Childhood Vaccination and Juvenile Diabetes OT

[Guest guest]

Hi all. I found this on the internet at: www.whale.to/v/coulter.html

So apparently, MMR might have caused my son's autism AND my juvenile

diabetes!!!

Childhood Vaccinations and Juvenile-Onset (Type-1) Diabetes

by 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 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

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 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. 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. D. Gorham, G. Garland, Barrett-Connor, Cedric F.

Garland, Deborah L. Wingard and 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. Bearn, op cit, 36-37.

7. P. Stites, 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. D. Sekura, 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. son,

" 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. 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 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 , " 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. 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.

[Vaccination]  [Coulter]