A paper coming out in the next issue of the journal Clinical Infectious Diseases addresses the question of the link between vaccines and autism. This new review article examines three hypotheses linking vaccines to autism:
(1) the combination measles‐mumps‐rubella vaccine causes autism by damaging the intestinal lining, which allows the entrance of encephalopathic proteins;
(2) thimerosal, an ethylmercury‐containing preservative in some vaccines, is toxic to the central nervous system; and
(3) the simultaneous administration of multiple vaccines overwhelms or weakens the immune system.
[This is a repost in honor of Get Your Flu Vaccination Week. Which is now. Did you get your vaccination yet?]
The MMR hypothesis was first advanced in a paper by Andrew Wakefield, in 1998. The present study suggests that Wakefield’s MMR – Autism link was flawed for a number of reasons. Methodologically, the studied cohort was self selected among a large population. The MMR vaccine is given at about the same time autism is often diagnosed, exacerbating a confirmation bias effect. The MMR-Vaccine theory relies on an intestinal route for encephalopathic substances, which would be indicated by some kind of G.I. symptoms prior to the autism, but this was often not the aetiology of the disease. There are other problems with this study as well.
The paper examines other MMR-Vaccine link studies and finds them at fault as well.
The Thimerosal link hypothesis asserts that ethylmercury, an ingredient in Thimerosal, is the cause of autism. Thimerosal is an antibacterial that has been used for decades to preserve various vaccines, (not including MMR, which is a live vaccine). Although there are several reasons to not think that Thimerosal can cause autism, several studies have been conducted to test the relationship (probably not a bad idea given the importance of this problem) and all of these studies failed to link Thimerosal to autism. What is especially convincing are studies that show a complete discordance between Thimerosal use and autism.
In Sweden and Denmark, researchers found a relatively stable incidence of autism when thimerosal‐containing vaccines were in use (1980-1990), including years when children were exposed to as much as 200 μg of ethylmercury (concentrations similar to peak US exposures) . However, in 1990, a steady increase in the incidence of autism began in both countries and continued through the end of the study period in 2000, despite the removal of thimerosal from vaccines in 1992.
The third hypothesis …. that too many vaccines stress the patient and ultimately cause autism to develop … was also found to be flawed.
Vaccines do not overwhelm the immune system. Although the infant immune system is relatively naive, it is immediately capable of generating a vast array of protective responses; even conservative estimates predict the capacity to respond to thousands of vaccines simultaneously… The immune response elicited from the vast antigen exposure of unattenuated viral replication supersedes that of even multiple, simultaneous vaccines…. Multiple vaccinations do not weaken the immune system. Vaccinated and unvaccinated children do not differ in their susceptibility to infections not prevented by vaccines … Autism is not an immune‐mediated disease. Unlike autoimmune diseases such as multiple sclerosis, there is no evidence of immune activation or inflammatory lesions in the CNS of people with autism…
The present study is, essentially, a meta study of twenty or so other studies that in combination seem to force the conclusion that the three hypotheses mentioned at the outset do not explain an apparent increase in autism cases. The authors suggest that the apparent increase in cases is a matter of changes in reporting, although as we have seen in other studies, that is contested.
Full disclosure: One of the paper’s authors is “…a coinventor and patent coholder of the rotavirus vaccine Rotateq and has served on a scientific advisory board to Merck.”
Jeffrey S. Gerber, Paul A. Offit (2009). Vaccines and Autism: A Tale of Shifting Hypotheses Clinical Infectious Diseases, 48 (4), 456-461 DOI: 10.1086/596476