Why Heavy Metals Are Toxic?

Why heavy metals and toxic and must be taken into consideration when being treated for cancer.

Heavy metals are some of the most well-known toxins. They include the big guns: Lead, Mercury, Aluminum and the #1 substance on the Agency for Toxic Substances and Disease Registry (ATSDR) toxin priority list—Arsenic. Heavy metals are:

• Immunotoxic
• Carcinogenic
• Mutagenic (which is in and of itself carcinogenic)
• Teratogenic

In addition to their toxicity, all have been shown to have estrogenic activity and thus have been labeled metalloestrogens. Think of that, a heavy metal that has estrogenic activity. Not only are they toxic, but they are hormonal.

How is this possible? Studies have shown these heavy metals exert their estrogenic activity through direct binding to estrogen receptors; ER-alpha to be exact. This affinity is so strong that these metals will even block estradiol (the most potent estrogen) from binding.

Through the estrogen receptors, metals will provide direct genomic signaling via what are called Estrogen Response Elements (ERE) and non-genomic signaling via activation of the well-known pro-growth signaling pathway proteins, activated in most cancers, of ERK (of the famous RAS-RAF-MEK-ERK pathway) and PI3K/Akt that interacts with mTOR.

Heavy Metals And Cancer Explained By Dr. Nathan Goodyear

Both pathways are uniformly unregulated in most types of cancers. In addition, the heavy metal cadmium has been shown to block the repair of damaged DNA ^[32].

One heavy metal that stands head and shoulders above the rest is cadmium.  Cadmium is the most well-known metalloestrogen.  The half-life of cadmium is an astonishing 20 years. Cigarette smoking and welding are the 2 most prominent sources of cadmium exposure.

In vitro and In vivo studies of cadmium have shown cadmium increases the cancer risk of the estrogen-sensitive uterus ^[33], breast ^{[34] [35]} and prostate ^{[36] [37]} organs. Even cadmium’s strong link to lung cancer is through estrogen receptor signaling ^[38]. The more we know, the more we realize we don’t know.

 In so many cases, the source of estrogen exposure or estrogen signaling is not through endogenous estrogen production or even through Hormone Replacement Therapy (HRT), but via these environmental estrogen-mimicking compounds.  The next example of some of these estrogen-mimicking compounds are the mycotoxins.

³² Byrne C, Divekar SD, Storchan GB, Parodi DA, Martin MB. Metals and breast cancer. J Mammary Gland Biol Neoplasia. 2013;18(1):63–73. doi:10.1007/s10911-013-9273-9

³³ McElroy JA, Kruse RL, Guthrie J, Gangnon RE, Robertson JD. Cadmium exposure and endometrial cancer risk: A large midwestern U.S. population-based case-control study. PLoS One. 2017;12(7):e0179360. Published 2017 Jul 24. doi:10.1371/journal.pone.0179360

³⁴ McElroy JA, Shafer MM, Trentham-Dietz A, Hampton JM, Newcomb PA. Cadmium exposure and breast cancer risk. J Natl Cancer Inst. 2006;98:869–873.

³⁵ Gallagher CM, Chen JJ, Kovach JS. Environmental cadmium and breast cancer risk. Aging (Albany NY). 2010;2(11):804–814. doi:10.18632/aging.100226

³⁶ Waalkes MK. Cadmium carcinogenesis. Mutat Res.2003;533:107–120.

³⁷ Rapisarda V, Miozzi E, Loreto C, Matera S, Fenga C, Avola R, Ledda C. Cadmium exposure and prostate cancer: insights, mechanisms, and perspectives. Frontiers In Bioscience, Landmark. Mar 1 2018;23:1687-1700.

³⁸ Mary O. Huff, Sarah L. Todd, Aaron L. Smith, Julie T. Elpers, Alexander P. Smith, Robert D. Murphy, Allison S. Bleser-Shartzer, Jacob E. Hoerter, Brandie N. Radde, Carolyn M. Klinge, Arsenite and Cadmium Activate MAPK/ERK via Membrane Estrogen Receptors and G-Protein Coupled Estrogen Receptor Signaling in Human Lung Adenocarcinoma Cells, Toxicological Sciences, Volume 152, Issue 1, July 2016, Pages 62–71, https://doi.org/10.1093/toxsci/kfw064