Junk Science on Autism

  • by: |
  • 07/07/2011
A new study purports to show that environmental factors are more likley to cause autism than genetic mutations.  I won't get into the weeds on the methodological problems of the research since genetic association studies are, absent analysis or sequencing of genes, full of statistical assumptions that vary from paper to paper.  Moreover, when discussing the contributions of genes and 'environmental' factors to a behavior or disease, the term environment really means "anything we can explain by genetics that is not explained by demographics." 

http://archpsyc.ama-assn.org/cgi/content/full/archgenpsychiatry.2011.76#YOA15046T2

Which begs this question:  Since so many of the likely 'environmental' factors alleged to be linked to autism (, inflammatory diseases, mitochondrial disorders, vaccines, water supply, chemicals) have been discredited, how reliable is a study -- one that is at odds with every other genetic association study regarding autism -- that claims environmental factors are twice as likely to trigger autism than genes?  How good is a model that predicts things at odds with what experience demonstrates?

Of course the media never examines this question, never puts this study into context and never looks at the toxicological studies showing that certain toxins some swear cause autism, impotence, cancer, etc. are not even present in concentration levels necessary to cause of biological reaction (benign or not).      Not suprisingly, BPA is now being held up as the next new culprit causing autism.  Thus the recent EPA review of BPA levels in humans will go unmentioned:

EPA Study Findings:

·         Consistent with previous human and animal studies, this new study confirms that human exposure to BPA is extremely low, and BPA is efficiently metabolized and rapidly excreted in urine. Of particular importance, these results confirm the validity of the controlled human volunteer pharmacokinetic studies that have been used by regulators in BPA risk assessments. 

 

o   Based on how much total BPA (after hydrolysis of metabolites) was found in urine (average exposure was 21% greater than the 95th percentile exposure determined by CDC’s population-scale urine biomonitoring data), the authors concluded that “BPA exposures in this study can therefore be viewed as representative of, or exceeding, the high end of the U.S. BPA exposure distribution.”

 

o   Total BPA was detected in only 14% of the 320 blood samples, only one of which was above 1 ppb. Total BPA was below the sensitive limit of detection (0.3 ppb) for 86% of the samples.

 

o   Estimates of peak BPA levels in the blood were 1 to 3 orders of magnitude below levels associated with potentially adverse health effects in the most sensitive experimental rat models. 

 

o   Free BPA was below the limit of detection in all 320 blood samples analyzed by the CDC lab, even for samples with detectable total BPA. Based on their results the authors note that reported high levels of BPA in blood are unlikely to be valid. (“Furthermore, the current results obtained using analytical methodology 10-45 times more sensitive than the previous human study by Voelkel et al. suggest that reported BPA concentrations in human blood of 1.4-19.2 nM [~0.3-4.4 ppb] (Vandenberg, Chahoud et al. 2010) are highly unlikely in the general population exposed orally to amounts as much as ~4 times greater than the 95th upper percentile of aggregate exposure in the general U.S. population.”)

 

o   While subjects of this study did not include pregnant women, the authors also add that “recently reported mean urine concentrations in pregnant women are low enough that blood and serum levels are likely to be below current detection limits.”

 

o   Samples with detectable total BPA were further analyzed in the FDA lab to confirm the findings. Very low but detectable levels of free BPA were found in 3 of these samples, but further analysis revealed that contamination was most likely the source of the free BPA. The authors note, “the evidence presented here and elsewhere for low-level contamination (Markham et al., 2010; Twaddle et al., 2010), even in the face of extraordinary attention to this problem, suggests that these infrequent positive determinations near the detection limit should be suspect” and “Thus, some attributions of high blood BPA concentrations from oral exposure seem implausible.”

 

24-Hour Human Urine and Serum Profiles of Bisphenol A During High Dietary Exposure  tinyurl.com/3efsdw8

Will we -- and the media -- unlearn the lessons of Wakefieldism?





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