Reply #26: Well, in this case, she gives a very specific reference. [View All]

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Rodent models suggest that reactions to some infectious agents (e.g., bornavirus and group A streptococcus) lead to somewhat specific neuronal cell death and evidence of autoimmune reactions in the developing and adult brains of rodents. The animals also exhibit abnormal behaviors. These immunological and behavioral findings are similar to those seen in some humans after infection: the behavior in children with PANDAS or in the animal models resembles the behavior constellations in children with autism. A similar set of comparisons can be made with mercury exposures (Bernard et al., 2001), although autism has never been documented as a consequence of high-dose mercury exposure, including acrodynia. While analogies are useful for hypothesis generation, they do not substitute for direct evidence.

Other evidence offered for the vaccine-autism hypothesis includes analogies between rodent behavior and human behavior as well as clinical observations of metabolic or immunologic differences between individuals with autism and normal subjects or subjects with other conditions. In the clinical studies, it is not clear to what extent the abnormalities are antecedents or are comorbid disease expressions, rather than causal factors. That is, it is possible that some people with autism, perhaps even a subgroup that could be identified at some time in the future by genetic markers, also have abnormal immune reactions and abnormal mercury metabolism but that vaccination does not cause these abnormalities, nor do they cause autism.

The committee notes several factors that limit acceptance at this time of the hypothesis that vaccines cause autism. The evidence offered for the hypothesis includes data from in vitro experimental systems, analogies between rodent behavior, and human behavior and clinical observations that are at least as well explained as being comorbid disease expressions than as causal factors. That is, it is possible that some people with autism, perhaps even a subgroup that could eventually be identified by genetic markers, have abnormal immune reactions and abnormal mercury metabolism, but that vaccination of these individuals does not cause these abnormalities or autism itself. However, the experiments showing effects of thimerosal on biochemical pathways in cell culture systems and showing abnormalities in the immune system or metal metabolism in people with autism are provocative; the autism research community should consider the appropriate composition of the autism research portfolio with some of these new findings in mind. However, these experiments do not provide evidence of a relationship between vaccines or thimerosal and autism.

In the absence of experimental or human evidence that vaccination (either the MMR vaccine or the preservative thimerosal) affects metabolic, developmental, immune, or other physiological or molecular mechanisms that are causally related to the development of autism, the committee concludes that the hypotheses generated to date are theoretical only.

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There are many examples in medicine of disorders defined by a constellation of symptoms that have multiple etiologies, and autism is likely to be among them. Determining a specific cause in the individual is impossible unless the etiology is known and there is a biological marker. Determining causality with population-based methods such as epidemiological analyses requires either a well-defined at-risk population or a large effect in the general population. Absent biomarkers, well-defined risk factors, or large effect sizes, the committee cannot rule out, based on the epidemiological evidence, the possibility that vaccines contribute to autism in some small subset or very unusual circumstances. However, there is currently no evidence to support this hypothesis either.

The committee concludes that much more research must be conducted on autism. However, research should be directed towards those lines of inquiry most supported by the current state of knowledge. The vaccine hypotheses are not currently supported by the evidence. Much remains unknown about the etiology or etiologies of autism. Furthermore, there have not been many studies on treatments for autism. Research should be directed towards better understanding the etiology or etiologies of autism and on treatments for autism.

While the committee strongly supports targeted research that focuses on better understanding the disease of autism, from a public health perspective the committee does not consider a significant investment in studies of the theoretical vaccine-autism connection to be useful at this time. The nature of the debate about vaccine safety now includes the theory by some that genetic susceptibility makes vaccinations risky for some people, which calls into question the appropriateness of a public health, or universal, vaccination strategy. However, the benefits of vaccination are proven and the hypothesis of susceptible populations is presently speculative. Using an unsubstantiated hypothesis to question the safety of vaccination and the ethical behavior of those governmental agencies and scientists who advocate for vaccination could lead to widespread rejection of vaccines and inevitable increases in incidences of serious infectious diseases like measles, whooping cough, and Hib bacterial meningitis.

The committee encourages that research on autism focus more broadly on the disorders’ causes of and treatments for it. Thus, the committee recommends a public health response that fully supports an array of vaccine safety activities. In addition the committee recommends that available funding for autism research be channeled to the most promising areas.

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