Negative BPA Effects Begin When Metabolized
October 5, 2012

Negative BPA Effects Begin When Metabolized By Body

Alan McStravick for - Your Universe Online

Roughly 9 out of 10 Americans are walking around with a highly toxic synthetic chemical surging through their systems. Bisphenol A (BPA) is a petroleum-based chemical that is widely used in the production of plastic products such as bottles, food can linings and water supply lines. And as these plastics degrade over time, humans ingest more and more BPA.

Less than 3 months ago, the FDA acted upon evidence found in several studies and banned the use of BPA in baby bottles and sippy cups. The European Union had already banned the use of BPA in products used for the feeding of smaller children after testing showed that laboratory animals exposed to the chemical, either in the womb or very early in life, experienced noticeable detrimental affects to their neural development.

BPA is even used in a powdered form on thermal cash register receipts. The chemical is able to be transmitted to the holder of the receipt in statistically significant amounts in a relatively short amount of time.

And new study has shown that BPA can also cause pregnant women and their newborn boys to suffer from reduced levels of thyroid hormone. An imbalance in thyroid hormone levels has been linked to negative changes in cognitive abilities, behavior and growth.

BPA resembles estradiol on a molecular level, a naturally occurring steroid that is part of the estrogen family. While the exact reasons why the thyroid hormone reduction is noticed in newborn boys and not girls is unknown, researchers have hypothesized that its resemblance to estradiol may be the key. They believe boys are less able to detoxify the estrogen-like BPA from their systems than girls.

In the most recent study of this chemical compound, researchers from the University of California, San Diego School of Medicine (UCSD) suggest that metabolic changes that take place once the BPA has broken down inside the body is where the greatest threat to our health lies. Their findings were published yesterday in the open journal PLOS ONE.

Thanks to BPA´s close resemblance to estradiol, it is able to bind to estrogen receptors, causing a disruption of estrogen signaling. The human body´s receptors are designed to bind with naturally occurring estrogens. When a look-alike comes along and fools the receptor, the outlook isn´t good. Even if the look-alike only has a weak bond with that receptor.

Particularly for fetuses, newborns and toddlers, BPA toxicity can cause disruptions to the endocrine and hormone systems.

The real culprit, according to Dr. Shin´ichi Yoshihara and his colleagues at Hiroshima International University, is not actually the BPA that is in its original form when it is ingested. Rather, the dangers arise from a compound created by your body when BPA is metabolized in your system. Yoshihara has dubbed this new compound MBP, and his research has shown that it is capable of binding much more tightly with our natural estrogen receptors.

The co-authors of the UCSD study, Michael E. Baker, PhD, professor of medicine, and Charlie Chandsawangbhuwana, graduate student in the UCSD Department of Bioengineering, began their study where Yoshihara left off. They wanted to learn just why the compound MBP is able to make such a strong connection with estrogen receptors.

Baker and Chandsawangbhuwana utilized three-dimensional computer modeling of MBP and BPA to learn why and how the new compound adhered so strongly to the receptors. Their findings showed that BPA was a shorter molecule that only makes contact with the receptor at one end, which explains its weak connection. MBP, on the hand, has a longer structure which allows both ends to have interaction with the receptor in much the same way as estradiol does.

"In other words, MPB is basically grabbing onto the estrogen receptor with two hands compared to just one hand for BPA," explained Baker. "Two contact points makes a much stronger connection."

Baker says that their 3D modeling supports the idea "that BPA is not the endocrine disruptor culprit. Instead, MBP is one (of perhaps several BPA metabolites) that causes disruption of estrogen signaling in humans and other animals."

Baker believes that these findings suggest that MBP measurements need to start being collected via urine and blood analysis from patients whose health issues are thought to be related to BPA toxicity. Baker goes on to say that obtaining that data may fuel development of a new therapeutic treatment for conditions linked to excessive estrogen levels and activity that include forms of breast and prostate cancers.

Speaking on new therapeutic advances in pharmaceuticals, Baker said, "One could use MBP, which has a novel structure, as a template to develop a new class of chemicals that could bind to the estrogen receptor with high affinity. The goal would be to have these chemicals inhibit the action of estradiol instead of activating the estrogen response. These chemicals could control unwanted growth of estrogen-dependent tumors."