., opc. cit., 154, 158.
34. J. Barthelow Classen, "Childhood Immunisation and Diabetes Mellitus." New Zealand M.J., 109 (May 24, 1996), 195.
35. Arnon Dov Cohen and Yehuda Shoenfeld, "Vaccine-Induced Autoimmunity." J. Autoimmunity 9 (1996), 699-703.
36. Edward D. Gotham et al, op. cit.
37. G. Panzram, "Epidemiologic Data on Excess Mortality and Life Expectancy in Insulin-Dependent Diabetes Mellitus - Critical Review." Exp. Clin. Endocrinol. 83: 1(1984), 93-100, at 93.
