Causes of Cancer: Heavy Metals & Coffee Enemas
Metals contribute to the formation of cancer in many ways. It is important for every cancer patient to have proper provoked heavy metal testing performed to determine if these potentially cancer-causing agents exist in the body. The present body of literature supports at least 5 main mechanisms for induction of cancer, including:
(1) Many metals (such as Nickel, Arsenic, and Chromium) not only damage DNA but also interfere with the body’s repair mechanisms for such damage (Salnikow and Zhitkovich 2008). In particular, these metals stop or reactivate DNA replication by adding “methyl” groups and/or removing “acetyl” groups from structures that package genes, called histones (Arita and Costa 2009, Salnikow and Zhitkovich 2008). Ultimately, by altering the replication of genes in our cells, specific pathways of signals are activated, which promote the survival of these genetically-altered cells – i.e. cancer.
(2) Metal exposure also produces molecules called free radicals and reactive oxygen species (ROS). In turn, radicals and ROS damage mitochondrial and nuclear DNA as well as structures beyond DNA. Likewise, when the machinery of our mitochondria malfunctions, our ability to produce ATP decreases – or our bodies storage form of energy decreases (Lamson 2017). Metals known to disrupt our mitochondrial function include: Mercury, Alumnum, Arsenic, Cadmium, Lead, and Manganese.
(3) However, many metals are known to disrupt our body’s hormonal balance. Cadmium, Cobalt, Chromium, Iron, Manganese, and Zinc are found in significantly higher levels in breast cancer tissue than in benign, non-cancerous tissues (Pasha et al. 2008). Metals, such as cobalt and chromium, increase the proliferation of breast cancer cells (Martin et al. 2003). Likewise, these metals also increase the stimulation of estrogen receptors, indirectly increasing the activity of hormones in the body. In fact, drugs used for blocking estrogen receptors are not able to block all the hormonal effects of these metals (Martin et al. 2003). While the implication of metals in breast cancer has been extensively studied, research also supports the role of metal exposure in prostate cancer through the binding of androgen receptors (Martin et al. 2002).
(4) Although breast cancer can form in tissues with hormonal receptors for estrogen, progesterone, and HER2, some forms of breast cancer are derived from cells that lack these receptors – called triple-negative breast cancer cells. For example, Cadmium promotes the proliferation of these triple-negative breast cancer cells by stimulating the receptor for the epidermal growth factor (Wei et al. 2015).
(5) Lastly, metals, like Nickle, Lead, and Cadmium, stimulate the formation of cancer in tissues by increasing levels of our body’s transforming growth factor beta (TGF-beta) (Blobe et al. 2000). In turn, TGF-beta stimulates angiogenesis (or the formation of new blood vessels), suppresses the activity of immune cells, and increases the invasiveness and metastatic ability of cancer cells to distant organs (Pertovaara et al. 1994, Willems-Widyastuti et al. 2011).
Metals and Coffee Enemas
Auto-intoxication is where the levels of by-products of inefficient digestion and toxins increase within the intestines, resulting in numerous diseases as these accumulations poison our body (Chen and Chen 1989, Gots 1993, and Richards et al. 2006). The practice of detoxification aims to remove such toxins. Enemas have been used for centuries by many civilizations, including the Egyptians, Romans, and Sumerians, for such purposes. In the last 30 years, the use of coffee enemas in particular has increased – though please note that drinking coffee does not have the same effect. In fact, caffeine in a coffee enema is approximately 3.5 times less available than in coffee consumed orally (Teekachunhatean et al. 2013). Yet, research supports that extracts of green coffee beans increase levels of anti-oxidants like glutathione within the small intestine and liver (Lam et al. 1982). Furthermore, Kim et al. (2014) support that this procedure aids detoxification by dilating our blood vessels, relaxing the smooth muscles of our gastrointestinal tract and enhancing circulation. As such, coffee enemas are widely used within the alternative medicine field for the removal of toxins from the body.
Nonetheless, metals toxins that accumulate within the body are often lipophilic – or “fat-loving” (Tchounwou et al. 2012). This property makes their removal more difficult as they require fat solvents to be excreted. On one hand, Lee (2004) maintains that coffee enemas induce relaxation of muscles of the liver and gallbladder ducts, which releases the toxins produced by tumours – as well as the byproducts from the body’s systems to eliminate cancer cells – into the intestines to be excreted from the body. However, chelation therapy – used by both conventional and alternative medicine – is the most widely used and well-researched method of detoxifying these lipid-soluble toxins (Sears 2013).
The first step in the effective detoxification of toxins is to check your levels of toxic metals reliably (Lamson 2017). At our clinic, a urine toxic metal test is performed after IV EDTA & DMPS is given. This urine test confirms what heavy metals are present in the body. The ability of chelating agents to remove metals depends on how accessible that agent is to tissues, the metal and its characteristics, and the amount of metal ions in tissues (Apostoli et al. 2006). Likewise, in order to remove metals, chelators that are also fat-loving penetrate deeper into tissues and cells – including the central nervous system, like the brain – and are released in larger amounts through bile into the intestines for excretion. In this way, we support your body through the process of detoxification of these specific harmful toxins by choosing the most appropriate chelating agent for you.
The most well-researched chelating agents are called EDTA (ethylene diamine tetra-acetic acid), DMSA (2,3-Dimercapto-1-propanesulfonic acid), or DMSA (Dimercaptosuccinic acid) (Sears 2013). During a urine test, these agents will pass through cell membranes to form complexes with the metal and glutathione as well as other small molecules (Flora 2009). These now-water-soluble complexes pull heavy metals from your tissues into the bloodstream, where the toxins can be removed by the kidneys and then released from the body. IV EDTA & DMPS are excreted via urine within 6h (Sears 2013).
In comparison, IV DMPS significantly increases the excretion of arsenic, cadmium, lead methylmercury, and inorganic mercury (Aposhian 1983, Hurlburt et al. 1994). However, the urine test also increases the excretion of copper, selenium, zinc, and magnesium such that the replacement of these minerals before and after treatment is required (Torres-Alanis et al. 2000). DMSA removes arsenic, cadmium, lead, and methylmercury (Aposhian 1983, Anderson and Neilsen 1988). Lastly, EDTA removes lead and cadmium (Sears 2013). Nonetheless, caution should be used with all these agents in treating metal exposures in children and the close monitoring of patients is required to prevent the onset of hypocalcemia (i.e. low blood calcium levels).
More on Metals
Aluminum can be ingested through food but also absorbed dermally (through for example, antiperspirants with aluminum) (ATSDR 2008). Higher levels of aluminum are present in breast tissues – particularly in the upper outer quadrant or the site of 53% of breast cancer (Darbre 2016). Aluminum leads to genetic instability as well as the over-proliferation of normal breast cells. Likewise, the metal increases the migration and invasion of breast cancer cells (Darbre 2016). As a metalloestrogen, aluminum also mimics estrogen in the body.
The Department of Health and Human Services (DHHS), Environmental Protection Agency (EPA), International Agency for Research on Cancer (IARC) have all deemed arsenic as a “carcinogen”. Arsenic cannot be destroyed in the environment; however, the metal can change its form and dissolve in water (ATSDR 2007a). Exposure occurs through ingestion of food and water or breathing in air containing arsenic. Furthermore, breathing in the sawdust or smoke of wood that has been treated with the metal can also lead to toxicity. Beyond the feeling of “pins and needles” in hands and feet, toxicity decreases the production of red and white blood cells, causes abnormal heart rhythm, and damages blood vessels.
As a carcinogen, arsenic converts normal stem cells into cancer stem cells (Barrett 2012). Typically, stem cells replenish our levels of damaged or dead cells; however, cancer stem cells feed the growth and spread of tumours in our body. Likewise, preliminary studies indicate that even indirect exposure may also induce cancer cells (Xu et al. 2012). For example, exposure in the womb and early childhood leads to an increases the rate of death from lung cancer and bronchietesis in young adults (Barrett 2012). Proposed mechanisms include inflammatory cytokines. Studies ultimately have determined that ingesting inorganic arsenic increases the risk of skin, liver, bladder and lung cancer (ATSDR 2007a). Likewise, inhaling inorganic arsenic increases the risk of lung cancer. Some forms of arsenic can also act as a metalloestrogen within the body (Darbre 2006).
By 2002, the International Agency for Research on Cancer (IARC) determined that Cadmium was a human carcinogen. The mechanism is in part due to increased DNA and lipid damage by free radicals (Bagchi et al. 1996). However, Cadmium is the best studied metalloestrogen (Byrne et al. 2013). That is to say, this metal exhibits an estrogenic effect in mammary glands (Johnson et al. 2003). Furthermore, this metal converts normal breast tissue into cancer cells (Benbrahim-Tallaa et al. 2009). The longer the exposure the more aggressive the cancer cells become, in terms of increase cell growth, migration and invasion. Beyond its implication in breast cancer, Qu et al. (2012) found Cadmium exposure leads to the formation of cancer in the lungs, prostate and pancreas. In fact, this metal has a stronger binding affinity for the androgen receptor than androgen itself, stimulating the growth of cancer cells in prostate tissue (Martin et al. 2002). While breast cancer can form in tissues with hormonal receptors for estrogen, progesterone, and HER2, some forms of breast cancer are derived cells that lack these receptors – called triple-negative breast cancer cells. Furthermore, Cadmium promotes the proliferation of these triple-negative breast cancer cells by stimulating the receptor for the epidermal growth factor (Wei et al. 2015). Lastly, Cadmium stimulates the proliferation of leiomyoma (i.e. fibroids that can form on smooth muscle organ, such as the uterus) through increases of a protein called mitogen-activated protein kinase (MAPK). We commonly find cadmium in our tests with cancer patients, particularly in those that have smoked cigarettes.
Most contaminations of lead in the environment are a result of human activities, such as burning fossil fuels, mining, and manufacturing (ATSDR 2007b). Human exposure of lead includes eating food or drinking water with lead. For example, lead can leach out of water pipes in some older homes with lead solder. However, airborne exposure is also possible through the deterioration of lead-based paints. Inside the human body, lead can damage nearly every organ and system (ATSDR 2007a). Nonetheless, the primary organ system affected by lead toxicity in adults and children is the nervous system. In fact, long-term exposure decreases the performance of the nervous system in adults. Lead causes weakness of the fingers, wrists, and/or ankles (ATSDR 2007a). Likewise, exposure not only increases in blood pressure in middle-aged and older people but also can cause anemia. High level exposure of leads can severely impair the function of the brain and kidneys in adults or children, leading to death (ATSDR 2007a). From exposure to lead, pregnant women are at risk of a miscarriage and male reproductive organs responsible for making sperm may be damaged.
Present studies have focused on the health effects of low exposure of lead (Waldron and Stofan 1974, Landrigan 1989). These levels were formerly deemed as safe, which brings to light the notion of “subclinical toxicity” of lead. These findings support the notion that despite a lack of clinical manifestations, lead exposure can have asymptomatic effects (Landrigan et al. 2000). While the IARC had initially deemed the present evidence as ‘inadequate’ towards determining the cancer risk of lead, new research has been collected on its carcinogenic risk (Silbergeld 2000). New research has found lead to cause renal cancer (Bofetta et al. 2011, Ilychova and Zaridze 2012, Southard et al. 2012), lung cancer (Jones et al. 2007, Rousseau et al. 2007, Steenland and Boffetta 2000) and brain tumors (Anttila et al. 1996, Bhatti et al. 2009, Rajaraman et al. 2006) in humans. Some proposed mechanisms of action include: inhibition of DNA synthesis and repair, oxidative damage, and interaction with DNA-binding proteins and tumor-suppressor proteins (National Research Council 2012).
Agency for Toxic Substances and Disease Registry (ATSDR). (2008). Toxicological Profile for Aluminum. Atlanta, GA: U.S. Department of Health and Human Services, Public Health Services.
Agency for Toxic Substances and Disease Registry (ATSDR). (2007a). Toxicological Profile for Arsenic (Update). Atlanta, GA: U.S. Department of Health and Human Services, Public Health Service.
Agency for Toxic Substances and Disease Registry (ATSDR). (2007b). Toxicological Profile for Lead (Update). Atlanta, GA: U.S. Department of Health and Human Services, Public Health Service.
Andersen, O. and Nielsen, J. B. (1988) Oral cadmium chloride intoxication in mice: effects of penicillamine, dimercaptosuccinic acid and related compounds. Pharmacol Toxicol. 63: 386–89.
Anttila, A., Heikkila, P., Nykyri, E., et al. (1996) Risk of nervous system cancer among workers exposed to lead. J Occup Environ Med. 38(2):131–6.
Aposhian, H. V. (1983) DMSA and DMPS—water soluble antidotes for heavy metal poisoning. Annu Rev Pharmacol Toxicol. 23:193–215.
Apostoli, P., Cornelis, R., Duffus, J., et al. (2006) Elemental speciation in human health risk assessment. Geneva: United Nations Environment Programme, the International Labour Organization and the World Health Organization.
Arita, A. and Costa, M. (2009) Epigenetics in metal carcinogenesis: nickel, arsenic, chromium and cadmium. Metallomics. 1(3): 222–8.
Bagchi, D., Bagchi, M., Hassoun, E. A., et al. (1996) Cadmium-induced excretion of urinary lipid metabolites, DNA damage, glutathione depletion, and hepatic lipid peroxidation in Sprague-Dawley rats. Biol Trace Elem Res. 52(2): 143–54.
Barrett, J. R. (2012) Bad Neighbors: Arsenic-Induced Tumor Cells Convert Normal Stem Cells into a Cancerous Phenotype. Environ Health Perspect. 120(6): a244.
Benbrahim-Tallaa, L., Tokar, E. J., Diwan, B. A., et al. (2009) Cadmium malignantly transforms normal human breast epithelial cells into a basal-like phenotype. Environ Health Perspect. 117(12): 1847–52.
Bhatti, P., Stewart, P. A., Hutchinson, A., et al. (2009) Lead exposure, polymorphisms in genes related to oxidative stress, and risk of adult brain tumors. Cancer Epidemiol Biomarkers Prev. 18(6):1841–8.
Blobe, G. C., Schiemann, W. P., and Lodish, H. F. (2000) Role of transforming growth factor beta in human disease. N Engl J Med. 342(18): 1350–8.
Boffetta, P., Fontana, L., Stewart, P., et al. (2011) Occupational exposure to arsenic, cadmium, chromium, lead and nickel, and renal cell carcinoma: A case-control study from Central and Eastern Europe. Occup Environ Med. 68(10):723–8.
Byrne, C., Divekar, S. D., Storchan, G. B., et al. (2013) Metals and breast cancer. J Mammary Gland Biol Neoplasia. 18(1): 63–73.
Chen, T. S. and Chen, P. S. (1989) Intestinal autointoxication: a medical leitmotif. J Clin Gastroenterol. 11(4): 434–41.
Darbre, P. D. (2016) Aluminium and the human breast. Morphologie. 100(329): 65–74.
Flora, S. J. S. (2009) “Metal poisoning: threat and management. Al Ameen J Med Sci. 2:4–26.
Gao, X., Yu, L., Moore, A. B., et al. (2015) Cadmium and proliferation in human uterine leiomyoma cells: evidence of a role for EGFR/MAPK pathways but not classical estrogen receptor pathways. Environ Health Perspect. 123(4): 331–6.
Gots, R. E. (1993) Medical hypothesis and medical practice: autointoxication and multiple chemical sensitivities. Regul Toxicol Pharmacol. 18(1):2–12.
Hurlbut, K. M. Maiorino, R. M. Mayersohn, M. et al. (1994) Determination and metabolism of dithiol chelating agents XVI: pharmacokinetics of 2,3- dimercapto-1-propanesulfonate after intravenous administration to human volunteers. J Pharm Exp Ther. 268(2): 662–8.
Ilychova, S. A. and Zaridze, D. G. (2012) Cancer mortality among female and male workers occupationally exposed to inorganic lead in the printing industry. Occup Environ Med. 69(2):87–92.
Johnson, M. D., Kenney, N., Stoica, A., et al. (2003) Cadmium mimics the in vivo effects of estrogen in the uterus and mammary gland. Nat Med. 9(8):1081–4.
Jones, S. R., Atkin, P., Holroyd, C., et al. (2007) Lung cancer mortality at a UK tin smelter. Occup Med. 57(4):238–45.
Kim, E. S., Chun, H. J., Keum, B., et al. (2014) Coffee enema for preparation for small bowel video capsule endoscopy: a pilot study. Clin Nutr Res. 3(2): 134–41.
Lam, L. K., Sparnins, V. L., and Wattenberg, L. W. (1982) Isolation and identification of kahweol palmitate and cafestol palmitate as active constituents of green coffee beans that enhance glutathione S-transferase activity in the mouse. Cancer Res. 42(4): 1193–8.
Lamson, D. (2017, Feb 17-19) Maintaining the Remission and Connections of Toxic metals to Cancer. Presented at the 6th Annual Conference of OncANP, Tempe, Arizona.
Landrigan, P. J. (1989) Toxicity of lead at low dose. Br J Ind Med. 46(9): 593–6.
Landrigan, P. J., Boffetta, P., and Apostoli, P. (2000) The reproductive toxicity and carcinogenicity of lead: a critical review. Am J Ind Med. 38(3): 231–43.
Lee, M. J. (2004) The Study of Enema Therapy as One of the Detoxification Therapy. J of Orient Neuropsychiatr. 15(2): 24–36.
Martin, M. B., Reiter, R., Pham, T., et al. (2003) Estrogen-like activity of metals in MCF-7 breast cancer cells. Endocrinology. 144(6): 2425–36.
Martin, M. B., Voeller, H. J., Gelmann, E. P., et al. (2002) Role of cadmium in the regulation of AR gene expression and activity. Endocrinology. 143(1): 263–75.
Pasha, Q., Malik S. A., Iqbal, J., et al. (2008) Comparative evaluation of trace metal distribution and correlation in human malignant and benign breast tissues. Biol Trace Elem Res. 125(1):30–40.
Pearce, M. S., McConnell, J. C., Potter C., et al. (2012) Global LINE-1 DNA methylation is associated with blood glycaemic and lipid profiles. Int J Epidemiol. 41(1): 210–7.
Pertovaara, L., Kaipainen, A., Mustonen, T., et al. (1994) Vascular endothelial growth factor is induced in response to transforming growth factor-beta in fibroblastic and epithelial cells. J Biol Chem. 269(9): 6271–4.
Qu, W., Tokar, E. J., Kim, A. J. et al. (2012) Chronic Cadmium Exposure in Vitro Causes Acquisition of Multiple Tumor Cell Characteristics in Human Pancreatic Epithelial Cells. Environ Health Perspect. 120(9): 1265–71.
Rajaraman, P., Stewart, P. A., Samet, J. M., et al. (2006) Lead, genetic susceptibility, and risk of adult brain tumors. Cancer Epidemiol Biomarkers Prev. 15(12):2514–20.
Richards, D. G., McMillin, D. L., Mein, E. A., et al. (2006) Colonic irrigations: a review of the historical controversy and the potential for adverse effects. J Altern Complement Med. 12(4): 389–93.
Rousseau, M. C., Parent, M. E., Nadon, L., et al. (2007) Occupational exposure to lead compounds and risk of cancer among men: A population-based case-control study. Am J Epidemiol. 166(9):1005–14.
Salnikow, K. and Zhitkovich, A. (2008) Genetic and epigenetic mechanisms in metal carcinogenesis and cocarcinogenesis: nickel, arsenic, and chromium. Chem Res Toxicol. 21(1): 28–44.
Sears, M. E. (2013) Chelation: Harnessing and Enhancing Heavy Metal Detoxification—A Review. Scientific World J. 2013: 219840.
Silbergeld, E. K., Waalkes, M., and Rice, J. M. (2000) Lead as a carcinogen: experimental evidence and mechanisms of action. Am J Ind Med. 38(3): 316–23.
Southard, E. B., Roff, A., Fortugno, T., et al. (2012) Lead, calcium uptake, and related genetic variants in association with renal cell carcinoma risk in a cohort of male Finnish smokers. Cancer Epidemiol. Biomarkers Prev. 21(1): 191–201.
Steenland, K. and Boffetta, P. (2000) Lead and cancer in humans: Where are we now? Am J Ind Med. 38(3):295–299.
Tchounwou,P. B., Yedjou, C. G., Patlolla, A. K., et al. (2012) Heavy Metals Toxicity and the Environment. EXS. 101: 133–64.
Teekachunhatean, S., Tosri, N., Rojanasthien, N., et al. (2013) Pharmacokinetics of Caffeine following a Single Administration of Coffee Enema versus Oral Coffee Consumption in Healthy Male Subjects. ISRN Pharmacol. 2013: 147238.
Torres-Alanis, O. Garza-Ocanas, L. Bernal, M. A., et al. (2000) Urinary excretion of trace elements in humans after sodium 2,3-dimercaptopropane-1-sulfonate challenge test. J Toxicol Clin Toxicol. 38(7): 697–700.
Wie, Z., Song, X., and Shaikh, Z. A. (2015) Cadmium promotes the proliferation of triple-negative breast cancer cells through EGFR-mediated cell cycle regulation. Toxicol Appl Pharmacol. 289(1): 98–108.
Waldron, H. A., and Stofen, D. (1974) Subclinical Lead Poisoning. London: Academic Press.
Willems-Widyastuti, A., Alagappan V. K., Arulmani, U., et al. (2011) Transforming growth factor-beta 1 induces angiogenesis in vitro via VEGF production in human airway smooth muscle cells. Indian J Biochem Biophys. 48(4): 262–9.
Xu, Y., Tokar, E. J., Sun, Y. et al. (2012) Arsenic-Transformed Malignant Prostate Epithelia Can Convert Noncontiguous Normal Stem Cells into an Oncogenic Phenotype. Environ Health Perspect. 120(6): 865–71.