The Matrix: Decoded
May 6th, 2010
I’m sorry to have been so long between new posts, but this review of two articles required a lot of additional work and - as I often have to remind myself - I already have a full-time job.
On November 17th and November 24th, researchers from the MIND Institute published two papers in the journal Neurotoxicity Research. These two papers were:
Tian Y, Green PG, Stamova B, et al. Correlations of gene expression with blood lead levels in children with autism compared to typically developing controls. (pub online 17 Nov 2009; rec’d 15 Sept 2009; accepted 12 Oct 2009)
and
Stamova B, Green PG, Tian Y, et al. Correlations between gene expression and mercury levels in blood of boys with and without autism. (pub online 24 Nov 2009; rec’d 15 Sept 2009; revised 15 Oct 2009; accepted 10 Nov 2009)
[Note: both author lists are almost perfectly identical. Alphabetically, the authors are: Paul Ashwood, Peter G. Green, Jeffrey P. Gregg, Robin Hansen, Irva Hertz-Picciotto, Isaac N. Pessah, Frank R. Sharp, Boryana Stamova, Yingfang Tian, Judy Van de Water and Xiaowei Yang. The Tian et al paper includes Glen Jickling as an author; the Stamova et al paper includes Jennifer Teng. Otherwise, both articles are written by the same group of people.]
Both studies were done as part of the Childhood Autism Risks from Genetics and Environment (CHARGE) study at the University of California at Davis.
In both studies, blood samples were analysed for lead or mercury and the RNA (in the white blood cells) was isolated and copied using reverse transcriptase to make cDNA copies of the RNA present. This cDNA was hybridized with an Affymetrix Human U133 Plus 2.0 GeneChip microarray to determine the gene expression levels. (If none of this sounds like English to you, hang on – I will try to explain it all in a moment)
The lead study (Tian et al) subjects were 37 children with autism (32 male, 5 female) and 15 typically developing children (11 male, 4 female). Their ages were similar, with mean ages of 44.2 and 41.2 months, respectively.
The mercury study (Stomova et al) had 33 autistic subjects and 51 typically developing control subjects – all male. Their mean ages were 45.3 and 43.3 months, respectively.
Autism diagnoses were confirmed through the use of the ADI-R and ADOS tests (both well-validated diagnostic tests for autism) and the typically developing control subjects were examined to exclude overt behavioral, developmental or autism spectrum disorders.
The Stomova et al study (mercury) makes reference to the fact that the blood tests for mercury and the gene expression data had been collected prior to the study as part of the CHARGE study. The Tian et al study (lead) does not explicitly state this, leaving it an open question whether their data was “fresh” or “canned”. However, that makes little difference.
First, let me discuss the blood lead and mercury levels, since I know some of you have been holding your breath waiting for the answer.
Lead: there was NO significant difference between the two groups (breathe). The mean (+/- SD) blood lead levels were 1.30 +/- 1.01 mcg/dL in the autistic subjects and 1.30 +/- 0.58 mcg/dL in the typically developing subjects.
Mercury: there was NO significant difference between the two groups (breathe). The mean (+/- SD) blood mercury levels were 0.46 +/- 0.73 mcg/L in the autistic subjects and 0.60 +/- 0.82 mcg/L in the typically developing subjects. Among the autistic subjects (n=33), four had blood mercury levels below the detection limit (0.01 mcg/L) and the highest level was 3.0 mcg/L; the typically developing controls (n=51) has one subject with blood mercury below the detection limit and the highest blood mercury level was 4.3 mcg/L.
So much for the “poor excretor” hypothesis, eh?
Those of you who just wanted to see the blood lead and mercury levels can leave now - please gather your coats and books and leave quietly.
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