Merry
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http://www.clinicalepigeneticsjournal.com/content/4/1/6/abstract
A macroepigenetic approach to identify factors responsible for the autism epidemic in the United States
Renee Dufault, Walter J Lukiw, Raquel Crider, Roseanne Schnoll, David Wallinga and Richard Deth
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Clinical Epigenetics 2012, 4:6 doi:10.1186/1868-7083-4-6
Published: 10 April 2012
Abstract (provisional)
The number of children ages 6 to 21 in the United States receiving special education services under the autism disability category increased 91 % between 2005 to 2010 while the number of children receiving special education services overall declined by 5 %. The demand for special education services continues to rise in disability categories associated with pervasive developmental disorders. Neurodevelopment can be adversely impacted when gene expression is altered by dietary transcription factors, such as zinc insufficiency or deficiency, or by exposure to toxic substances found in our environment, such as mercury or organophosphate pesticides. Gene expression patterns differ geographically between populations and within populations. Gene variants of paraoxonase-1 are associated with autism in North America, but not in Italy, indicating regional specificity in gene-environment interactions. In the current review, we utilize a novel macroepigenetic approach to compare variations in diet and toxic substance exposure between these two geographical populations to determine the likely factors responsible for the autism epidemic in the United States.
The complete article is available as a provisional PDF. The fully formatted PDF and HTML versions are in production.
Conclusion from the PDF:
The number of children ages 6 to 21 in the U.S. receiving special education services under
the autism disability category increased 91 % between 2005 to 2010 despite fewer children
receiving special education services overall during the same time period. A comparison of
autism prevalence between the U.S. and Italy using the Mercury Toxicity Model suggests the
increase in autism in the U.S. is not related to mercury exposure from fish, coal-fired power
plants, thimerosal, or dental amalgam but instead to the consumption of HFCS [high fructose corn syrup]. Consumption of HFCS may lead to mineral imbalances, including Zn, Ca and P loss and Cu gain and is a
potential source of inorganic mercury exposure. These mineral imbalances create multiple
pathways for oxidative stress in the brain from exposure to OP pesticides and heavy metals,
such as Pb or Hg. Inorganic mercury and fructose exposure from HFCS consumption may
both modulate PON1 gene expression. With a reduction in PON1 activity, there is a potential
for increasing homocysteine levels which are associated with genome-wide DNA
hypomethylation that may carry over from one generation to the next, affecting both
neurodevelopment and autism prevalence.
A macroepigenetic approach to identify factors responsible for the autism epidemic in the United States
Renee Dufault, Walter J Lukiw, Raquel Crider, Roseanne Schnoll, David Wallinga and Richard Deth
For all author emails, please log on.
Clinical Epigenetics 2012, 4:6 doi:10.1186/1868-7083-4-6
Published: 10 April 2012
Abstract (provisional)
The number of children ages 6 to 21 in the United States receiving special education services under the autism disability category increased 91 % between 2005 to 2010 while the number of children receiving special education services overall declined by 5 %. The demand for special education services continues to rise in disability categories associated with pervasive developmental disorders. Neurodevelopment can be adversely impacted when gene expression is altered by dietary transcription factors, such as zinc insufficiency or deficiency, or by exposure to toxic substances found in our environment, such as mercury or organophosphate pesticides. Gene expression patterns differ geographically between populations and within populations. Gene variants of paraoxonase-1 are associated with autism in North America, but not in Italy, indicating regional specificity in gene-environment interactions. In the current review, we utilize a novel macroepigenetic approach to compare variations in diet and toxic substance exposure between these two geographical populations to determine the likely factors responsible for the autism epidemic in the United States.
The complete article is available as a provisional PDF. The fully formatted PDF and HTML versions are in production.
Conclusion from the PDF:
The number of children ages 6 to 21 in the U.S. receiving special education services under
the autism disability category increased 91 % between 2005 to 2010 despite fewer children
receiving special education services overall during the same time period. A comparison of
autism prevalence between the U.S. and Italy using the Mercury Toxicity Model suggests the
increase in autism in the U.S. is not related to mercury exposure from fish, coal-fired power
plants, thimerosal, or dental amalgam but instead to the consumption of HFCS [high fructose corn syrup]. Consumption of HFCS may lead to mineral imbalances, including Zn, Ca and P loss and Cu gain and is a
potential source of inorganic mercury exposure. These mineral imbalances create multiple
pathways for oxidative stress in the brain from exposure to OP pesticides and heavy metals,
such as Pb or Hg. Inorganic mercury and fructose exposure from HFCS consumption may
both modulate PON1 gene expression. With a reduction in PON1 activity, there is a potential
for increasing homocysteine levels which are associated with genome-wide DNA
hypomethylation that may carry over from one generation to the next, affecting both
neurodevelopment and autism prevalence.
The hypothesis that diet contributes to the onset of autism I had never thought of. I'll have to do some more reading.