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Xenoestrogens Part 1: Hormone Disrupting Compounds Linked to Cancer Growth

Xenoestrogens Part 1: Hormone Disrupting Compounds Linked to Cancer Growth

Xenoestrogens are a group of environmental chemicals, which mimic estrogen in the body. This family of molecules have been linked to the development and promotion of hormonally sensitive cancers.  
Research is just beginning to uncover the wide-ranging effects of this class of compounds. This topic is so important; I have devoted a 3-part article to expanding and explaining this important topic. As of 2003 there were over 160 xenoestrogens that may be involved in breast cancer development (Brody and Rudel 2003). Cancer types that have been well documented in literature to be related with environmental exposure include the reproductive system, breast, lung, kidney, pancreas, and brain (Fucic et al 2012).
New research is always emerging that confirms the negative impact of environmental chemicals such as dioxins, phthalates and parabens which are found in pesticides, cosmetics, cleaners and processed foods. Specifically in cancer, there is evidence the xenoestrogens play a role in in all phases of cancer development including initiation, transformation, and invasion (Fernandez and Russo 2010). For example, a number of studies have now confirmed that a chemical (a polycyclic aromatic hydrocarbon) produced during meat frying and grilling strongly increases DNA damage in breast cells and promotes breast cancer growth (Rohrmann et al 2009).
Two emerging concepts to consider is that individual differences in genes responsible for detoxification many predispose some people more than others to the harmful effects of xenoestrogens. Secondly, a very concerning aspect of xenoestrogens is that studies are now confirming that exposure not only poses a health risk immediately, but also increases susceptibility to cancer and other diseases later in life (Wadia et al 2007). There is still more research to be done to fully understand the broad health impact of xenoestrogens but the emerging evidence is frightening do to their wide spread prevalence and pervasiveness in our food products, water supply, and environment.
As part of a hormonal balancing and breast cancer prevention plan, it is paramount to consider reducing the exposure to these compounds that contribute to detrimental estrogenic activity in the body. You must also support the natural detoxification pathways (i.e. phase 1 and 2 in the liver) that remove excess hormones and xenoestrogens. Most people are inefficiently removing these compounds after they are exposed which increases their damaging effects. Natural compounds found in vegetables and certain herbs like mike thistle can promote healthy detoxification and therefore indirectly balance your hormones and reduce your cancer risk.
 To learn more visit your Naturopathic Doctor at pureBalance Wellness Centre to safely and effectively stimulate the elimination of harmful xenoestrogens and reduce your cancer risk. Stay tuned for part 2 of this 3 part article where I highlight Top ways to reduce your exposure to xenoestrogens.

By: Dr. Paul Hrkal, ND
Join Dr Hrkal as he takes you on a tour of your house to explore the various potentially toxic and hazardous products that could be contributing to your cancer risk. The workshop is called Cancer Proof Your Home, it will be presented at pureBalance Wellness Centre on November 6 at 7:30pm. Click Here to learn more about this event.
Brody and Rudel. Review Environmental pollutants and breast cancer.
Environ Health Perspect. 2003 Jun; 111(8):1007-19.
Fucic et al.  Environmental exposure to xenoestrogens and oestrogen related cancers: reproductive system, breast, lung, kidney, pancreas, and brain. Environ Health. 2012 Jun 28;11 Suppl 1:S8.
Rohrmann et al. Dietary intake of meat and meat-derived heterocyclic aromatic amines and their correlation with DNA adducts in female breast tissue. Mutagenesis. 2009 Mar;24(2):127-32.
Wadia et al. Perinatal bisphenol A exposure increases estrogen sensitivity of the mammary gland in diverse mouse strain. EHP. 2007;115(4):592–598

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