re: Di(2-ethylhexyl)phthalate and ASDs - thyroid - α-PPAR

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from the study:

Phthalate metabolites activate peroxisome proliferator-activated

receptor (α-PPAR), interfering with cellular proliferation and lipid

metabolism. Activation of α- PPAR by phthalates may alter lipid

metabolism in the brain (- et al. 2004). Recently, a signal

transduction pathway of α-PPAR was correlated to progression of

neurodegenerative and

psychiatric diseases.

Phthalates also interfere with the thyroid hormone system by inducing

hypothyroidism. Recent studies correlated in utero hypothyroxinemia to

decreased intellectual capacity, mental retardation, and ASDs (Roman

2007). Thus reinforcing our speculation. Moreover, exposure to

di-n-butyl phthalate (DBP) seems to affect thyroid activity in pregnant

women, thus leading to adverse effects in the foetus (Huang et al. 2007).

On the other hand, transient intrauterine deficits of thyroid hormones

have been shown to result in permanent alterations of cerebral cortex

similar to those found in brains of children with autism (Roman 2007).

As a consequence, the current surge of this disease could be related to

transient maternal hypothyroxinemia resulting from exposure to

antithyroid environmental contaminants.

For the first time in this study we correlated different levels of the

primary and secondary metabolites with ASDs compared to HC children.

These data generate the idea that either current exposure is higher in

children with ASDs, or alternatively and more likely, ASD children may

differ in their ability to metabolize phthalates.

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http://www.asnneuro.org/an/imps/abs/AN20120015.htm

open access:

Di(2-ethylhexyl)phthalate and Autism Spectrum Disorders

Chiara Testa, Francesca Nuti, Joussef Hayek, Claudio De Felice,

Chelli, Paolo Rovero, Giuseppe Latini and Papini

Polo Scientifico e Tecnologico of the University of Florence, Sesto

Fiorentino, Italy. annamaria.papini2@...