Autoimmune diseases: Vaccines as a possible trigger



Screening for genetic susceptibility to vaccine-injury and vaccine non-response could reduce the incidence of autoimmune diseases as juvenile diabetes and juvenile rheumatoid arthritis. For details on one potential genetic marker, see Potential genetic marker for susceptibility to vaccine-injury.



Autoimmune diseases in children have increased so dramatically that incidence study states that the coincidental explosions in juvenile type 1 diabetes and rheumatoid arthritis, for example, must be due to “some major environmental effect” [1]. Many of these children appear to share a genetic susceptibility that places them in a high-risk category for adverse events following vaccination [2].  Ironically, these same vulnerabilities appear to to increase the risk of being a non-responder to vaccination.  In other words, these children do not develop immunity even though they are vaccinated, so they incur higher risk of vaccine-injury without gaining the vaccine benefit of disease protection. Screening for genetic susceptibility to vaccine-injury and/or vaccine non-response, and exempting or alternatively vaccinating based upon the screening results, could be a smarter approach to vaccination policy.  Further, research into the causal mechanisms behind this genetic susceptibility could gain knowledge that would assist in developing newer versions of existing vaccines and future vaccines that are both safer and more-effective.

Medical literature demonstrates how vaccine ingredients such as viruses, bacteria and aluminum are triggers for such autoimmune conditions as juvenile diabetes and juvenile arthritis.

A component in the Hib vaccine has been linked to juvenile diabetes. Hib was first licensed in 1985, and at the same time an exceptionally large increase in the age group 0-4 yrs of age was observed between 1985 and 1989:

For the first time a major increase in IDDM was seen (1985-1989). … and an exceptionally large increase in the youngest age-group (0-4 yr of age) was observed [3].

In 1990-1994, juvenile diabetes incidence increased again “more than two times higher” than the 1985-1989 group.  In this period Hib vaccination increased from 1 dose to 4 doses and was administered earlier at 2, 4, 6 and 15 months instead of between 2 and 5 years [4]. Following this development, further study confirmed that a “Causal relation is likely” between insulin-dependent diabetes mellitus and a component in the Hib vaccine [5].

In addition to juvenile diabetes, the expanded vaccination schedule of the late 1980s and early 1990s resulted in a spike in prevalence of juvenile rheumatoid arthritis.

The incidence of JRA was significantly higher than in the earlier years (1980, 1985 and 1990) in the same district. … There was both temporal and regional variation in the incidence of JRA. Results of the present study suggest that environmental factors may influence the frequency of JRA [6].

In those who developed juvenile rheumatoid arthritis (RA) after vaccination, a genetic marker called HLA-DR4 was a common thread that linked the children: “In a new series of RA patients the association with HLA-DR4 was again found to be highly significant [7].” Children and adults with this marker are vulnerable to adverse reactions to vaccine ingredients.  Some doctors have recognized the importance of screening for this genetic marker before vaccinating:

Perhaps, the assessment of autoantibody and HLA status prior to immunization will serve as a marker for individuals at risk. More research is required to identify those individuals who may develop autoimmune diseases following immunizations. It is not clear if genomics or proteomics will reveal the individuals with an increased risk to develop autoimmune phenomena [8].

The genetic HLA marker is associated with a “non-response” to certain vaccines [9].  These vaccines include measles, rubella, influenza and more.  Research confirms that poor antibody production after immunization may be directly related to HLA types [10].



[1] K.M. Gillespie, et al., “The rising incidence of childhood type 1 diabetes and reduced contribution of high-risk HLA haplotypes,” The Lancet, 364 (Nov. 2004): 1645-7.

[2] M.C. Levin, et al., “Autoimmunity due to molecular mimicry as a cause of neurological disease,” Nature Medicine, 8, 5 (May, 2002): 509-13.

[3] TM Dokheel, “An epidemic of childhood diabetes in the United States?” Diabetes Care, 16, 12 (Dec., 1993): 1606-11.

[4] Libman et al. Was there an epidemic of diabetes in nonwhite adolescents in Allegheny County, Pennsylvania? Diabetes Care. 1998 Aug;21(8):1278-81.

[5] J. Barthelow Classen, “Association between type 1 diabetes and Hib vaccine, Causal relation is likely,” British Medical Journal, 319 (Oct. 1999): 1133.

[6] O.Kaipiainen-Seppanen and A. Savolainen, “Changes in the incidence of juvenile rheumatoid arthritis in Finland,” Rheumatology, 40, 8 (Jan. 31, 2001): 928-932.

[7] P. Stastny, et al., “HLA-DR4 and other genetic markers in rheumatoid arthritis,” Rheumatology, 27, 2 (1988): 132-138.

[8] H. Orbach, “Vaccines and autoimmune diseases of the adult,” Discovery Medicine, (Feb. 4, 2010).

[9] HLA-DR4 has been associated with “nonresponse to hepatitis B vaccine”

[1][10] According the article, “Genetic Variation in the Response to Vaccination” by T.G. Kimmana, R.J. Vandebrielb, B. Hoebeeb,