Most studies have not found vaccines to be associated with the development of type 1 diabetes or type 1-associated autoantibodies. For example:
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, dogs, and men page for more on this point). A large Canadian study found that the BCG vaccine in the first year of life did not affect the overall risk of childhood type 1 diabetes (Rousseau et al. 2015).
Note that the presence of environmental chemicals in the body may affect the efficacy of vaccines. Infants with higher levels of persistent organic pollutants in their bodies (PCBs and DDE) had lower levels of antibody response to the BCG vaccine (Jusko et al. 2015).
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 as an adjuvant, such as some flu shots.
A Swedish study found that the H1N1 flu (swine flu) vaccine may affect the development of type 1 diabetes in young children, although exactly how is a bit unclear. The levels of some autoantibodies associated with type 1 diabetes were higher during and after the vaccine was administered, but the proportion of young children with a certain genetic risk diagnosed with type 1 diabetes decreased after vaccination. The authors state, "it cannot be excluded that the vaccine affected clinical onset of type 1 diabetes" and that, "it can therefore not be excluded that the vaccination campaign may have delayed the clinical onset in young high-risk children but induced an earlier diagnosis in others" (Svensson et al. 2014).
A study of the H1N1 vaccine and autoimmune disease did not find a different between those given shots with adjuvant and without. Rates of type 1 and other autoimmune diseases were also not different than background rates would predict (Isai et al. 2012). Another study of the H1N1 vaccine also found no increased risk of type 1 diabetes (Bardage et al. 2011).
There is ongoing debate about a Swedish study of the swine flu vaccine Pandemrix used in 2009-2010 (e.g., Andersson 2014; Persson 2015; Persson et al. 2017). The original study found no increased risk of type 1 diabetes from this vaccine (Persson et al. 2014). A different researcher, however writes that the authors of the original study excluded people with type 1 diabetes from the analysis, and that when you include them, the risk increases (Andersson 2017). I'm not sure what the truth is, but in any case, this vaccine was never used in the U.S. The original study did find an increased risk of narcolepsy from Pandemrix (which has not been used since 2010), but in the U.S., other swine flu vaccines did not increase the risk of narcolepsy (Duffy et al. 2014).
The HPV vaccine Gardasil did not increase the risk of type 1 diabetes, or any of the other 15 autoimmune conditions analyzed (Chao et al. 2012).
Some vaccines (e.g., BCG) may be able to accelerate the progression of type 1 diabetes, although most studies have not found associations between vaccines and type 1 diabetes. In case you were wondering, my children are fully vaccinated, and we also all get flu shots every year.
To see or download the references cited on this page, see the collection Vaccines and diabetes/obesity in Pubmed.