What do you get when you cross pro-life advocates with vaccine deniers? The implausible idea that vaccines originally derived from aborted fetal tissue are responsible for the rise in autism. A mother of a child with autism sent me an e-mail today asking if I had any information about the recent chirping in the pro-life community about a new study they say proves a correlation between autism and their ingredients derived from aborted fetal tissue. She writes…
Just when I thought all that nonsense was dying a slow death, someone comes on one of the autism support group sites and posts something about a new EPA study linking autism to abortion cell use in vaccines.
It seems like autism is a magnet for woo woo because its origins can’t be fully explained. The idea that a study was being interpreted by pro-life activists as showing a correlation between autism and aborted fetal tissue really raised my skeptical alarm bells, obviously. My first thought was that this was a simple case of correlation being confused with causation. My second thought was that I better check out the study and see what it says. My third thought was that the best person to answer this question would be the study’s author, Mike McDonald. I bet the pro-life anti-vaccine activists never thought to ask the person who did the research.
Fortunately, Mike McDonald replied to me about whether his study can be interpreted to show a link between autism and aborted fetal ingredients in vaccines. (Honestly, I think this is just a trick to get people like me to acknowledge that some cells in vaccines were derived from aborted fetal tissue). Here’s what he had to say…
The statements made on the website incorrectly represent, and far overreach, our study findings. Our study draws no causal linkages with anything and the recent increase in autistic disorder, and certainly not to the use of fetal tissues in vaccines. Our research serves as a screening tool to direct future research to a potentially more productive time frame for additional study. Without additional screening approaches there are potentially a huge number of possible exogenous factors and explanations that could be associated with autism. The data we used suggest that the timing would be similar in Denmark and in California (the Japanese data may be earlier in occurrence, but we were not able to determine a change point from the study we used), suggesting that something similar may have been occurring in at least developed countries at this time. Autistic disorder increased in California and Denmark beyond the time frame of our study, but at different rates. If we assume a dose response relationship, then exposure to whatever exogenous factor or
factors, that might be associated with AD, would have had to increase in parallel to the AD levels in different places. But, the levels of exposure may have been different. However, in no case is a correlation with any of these things, including with the timing of the change point, with some other occurrence any indication of causation.
I hope this helps.
Yes, it helps. Thank you so much!