Most studies to date have offered equivocal links between BPA and cancer, using terms like “associated with” and “linked to.” These vague connections fail to alert consumers to the actual connections.
However, the original research we did at our old, proog-of-concept site, Nano-Active discovered solid, causal connections. This post is from the first connection we made where we can accurately and definitively state that “BPA causes the exact same harm in a cell that triggers one of the stages needed for cancer to develop.”
Bisphenol A (BPA) has been suspected in many studies(1-5) of disrupting thyroid hormones.
In addition, BPA exposure in pregnant mice has been shown to induce epigenetic changes in offspring(6). Epigenetic changes are those that alter the functioning of a gene without actually changing the DNA sequence.
Various mechanisms have been proposed including hypomethlyation (adding a CH3 – methyl group) in early development, specifically, “CpG methylation also was decreased at another metastable locus, the CDK5 activator-binding protein (Cabp IAP)(7) .
This previous work with BPA as a thyroid endocrine disruptor may offer significant insight into the origins of medullary thyroid carcinoma (MTC) when viewed in light of a recent accidental discovery in Texas.
According to a study published Oct 14 in Cancer Cell(8) research at The University of Texas Southwestern’s Department of Psychiatry were investigating the origins of dementia and created a transgenic mouse that over-expressed the Cdk5 protein they felt could be connected with myloid plaques.
The study, run by Dr. James Bibb, Associate Professor of Psychiatry and Neurology and Neurotherapeutics, quickly found that the mice had all developed medullary thyroid carcinoma.
According to this news release from UT Southwestern, although rare, medullary thyroid cancer is often fatal and that the causes for 75% of the cases are unknown.
“More than 20 years ago, mutations in a gene were found to cause about 25 percent of these cancers,” said the UT Southwestern news release. “Genetic sequencing and screening has become an important diagnostic and prognostic tool for those families that share such mutations. But the causes for the remaining 75 percent of patients with this dangerous cancer have remained unknown and a source of frustration for endocrinologists and surgeons such as Dr. Nwariaku, also Associate Dean of Global Health.
Those causes may be epigenetic — rather than genetic — changes due to exposure to endocrine disruptors such as BPA.
This ad-free article is made possible by the financial support of the
Center for Research on Environmental Chemicals in Humans: a 501(c)(3) non-profit.
Please consider making a tax-deductible donation for continued biomedical research.
CAUSAL ROLE FOR BPA IN MEDULLARY THYROID CARCINOMA?
The UT Southwestern study showed that over-expression of Cdk5 resulted in MTC in the test animals. And the studies cited above demonstrate that BPA exposure results in hypomethylation (resulting in over expression) of Cdk5 genes.
Because epigenetic hypomethylation results in overproduction of the relevant protein, this suggests a cause for the remaining 75% of MTC that has not yielded its secrets to standard genome base-pair sequencing and screening.
Because epigenetics could be indicated, this offers avenues for further investigation into potential compounds that may reverse the hypomethylation. It also suggests a plausible route for thyroid effects already shown with BPA exposure.
(2) Do Thyroid Disrupting Chemicals Influence Foetal Development during Pregnancy? Marie-Louise Hartoft-Nielsen, Malene Boas, Sofie Bliddal, Åase Krogh Rasmussen, Katharina Main, Ulla Feldt-RasmussenJ Thyroid Res. 2011; 2011: 342189. Published online 2011 September 11. doi: 10.4061/2011/342189
(4) Endocrine Disruptors and the Thyroid Gland—A Combined in Vitro and in Vivo Analysis of Potential New Biomarkers Cornelia Schmutzler, Inka Gotthardt, Peter J. Hofmann, Branislav Radovic, Gabor Kovacs, Luise Stemmler, Inga Nobis, Anja Bacinski, Birgit Mentrup, Petra Ambrugger, Annette Grüters, Ludwik K. Malendowicz, Julie Christoffel, Hubertus Jarry, Dana Seidlovà-Wuttke, Wolfgang Wuttke, Josef KöhrleEnviron Health Perspect. 2007 December; 115(Suppl 1): 77–83. Published online 2007 June 8. doi: 10.1289/ehp.9369
Endocrinol Metab. 2002; 87:5185–5190. [PubMed: 12414890](6) Epigenetic Responses Following Maternal Dietary Exposure to Physiologically Relevant Levels of Bisphenol A Olivia S. Anderson, S. Nahar, Christopher Faulk, Tamara R. Jones, Chunyang Liao, Kurunthachalam Kannan, Caren Weinhouse, Laura S. Rozek, and Dana C. Dolinoy Environ Mol Mutagen. 2012 June ; 53(5): 334–342. doi:10.1002/em.21692.