On the other hand, a Swedish study found that the HiB (hemophilus influenza B) vaccine may induce type 1-related autoantibodies in 1 year old children (Wahlberg et al. 2003). Another study compared Finnish children who had received the HiB vaccine and those who had not (in the two years prior to the introduction of the vaccine). They found that children receiving 4 doses as compared to those receiving no doses had slightly higher rates of type 1 diabetes, beginning about 3-3.5 years after immunization. Yet HiB vaccination in the first month of life may also be associated with a decreased risk of type 1 diabetes (Classen and Classen 2002).
The case of the bacillus Calmette-Guerin (BCG) vaccine is interesting, in that it shows how animal studies may not translate well to human studies. The BCG vaccine prevents the development of diabetes in NOD (non-obese diabetic) mice, an animal model of autoimmune diabetes (Harada et al. 1990). In humans, the BCG vaccine sometimes has been shown to preserve beta cell function when given just after diagnosis. On the basis of these studies, a prospective study in Germany examined whether vaccination might prevent beta cell damage in children genetically at risk for type 1 diabetes. The study compared children who received this vaccine before 3 months of age, after 3 months of age, and not at all. It found that the vaccine did not affect the development of type 1 diabetes-related autoantibodies. But, instead of being protective to beta cells, it actually sped up the rate of progression to type 1 in children who had these antibodies. And, the age of diabetes onset was significantly younger in children who had BCG vaccination (2.8 years) than in children who were not vaccinated (5 years). While this study does not suggest that BCG vaccination will increase the overall incidence of type 1 diabetes, it was found to accelerate development of the disease. The mechanism may involve stimulation of the immune system via inflammation (Huppmann et al. 2005). This is an interesting example of a case where something that can prevent diabetes in NOD mice accelerates type 1 diabetes in humans (see the of mice and men page for more on this point).
Vaccines are one instance where the presence of potentially toxic chemicals are included by design, not by accident. The vaccine preservative thimerosal, for example, is a mercury compound. The effect of thimerosal on the immune system is largely unknown (Havarinasab et al. 2005). A few Swedish researchers have tried to elucidate these effects in animal studies. One study showed, for example, that thimerosal exposure in mice was associated with the development of autoantibodies, and accelerated disease, at doses similar to those in infant vaccines (Havarinasab and Hultman 2006). Another found that thimerosal treatment of genetically susceptible mice leads first to an immunosuppression stage, followed by a second phase of immunostimulation and autoimmunity (Havarinasab et al. 2005). Thimerosal was removed from most childhood vaccines in 2001 in the U.S., but remains in some, such as some flu shots.
Some vaccines (BCG, and possibly HiB) may be able to accelerate the progression of type 1 diabetes, although most studies have not found associations between vaccines and type 1 diabetes.