One of the maddening aspects of the dismissal of the environmental hypothesis for autism is that the counter-evidence provided is never allowed to be seen in context. The environmental hypothesis is rejected in favor of an ostensibly “pure” genetic hypothesis and that’s that. Evidence for the genetic hypothesis—which is indeed plentiful—is allowed to displace the environmental hypothesis as if the one excluded the other.

It is of course much more “ecological” to assume that just as the genetics of autism is turning out to be complex, environmental influences are likely to be complex as well. Ruling out environmental factors is not at all a trivial matter, and epidemiology is not up to the task. We are now aided in this discussion by a new study just published in the American Journal of Biochemistry and Biotechnology {4(2), 73-84 (2008!)}. The lead author, Elizabeth M. Sajdel-Sukowska, is at the Harvard Department of Psychiatry.

The overarching model is that oxidative stress wreaks havoc with brain function; mercury contributes famously to such oxidative stress; and the autistic brain may have difficulty with detoxing mercury itself, or it may have difficulty with mounting counter-measures, as with anti-oxidants such as selenium and glutathione.

In this study, the authors measured the post-mortem cerebellar concentrations of a marker for oxidative stress, 3-nitrotyrosine (3-NT), in ten normal brains and in nine brains of autistic children. They also measured levels of mercury and of selenium. The levels of 3-NT averaged 70% higher in the autistic children, and this was statistically significant (p=0.045). The mercury level was similarly 70% higher in the autistic children, but in this case the elevation was not statistically significant. Remarkably, however, the correlation of 3-NT with mercury level was an astonishing 80%. The corresponding p-value was 0.001. Whenever you get a correlation coefficient this large out of population of subjects this small, one is no doubt looking at a robust effect.

Corroborative evidence was also furnished by the selenium assays. As was the case with mercury, there was no statistically significant difference in selenium levels between the two populations. However, there was a significant correlation of Se/Hg molar ratios: the ratio was 43% lower in the autistic population, suggestive of reduced ability to counter oxidative stress.

If the starting point of the discussion is oxidative stress, then mercury fits nicely into the discussion. But the discussion also does not end with mercury. The nervous system subject to oxidative stress is going to be vulnerable to a variety of environmental factors that are now plentiful in our modern existence: pesticide residues, lead, polychlorinated biphenyls (PCBs), etc. So mercury does not have to stand out as the singular culprit in the general case.

Unfortunately, this is not the kind of paper that is going to draw headlines in the newspaper. But it does answer the loose lips at the NIMH that persist in trying to bury mercury as an issue in autism.

It is also comforting that autism isn’t an issue entirely unto itself with regard to oxidative stress. There is increasing evidence that the same issues arise in connection with the degenerative conditions of ALS, Parkinson’s, and Alzheimer’s. And among the children’s issues we work with, increasingly we are coming to recognize the commonality of biomedical stressors that impinge on ADHD, autism, Tourette Syndrome, and childhood Bipolar Disorder.

This entry was posted on Tuesday, November 6th, 2007 at 11:54 pm and is filed under Autism, Research. You can follow any responses to this entry through the RSS 2.0 feed. You can leave a response, or trackback from your own site.