Diabetes, a disease caused by failure of the pancreas to generate insulin, is a major health problem in the United States. The number of diabetics, both juvenile-onset (Type I) and adult-onset (Type Il), is increasing every year.

The Metropolitan Life Insurance Co. estimates that diabetics make up 5 percent of the US population, or 13 million persons. Of these 85-90 percent (11,375,000) are adult onset, which is more or less controlled by diet, oral medication, and exercise; the other 1015 percent (1,625,000) require daily injections of insulin.

While the US population has approximately doubled since the 1940s, the number of diabetics has risen more than 20 times since 1946. Diabetics consume about 15 percent of all health care costs, again according to Metropolitan Life. It is the third or fourth leading cause of death (160,000 deaths in 1994), and the disease leads to cardiovascular complications, stroke, gangrene of the extremities requiring amputation, kidney failure, and blindness. It is the leading cause of blindness in adults. Twenty-percent of cases of kidney failure are due to diabetes, and most patients undergoing kidney dialysis are diabetics. Nearly 50 percent of all nontraumatic foot and leg amputations are caused by diabetes. Maternal diabetes is a major cause of birth defects and infant mortality. Diabetics are 2 to 4 times more likely to develop heart disease than non-diabetics. Diabetics spend twice as many days in hospitals as other patients, and it is the fourth leading cause of visits to physicians' offices.

Of course, the emotional toll on diabetics and their families must be added to this account.

With an estimated total health bill in the United States of about $1 trillion/year at the end of the 20th century, the annual bill for the care and treatment of diabetes will shortly amount to over $100 billion -- of which $30 billion will go for Type-1 diabetes and $70 billion for Type-2 -- unless steps are taken to prevent this. If the Medicare and Medicaid expenditure on diabetes could be reduced by half, it would be a major budgetary saving. If only for this reason, my testimony should be of great interest to the Committee on Appropriations.

Of particular concern is the heightened prevalence of diabetes in the American black population. The death rate for blacks is 2-3 times as high as for whites.

This is an especially serious problem in the armed services, where the incidence of Type-1 (insulin-dependent) diabetes for white servicemen and women is eight times higher than for the population at large, while for black servicemen and women it is 22 times higher. No one knows why the diabetes incidence is so high in the armed services, or why it is higher in black service personnel.

In any case, the very origin of diabetes is itself a mystery. What causes the pancreas to stop producing insulin?

One causal factor in Type-1 diabetes which has hardly been investigated at all is the relationship with childhood vaccinations. However, there is much hard scientific data, as well as "anecdotal" evidence (meaning case histories), in favor of a vaccination connection with Type-1 diabetes.

The first vaccine implicated in this way is the one for pertussis (whooping cough) -made from the "pertussis toxin" secreted by the microbe which causes whooping cough. This toxin acts specifically and directly on the insulin-secreting parts of the pancreas.

At least since the 1970s the pertussis vaccine has been shown in animal experiments to stimulate overproduction of insulin by the pancreas followed by its exhaustion and destruction, leading to underproduction of insulin; in the first case the outcome is hypoglycemia, and in the latter it is diabetes. Physicians as early as 1949 called attention to low blood sugar in children with severe reactions to the pertussis vaccine. Dutch researchers observed in 1978: "infants who show serious reactions following pertussis vaccination suffer from a failure to maintain glucose [sugar] homeostasis." And German researchers found in 1979 that 59 out of 149 children who manifested adverse reactions to the pertussis vaccine developed symptoms of hypoglycemia.

One could logically conclude that the steady increase in Type-1 diabetes since the late 1940s is due to the widespread introduction of vaccination against whooping cough which occurred in this same time period. This is borne out by much epidemiologic data. Today the issue is being studied closely in Sweden, and the results of these investigations are expected within the next few months.

The MMR (measles, mumps, rubella) vaccine, especially its rubella (German measles) component, has been especially implicated in the causation of Type-1 diabetes.

German measles itself is known to cause Type-1 diabetes. The "congenital rubella syndrome" -- the name given to the group of impairments and disabilities often seen in babies whose mothers become iii with German measles during pregnancy -- leads to Type-1 diabetes in up to 20 percent of these babies.

In 1989 scientists infected laboratory cultures of human pancreatic cells with rubella virus and found that these infected cells produced much lower levels of insulin.
While German measles can cause Type-1 diabetes, the rubella vaccine can cause clinical German measles, -- with rash, fever, sore throat, and headache -- in up to half of the women who receive it.

It stands to reason that, if German measles can cause Type-1 diabetes, and the rubella vaccine can cause German measles, this vaccine can also cause Type-1 diabetes. The rubella virus probably attacks the islet cells of the pancreas, exacerbating an existing allergic (autoimmune) condition of that organ.

The reasonableness of this explanation is enhanced by the observation that the rubella vaccine often causes an allergic reaction. A Canadian survey in 1987 found "allergic reactions" in 30 children who reacted adversely to the MMR vaccine.

Indeed, the possibility of an allergic or 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 Compensation Act of 1986 [100 Stat. 3780, 3781. Public Law 99- 660]).

The hepatitis-B vaccine is another suspect. According to J. Barthelow Classen, M.D., a 1988 hepatitis-B vaccination program in New Zealand caused a 60 percent increase in Type-1 diabetes in the recipients. In Ciassen's view, the hepatitis B vaccine provokes the release of interferons -- which are known to be implicated in the causation of autoimmunity and of Type-1 diabetes.

The vaccine "package inserts," and the FDA itself, recognize that the various hepatitis-B vaccines on the market cause several autoimmune diseases.

The hemophilus influenzae B vaccine is the final suspect. It was also found to cause Type-1 diabetes in a randomized clinical trial performed recently on 114,000 children in Finland. The group receiving 4 doses of the hemophilus influenzae vaccine had a higher incidence of Type-I diabetes than those receiving one dose only.

Thus we feel that these and possibly other childhood vaccinations are the principal cause of the steadily rising incidence of Type-1 diabetes in the US population
And we suggest that the Congress consider the following suggestions for action.

Here it must be borne in mind that the FDA, the Public Health Service, the Centers for Disease Control, 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 Compensation Act of 1986 (over the protests of these same agencies, supported by a presidential veto), compelling these agencies to investigate areas they would have preferred to ignore. In the light of the possible budgetary savings involved, the Congress should overcome the inertia of the federal health establishment on the question of vaccines and Type-I diabetes. -- the FDA should be compelled to fulfil its statutory duty of ensuring that only "safe" vaccines are marketed. At present the FDA disregards the law in this respect and allows vaccines to be marketed based on studies that register adverse reactions only during the first 15 days after administration. Vaccines are thus marketed based on a presumption of safety without any long-term data demonstrating safety. But the first symptoms of Type1 diabetes may appear several weeks or months after the vaccination. Hence Congress should require vaccine manufacturers to record all adverse reactions occurring within five years after receiving any vaccine, with these data then being factored into the cost-benefit equation.

Vaccination campaigns are justified on cost-benefit grounds, but the equations may yield different outcomes when the real costs are factored in.

-- physicians should be alerted to Type-1 diabetes as a possible consequence of mumps, rubella, pertussis, and other childhood vaccinations; if that were done, the reporting of Type-1 diabetes would be intensified.

-- alternative scheduling of childhood vaccinations, as a way of minimizing the incidence of Type-1 diabetes, could be studied; or these vacinations could be suspended until the relationship with diabetes and other diseases has become more clear.

-- consideration should be given to including Type-1 diabetes in the Vaccine Injury Table of the National Vaccine Injury Compensation Program.

-- an effort should be made to seek out armed services personnel who contracted Type-1 diabetes while on active service. Since diabetes is a bar to military service, 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. Here follows the testimony of one servicewoman who did contract diabetes in this way:

A Personal Account of Acquiring Type-1 Diabetes While on Active Service Susan Savastuk MEd, BSN, RN, CDE Western Reserve Health Care, Youngstown, Ohio
Here are the details surrounding my diagnosis of Type-1 diabetes while in the USAF. I have supplied all known facts that I have available to me as well as my recollection of the events that led to my medical discharge. This information has been obtained from medical records and hearing records from the time of my discharge.

I entered the USAF on May 23, 1977. I spent 6 weeks in Basic Training at Lackland AF Base in San Antonio, Texas. While there I received multiple vaccinations but have no record of what they were or their doses. I presume that they were the typical Recruit vaccines. I had no immediate reaction to the vaccines that I recall. After basic training I was sent to Wichita Falls, Texas, for training to become a Medical Service Specialist (Medic). After graduation I was assigned to Wilford Hall Medical Center at Lackland AF Base, San Antonio, Texas.

In early February, 1978, I began to have the classic symptoms of Type- I diabetes me!!itus: polyuria [frequent urination], polydypsia [excessive thirst], nocturia (2-4) per night, a vaginal yeast infection, an eight-pound weight loss without trying, fatigue, weakness and lethargy.

These symptoms lasted approximately one week. I did a self urine test and found 4+ glucose and positive for ketones. The nurses on the floor were I worked as a medic did a random blood sugar on me and found it to be above 400 mg/dcl.

I was sent to the Emergency Room of Wilford Hall Medical Center and given the diagnosis of Maturity Onset Diabetes. I was not admitted as an inpatient. I feel I was given the diagnosis of Maturity Onset Diabetes (Type-2) instead of Juvenile Onset (Type-1), because it gave me a smaller severance pay and disability rating. I was never started on an oral antidiabetic agent nor was diet control attempted. After my discharge the diagnosis was changed by the veterans association to Type-I diabetes which gave me a 30% disability rating and money to attend college.

I do not posses medical records from the time of my diagnosis; thus I do not have the name of the physician who diagnosed my diabetes. I do have copies of records from the time of my discharge which refer to my initial diagnosis, and much of the information I am providing is from these records. I can make these records available to Congress, if that is desired.

At the time of my diagnosis I was given 10 units of NPH Insulin which over a 3 to 4 week period was increased to 33 units of NPH every morning. This dosage was subsequently reduced by two units daily until a maintenance dose of 26 units was achieved.

In early August of 1978 I entered into my "honeymoon phase" of Type-1 diabetes. After experiencing frequent low blood sugars I began to taper my dose of NPH to 4 units and eventually stopped the insulin altogether. I remained insulin-free until late September, 1978, when I developed an upper respiratory infection and had to resume the NPH Insulin.

The infection did not resolve, necessitating a hospital admission due to hyperglycemia and weakness. It was during this admission that the process was started to medically discharge me from Active Duty. On November 7, 1978, I was found by the USAF Physical Evaluation Board to be unfit for Military duty because of Maturity Onset Diabetes, Insulin Dependent. My official discharge date was January 2, 1979. I fought my discharge all the way to the Secretary of the Air Force without success, claiming that as a Medic I would be stationed in a health care environment which would allow for easy monitoring of my condition.

I truly believe that the discharge practices of the military at the time of my discharge were discriminatory. I was fully able to perform my job responsibilities at that time and should have been given the opportunity to prove that. Just the cost alone of putting me through basic training was wasted by an unjustified discharge. I have only been hospitalized once since my military medical discharge because of diabetes or a diabetesrelated illness. I would be retiring next year with 20 years of service. Their loss, I guess.

Also, at the time of my diagnosis there was no history of diabetes in my family. l now have a maternal aunt in her late 70's who has Type-2 diabetes.

My current treatment plan includes: a mix of Humulin Ultralente and regular insulins 3-4 times a day. I take 16 units of UItralente and between 16 and 22 units of regular. I exercise regularly, I see an endocrinologist, dentist, family physician, opthalmologist, podiatrist and massage therapist at regular intervals, I do home glucose testing 2-4 times per day, I eat a mostly vegetarian diet.

I have a Masters Degree in Health Education; I am a Registered Nurse (15 years) and a Certified Diabetes Educator (7 years). I frequently do public speaking on the subject of diabetes and am considered a resource person at my hospital for new employees, student nurses and patients who have diabetes. I have also organized a support group for hospital employees with diabetes. I have been employed at the same hospital for 15 years and have not missed one day of work due to my diabetes.

I would be happy to testify under oath to the contents of this communication.

A longer version of Harris L. Coulter's testimony, together with notes, is available from the Center for Empirical Medicine, 4221 45th Street, NW, Washington, DC 20016.