The letter, written by J Barthelow Classen, director of American based Classen Immuno Therapies in Baltimore, Maryland, provided some astonishing evidence of the relationship between childhood immunization and the development of diabetes mellitis.
In his letter, Classen wrote that his research team has demonstrated in a published paper that vaccines given six weeks after birth are associated with an increased risk of developing insulin dependent diabetes in humans and rodents (PCT patent application, 1994; PCT/US94/08825).
They have also provided evidence that immunization given at birth is associated with a decreased incidence of diabetes in humans and rodents (Diabetolia, 1996, April: 39).
After publication of their data, Classen and his research team evaluated the effect of the recent hepatitis B immunization programme in New Zealand on the development of insulin dependent diabetes.
New Zealand was a good country to test the hypothesis since takeup rate among children and adolescents was widespread and administered at the same time. When the programme was launched, nearly three quarters of all children and teenagers were immunized against hepatitis B.
The programme began with the vaccination of children aged 5 or under, but soon was extended to include all children under age 16.
In Classen’s view, based on his previous data, those children born in 1988 and 1989 who were immunized at birth would be expected to have a lower incidence of diabetes, but all others would suffer an epidemic increase in diabetes.
Classen located the Christchurch diabetes registry, the only such registry in New Zealand, which has followed the health of a group of 100,000 people under 20 since 1982 (Care, 1992; 15: 895-9; Care, 1995; 18: 1428-33). Between 1982 to 1987, before the launch of the New Zealand hepatitis B campaign, the registry recorded the incidence of diabetes at 11.2 cases per 100,000 people every year.
>From 1989 to 1991, the years immediately following the vaccination campaign, the incidence of diabetes leapt to 18.2 cases per 100,000 per year an increase of 60 per cent.
“We . . . believe the most likely explanation is that the immunization programme caused the diabetes epidemic,” writes Classen.
The data Classen has collected also indicates that diabetes epidemics have followed the recent widespread use of the hemophilus influenzae b vaccine (PCT patent application, 1994; PCT/US94/08825).
Classen believes that the mechanism by which the damage occurs is no mystery. The manufacturers of the hepatitis B vaccine acknowledge that the vaccine can cause a number of autoimmune diseases.
Other studies have shown that the hepatitis B vaccine, among other immunizations, has the potential of causing insulin dependent diabetes because it releases interferons. These interferons have been shown to cause autoimmune disease, including insulin dependent diabetes (Science, 1993; 260: 1942-6; Diabetes, 1995; 44: 658-64; Ann Intern Med, 1995; 123: 318).
Classen is attempting to enlist the support of researchers in New Zealand to help perform epidemiological studies to substantiate observations about the Hib vaccine, which was introduced in that country in 1993.
As Classen wrote in a letter to Hilary Butler, of the Immunization Awareness Society in New Zealand, “This epidemic could have been avoided by being more selective of who receives the hepatitis B vaccine and by starting immunization before four weeks instead of after four weeks.”
Harald Gaier is on holiday this month.