Vas Aposhian is – like Sander Greenland – an expert witness for petitioners (the families) and a professor of molecular and cellular biology as well as a professor of pharmacology.
On Day 2 and 3 he testified as to what seemed to be the main hypothesis behind the whole thiomersal/autism idea.
The basic idea is that some people are genetically predisposed to something called _mercury efflux disorder_ (plain english, they can’t get rid of mercury as well as most people can, it crosses the blood brain barrier and triggers autism). Mercury Efflux Disorder is itself an unproven hypothesis but Aposhian passionately believes in it.
He came under heavy cross exam (I won’t go through his performance whilst testifying to his own ‘side’ – we all know the basic hypothesis), that compromised a lot of day two and most of the morning of day three (the audio is released slowly so I’m a couple of days behind). The part I’m writing about today starts about an hour and a half into day three (NB: I’ve downloaded all the MP3’s and stitched them into one file).
Aposhian says that the mercury efflux hypothesis is supported by six papers:
…each piece of evidence alone leaves some doubt but taken all together the evidence implicates thimerosal/ethylmercury as the likely precipitating agent in the etiology of some of the autism spectral disorders.
Respondent counsel referred to these six papers as ‘pillars’ supporting the hypothesis. Aposhians’s pillars are:
First, Adams et al. (2007) demonstrated that teeth from autistic children contain more mercury than those from non-autistic children.
Respondent counsel asked Asphosian what he thought he could criticize about these papers he says ‘implicate thiomersal’. Regarding Adams et al, Asphosian said (and I’m paraphrasing slightly after scribbling notes furiously):
1) The number of controls should’ve been increased.
2) There were too few test subjects
3) When asked if raised mercury level was an indicator of toxicity, Asphosian answered “I don’t know”.
4) When asked if he would’ve expected mercury concentrations to vary depending on gender, Asphosian answered “Yes”.
5) When asked if Adams controlled for gender Asphosian answered, “No, he doesn’t control for gender”.
6) When asked if lead concentration of a tooth affected mercury concentration of a tooth, Asphosian answered, “I don’t know”.
7) Asphosian was asked, given the fact that the thiomersal hypothesis depended on the role of _ethyl_ mercury, what type of mercury did Adams et al measure in the teeth? Asphosian’s answer was “…did not do speciation” – in other words, he didn’t separate the types of mercury out. He recorded it all.
8) When asked if mercury levels in teeth tell you anything about amounts of mercury in the brain Asphosian replied that he didn’t know as no one had ever done that study.
These are fairly damning failings in what Asphosian’s assumptions were regarding the quality of that study. Of course, there is more wrong with the Adams paper than just the above, but these points are pretty damning. The failure to control for gender, the paucity of subjects and the fact Adams et al didn’t concentrate on ethyl-mercury raise serious questions over what exactly this study can add to the so-called Mercury Efflux Disorder.
I’ll keep appending to this post as I work through the rest of the audio.