Thursday, September 26, 2019
Insights From An Oasis Of Healing #16 The Best Treatment For Cancer Is Prevention
Watch on YouTube here: Insights From An Oasis Of Healing #16 The Best Treatment For Cancer Is Prevention
Via
Monday, September 23, 2019
Monday, September 16, 2019
Estrogen Metabolism Pathway And The 3 Primary Estrogen Metabolites
Estrogen metabolism pathway: there are three pathways and I label them as the good, bad, and ugly.
Previously, I mentioned the 3 primary estrogens: estradiol, estrone, and estriol. That is the simple. The complex is that there are many more estrogens that are actually produced by the body through the process of estrogen metabolism—estrogen metabolites.
Estrogen metabolites have been shown to have different effects on cancer risk. This difference in risk is the result of an interplay between an individuals genetics and their environment. The vast majority of the research on estrogen metabolism is with cancer. The majority of the research on estrogen metabolism with cancer is with breast cancer.
When it comes to estrogen metabolism and cancer there are 3 primary estrogen metabolism pathways to highlight. I call them the good, the bad and the ugly. There are 3 primary estrogen metabolites from these 3 pathways: 2-hydroxy estrone (2OH-estrone), 4-hydroxy estrone (4OH-estrone), and 16alpha-hydroxy estrone (16alphaOH-estrone).
The origin estrogens for these 3 metabolites are primarily Estradiol (the most potent estrogen) and Estrone (the second most potent estrogen). Estriol, the weakest estrogen, can be converted to the 16alpha-OH-estrone metabolite, but not to the 2OH-estrone or 4OH-estrone metabolites. Additional estrogen metabolites include:
- 2-OH Estradiol
- 4-OH Estradiol
- 16alpha-OH Estradiol
- 2-methoxy Estrone
- 2-methoxy Estradiol
- 16-epi Estriol
- 17-epi Estriol
- 16-keto Estradiol
For the purpose of the brevity of this blog post, I will stick to a brief discussion of these 3 primary estrogen metabolites.
Dr. Nathan Goodyear Explains The 3 Primary Estrogen Metabolism Pathways
2OH-Estrone Metabolite
The 2OH-estrone metabolite is the safest estrogen metabolite. The better descriptive term to describe the 2OH-estrone metabolite is “safest” or “lowest risk” and that may too be overly simplistic. The 2OH-estrone metabolite is the most prevalent estrogen metabolite circulating in the blood [63].
Research points to the 2OH-estrone metabolite as the byproduct of the CYP1A1, CYP1A2, and CYP1B1 detoxification enzymes [64] [65] though studies do suggest that CYP1A1 is the primary enzyme involved in the production of the 2OH-estrone metabolite [66] [67] [68]. This “good” term for the 2OH-estrone metabolite is also an oversimplification of the scientific evidence on this estrogen metabolite as some more recent evidence points to an increased breast cancer risk with the 2-hydroxyestrone metabolite.
There are several mechanisms that support 2OH-estrone metabolite as the safest estrogen metabolite. First, all of the estrogen metabolites are particularly unstable compounds. The 2OH-estrone metabolite is the most stable of the 3 estrogen metabolites discussed [69] which translates to less potential DNA damage.
It is DNA damage that is critical in carcinogenesis. Second, the 2OH-estrone metabolite elicits a very weak, almost anti-estrogenic activity [70] [71]. Low binding affinity for the estrogen receptor and increased removal from the estrogen receptor are the primary reasons for the weak estrogenic activity of the 2OH-estrone metabolite. This estrogenic activity is the weakest of the 3 estrogen metabolites.
Third, though weak as indicated above, the 2OH-estrone metabolite is easily methylated and thus inactivated. Last, the 2OH-estrone metabolite lacks significant anti-apoptosis activity [72] which maintains a strong anti-growth potential check through the active process of apoptosis (programmed cell death).
4OH-Estrone Metabolite
The bad estrogen or what I call the “ugly” estrogen metabolite is the 4OH-estrone metabolite. The overwhelming evidence points to the 4OH-estrone metabolite as pro-carcinogenic and pro-growth.
There are several reasons why the 4OH-estrone metabolite is the most dangerous estrogen metabolite. First, the 4OH-estrone metabolite is the most unstable of the estrogen metabolites and it is this instability that can lead to DNA damage which is important in carcinogenesis. Second, of the 3 metabolites, the 4OH-estrone metabolite elicits the strongest estrogenic activity via its high affinity and tight binding to the estrogen receptor and lower disassociation rate from the estrogen receptor.
Third, in contrast to the 2OH-estrone metabolite, the 4OH-estrone metabolite is not easily deactivated through methylation. Last, the 4OH-estrone metabolite has a significant anti-apoptotic effect which favors such cancer cell survival. All this at an estimated 15-25% less circulating volume than the 2OH-estrone metabolite.
16alphaOH-Estrone Metabolite
The 16alphaOH-estrone metabolite has been historically labeled as a “bad” estrogen. This pathway of estrogen metabolism, as a whole, is the dominant pathway of estrogen metabolism 16. The proposed high cancer risk of the 16alphaOH-estrone metabolite is due to its increased estrogen signaling and growth capacity through its tight binding to the estrogen receptor. In addition, it is not easily removed leaving the metabolite tightly bound to the estrogen receptor resulting in a prolonged growth signal.
In addition, the 16alphaOH-estrone metabolite does not down-regulate the estrogen receptor, which is a key mechanism by which cells can turn down the potential signal. Finally, 16alphaOH-estrone metabolite has a strong anti-apoptotic effect [73]. The jury is out on the “bad” label for this metabolite. The 16alpha-OH-estrone metabolite has a strong positive link to breast cancer in post-menopause women [74] yet, other studies have found no link between 16alpha-OH-estrone and cancer risk [75] [76].
The implication is that it may not only be the estrogen levels or the estrogen receptors that are involved in cancer risk, but it is, in fact, what the body is doing with the estrogens through estrogen metabolism that also poises the cancer risk.
[63] Adlercreutz H, Fotsis T, Hockerstedt K, Hamalainen E, Bannwart C, Bloigu S, Valtonen A & Ollus A 1989 Diet and urinary estrogen profile in premenopausal omnivorous and vegetarian women and premenopausal women with breast cancer. Journal of Steroid Biochemistry and Molecular Biology 34 527–530.
[64] Cribb AE et al. Role of polymorphic human cytochrome P450 enzymes in estrone oxidation. Cancer Epidemiol Biomarkers Prev. 2006 Mar. 15/551.
[65] Sowers MR et al. CYP1A1 and CYP1B1 polymorphism and their association with estradiol and estrogen metabolites in women who are premenopausal and perimenopausal. Am J Med. Sep 2006;119(9 Suppl 1): S44-51.
[66] Lee AJ, Cai MX, Thomas PE, Conney AH, Zhu BT. Characterization of the oxidative metabolites of 17β-estradiol and estrone formed by 15 selectively expressed human cytochrome p450 isoforms. Endocrinology 2003;144:3382–98.
[67] Shimada T, Watanabe J, Kawajiri K, et al. Catalytic properties of polymorphic human cytochrome P450 1B1 variants. Carcinogenesis 1999;20:1607–13.
[68] Kisselev P, Schunck WH, Roots I, Schwarz D. Association of CYP1A1 polymorphisms with differential metabolic activation of 17β-estradiol and estrone. Cancer Res 2005;65:2972–8.
[69] Bradlow HL, Telang NT, Sepkovic DW, Osborne MP. 2-Hydroxyestrone: the ‘good’ estrogen. J Endocrinol 1996;150 Suppl:S259–65.
[70] Schneider J, Huh MM, Bradlow HL, Fishman J. Antiestrogen action of 2-hydroxy estrone on MCF-7 human breast cancer cells. J Biol Chem. 1984;259:4840–5.
[71] Vandewalle B, Lefebvre J. Opposite effects of estrogen and catechol estrogen on hormone-sensitive breast cancer cell growth and differentiation. Mol Cell Endocrinol. 1989;61:239–46.
[72] Seeger H, Wallwiener D, Kraemer E, Mueck AO. Comparison of possible carcinogenic estradiol metabolites: effects on proliferation, apoptosis, and metastasis of human breast cancer cells. Maturitas 2006;54:72–7.
[73] Seeger H et al. Comparison of possible carcinogenic estradiol metabolites: effects on proliferation, apoptosis, and metastasis of human breast cancer cells. Maturitas. 2006 Apr;54(1):72-7.
[74] Kabat GC, Chang CJ, Sparano JA, et al. Urinary estrogen metabolites and breast cancer: a case-control study. Cancer Epidemiol Biomarkers Prev. 1997;6(7):505-509.
[75] Mackey RH et al. Hormone therapy, estrogen metabolism and risk of breast cancer in the Women’s Health Initiative. Cancer Epidemiol Biomarkers Prev. 2012 Nov;21(11):2022-2032.
[76] Arslan AA et al. Circulating estrogen metabolites and risk for breast cancer in premenopausal women. Cancer Epidemiol Biomarkers Prev. 2009 Aug;18(8):2273-9.
Thursday, September 12, 2019
Monday, September 9, 2019
Stage 4 Breast Cancer With Bone Metastasis PET Scan Is Clear
Stage 4 breast cancer with bone metastasis had Shirley M. searching for alternative treatments for cancer.
Ten years ago, Shirley M. was diagnosed with breast cancer. She had a mastectomy and chemotherapy and even adapted a (kind of) vegetarian diet. The cancer was gone.
Or so she thought.
Fast forward to early 2019: Shirley noticed a knot under her arm and had it checked out. It was cancer again.
Shirley knew that she could not go through the aggressive treatments again. She searched online and found An Oasis of Healing as the best website.
“I called, and talking to Andy, I never had any doubt that this was the best place to come,” she said. “I never would have dreamed of how caring and passionate everybody is here. Every person here cares truly and does their best to help and encourage.”
When she first arrived at the Arizona-based alternative cancer treatment center, she was understandably worried. As Dr. Nathan Goodyear, senior medical staff member, pointed out, stage 4 bone cancer metastasis is a “big challenge.”
Understanding Bone Cancer Metastasis
Bone cancer can start as primary or secondary cancer. Primary bone cancer is when “cancer starts in the bone.”
Secondary bone cancer, or bone metastasis, means that cancer started elsewhere but has now metastasized or spread to the bone. This is considered the most advanced stage of bone cancer aka stage 4.
Bone metastasis is more likely to occur in the spine, pelvis or thigh. Symptoms include broken bones, bone pain, urinary and bowel incontinence, weakness in the arms and legs, and hypercalcemia or high levels of calcium in the blood which can then cause nausea, vomiting, and constipation.
At stage 4, the tumor will have appeared in more than one part of the body—possibly the lungs, lymph nodes or other organs.
The Beginning Of A Healing Journey
Shirley imagined that the process might be some sort of a “little vacation” for her but as it turns out, the healing journey required “hard work” from her end. Although she’s had her doubts, fears, and struggles halfway through the process, her perseverance paid off.
Shirley had cancer in her bones, liver, and breast but when the PET (positron emission tomography) scan came back, the cancer was gone. There were no more tumors.
Shirley’s favorite therapy was hyperthermia. “I got to sleep the day away. That was kind of fun,” she shared.
Hyperthermia, also sometimes called thermal therapy or thermotherapy, is a type of treatment wherein the body tissue is exposed to high temperatures with the intent of damaging and eventually, killing cancer cells. Hypothermia damages the proteins and structures within cancer cells to facilitate the shrinking of tumors.
Lymphatic Drainage Therapy As Part Of Shirley’s Bone Metastasis Treatment Allowed The Immune System To Do Its Job
Shirley added, “I loved going to lymphatics. Without that, my arm would just balloon and that kept it under control.” Lymphatic therapy helps the body “clear its informational highway” so that the body, especially the immune and lymphatic systems, can function at its optimal level.
The treatment device at An Oasis of Healing painlessly breaks down congestion using inert gas ionization. This allows trapped proteins to “become disassociated,” thus releasing the stagnate lymph. In effect, the excess, blocked, stagnate or retained fluid are released and flow out into normal filtration and reabsorption channels.
“If everybody knew about this healing center, they could forego all the negative side effects of conventional oncology,” she said. And as long as she stays with her current wellness routine, she knows that she can continue to enjoy the post-treatment quality of life she is living now.
Find out how An Oasis of Healing can help you or a loved one. Get in touch today.
Tuesday, September 3, 2019
Glyphosate Cancer Risk The Connection Is Evident
Glyphosate cancer risk is growing steadily with plenty of proof as we will explain in this article!
You may or may not be aware of the glyphosate. It is hard to miss it though. It can be found in your local community hardware store. The glyphosate cancer risk is very real.
The purpose? To kill those pesky, unsightly weeds. You know the commercial product as Roundup. Glyphosate is the active component within Roundup and other common anti-weed products available on the market. Glyphosate functions as a non-selective, broad-spectrum herbicide. Glyphosate has been approved for use in the U.S. for 42 years [56].
Glyphosate exposure is on the rise. A 2017 study out of University of California San Diego found that human glyphosate exposure has increased 500% since 1993 [57]. In fact, 70% of the individuals evaluated tested positive for glyphosate.
Glyphosate is found primarily in the soil and from the produce grown from the soil i.e. carrots, potatoes. Another 2017 study of soil samples from countries in the EU found that 45% of the soil samples submitted were contaminated with either glyphosate and/or metabolites of glyphosate [58].
So why the concern? How about a 41% increase in cancer risk. A February 2019 study found a 41% increase in Non-Hodgkin’s Lymphoma as a result of glyphosate exposure [59]. Glyphosate’s cancer risk connection was recently evident in a $78.5 million verdict against Bayer, who recently purchased Monsanto, out of California.
Listen to Dr. Nathan Goodyear Explain The Associated Cancer Risk from Glyphosate
Glyphosate toxicity has been the focus of intense debate in recent years, but has been shown to have numerous potential negative effects [60]:
- Carcinogenic
- Tumor growth promotion
- Endocrine disruption
- Tissue-specific toxicity
- Cytotoxicity
- Immune suppression
- Disruption of gap-junction intercellular signaling
- Oxidative stress
For the purpose of this blog, the estrogen effects of glyphosate are front and center. Glyphosate does have weak affinity and stimulators effect in binding to the estrogen receptors but it does so much more.
A recent study showed that glyphosate increased the up-regulation of ER-alpha expression in addition to pro-growth, carcinogenic VEGFR2, pERK, PI3K, and PCNA [61]. This was also evident in an earlier study that showed that glyphosate increased the expressed ratio of ER-alpha to ER-beta [62].
Let me restate that statement to clarify the significant impact that glyphosate has on potential ER activity. Remember that the ER expression in breast cancer, colorectal cancer, and other cancers is the ER-alpha form.
Glyphosate signals the DNA to increase the production of ER-alpha. As a result of the ER-alpha production and expression as a result of glyphosate, the cell has an increased capacity to respond to estrogen.
Add this to the increased exposure to endogenous estrogen production and an increase in estrogen in the environment through other xenoestrogens and the table is set up for an estrogenic signaling environment that favors cancer. This is how in utero exposure can change the body even prior to birth.
[56] Benbrook CM. Trends in glyphosate herbicide use in the United States and globally. Environ Sci Eur. 2016;28(1):3. doi:10.1186/s12302-016-0070-0.
[57] Mills P, Kania-Korwel I, Fagan J et al. Excretion of the Herbicide Glyphosate in Older Adults Between 1993 and 2016. JAMA. 2017;318(16):1610-1611. doi:10.1001/jama.2017.11726.
[58] Silva V, Montanarella L, Jones A, Fernandez-Ugalde O, Mol H, Ritsema C, Geissen V. Distribution of glyphosate and aminomethylphosphonic acid (AMPA) in agricultural topsoils of the European Union. Science of the Total Environment. April 15 2018;621: 1352-1359. https://doi.org/10.1016/j.scitotenv.2017.10.093.
[59] Zhang L, Rana L, Schaffer R, Taioli E, Sheppard L. Exposure to Glyphosate-Based Herbicides and Risk for Non-Hodgkin Lymphoma: A Meta-Analysis and Supporting Evidence. Mutation Research/Reviews in Mutation Research. Feb 10 2019. https://doi.org/10.1016/j.mrrev.2019.02.001.
[60] Tarazona JV, Court-Marques D, Tiramani M, et al. Glyphosate toxicity and carcinogenicity: a review of the scientific basis of the European Union assessment and its differences with IARC. Arch Toxicol. 2017;91(8):2723–2743. doi:10.1007/s00204-017-1962-5.
[61] Sritana N, Suriyo T, Kanitwithayanum J, Songvasin BH, Thiantanawat A, Satayavivad J. Glyphosate induces growth of estrogen receptor alpha positive cholangiocarcinoma cells via non-genomic estrogen receptor/ERK1/2 signaling pathway. Food and Chemical Toxicology. Aug 2018;118:595-607. https://doi.org/10.1016/j.fct.2018.06.014.
[62] Thongprakaisang S, Thiantanawat A, Rangkakilok N, Suriyo T, Satayavivad J. Glyphosate induces human breast cancer cells growth via estrogen receptors. Food and Chemical Toxicology. Sept 2013;59:129-136. https://doi.org/10.1016/j.fct.2013.05.057.
Monday, August 26, 2019
Mycotoxins Increase The Risk Of Cancer
Mycotoxins have been shown to obstruct apoptosis or programmed cell death.
Mycotoxins are toxins are just as their name implies: myco = fungus and toxin = toxin. These toxins originate from a fungus that commonly grows in the food supply and in water damaged areas. Mycotoxins will increase the chance of cancer developing in the human body.
Mycotoxins have been shown to be [39] [40]:
- Carcinogenic
- Mutagenic
- Teratogenic
- Immunotoxic
- Hepatoxic
- Hemorrhagic
- Nephrotic
- Neurotoxic
- Dermatoxic
- Endocrine (hormone) disruptors
Mycotoxins can be defined as “natural products produced by fungi that evoke a toxic response when introduced in low concentration to higher vertebrates and other animals by a natural route“ [41]. Mycotoxins are some of the most well-known toxins to contaminate the food supply including but not limited to aflatoxin, ochratoxin, fumonisins, patulin, zearalenone (ZEA), and trichothecenes from the fungus Aspergillus, Fusarium, and Penicillium.
In addition, mycotoxins are found in water-damaged walls, wallpaper in homes, buildings… Not all mycotoxins are inherently toxic as the antibiotic penicillin is a mycotoxin. The question lies in where is the toxicity directed?
Mycotoxins Are Affecting People Globally
Mycotoxins are a world-wide problem affecting an approximate 25% [42] of the world’s food supply. Mycotoxins are most commonly found in the grain and cereal foods i.e. wheat, barley, nuts, corn, rice… Even the coffee in your morning cup of joe is a potential source—so sad.
These food items are commonly stored at room temperature in containers on the counter in the kitchen or in foods stored in the pantry or on the store shelf which is in part the origin of the risk. Don’t forget about animal products, such as beef, chicken, milk, eggs… that are raised on mycotoxin contaminated rich foods are also a potential exposure source.
Zearalenone is one of the most common mycotoxins that the U.S. food supply is at risk for. Animal and human studies have shown that zearalenone does accumulate in the body [43] [44]. This is huge because if these low exposures to 1,000s of potentially toxic chemicals are quickly cleared, then the risk and concern is limited; however, if these toxins bioaccumulate, then the low exposures to 1,000s of potentially toxic chemicals are, in fact, accumulating ticking time bombs.
Zearalenone is an endocrine disruptor; specifically, zearalenone mimics estrogen [45]. Zearalenone readily binds to the estrogen receptors (ER). Zearalenone stimulates an estrogenic signal through the specific binding to the ER-alpha receptors, not ER-beta [46].
This preferential ER-alpha affinity shifts the ER-alpha/ER-beta receptor balance to an ER-alpha dominance. This affinity of zearalenone for ER-alpha and ER-alpha dominance has been shown to increase the risk of breast cancer [47], esophageal [48], colorectal cancer [49] and prostate cancer [50]. Specifically, this mycotoxin has been shown to inhibit apoptosis (programmed cell death) stimulate proliferation, promote cancer cell invasion and metastatic spread of cancer cells 45 [51] [52].
Most interesting is that this powerful estrogenic signal, peak proliferation, and invasion occurred at the lowest levels of exposure. This has enormous implication as most people are not exposed to acute, high toxic loads of mycotoxins, or any toxin for that matter, but instead are exposed to small, regular, indolent exposures to hundreds of toxins every day.
Again, evidence shows that toxins like zearalenone can bioaccumulate in the environment and the human body. It is this regular exposure, bioaccumulation and synergistic toxic effects of these multiple toxins that change the environment in our body to increase the risk of cancer.
The Effects of Mycotoxins and EMF’s
As in all things, disease such as cancer is never the result of 1 item. It is the collective, synergistic effects that come together to affect disease risk. This is no more evident than in the growing volume of research that points to the synergistic effect of EMFs and mycotoxins. EMFs are all around us in our day-to-day activities and our home is the biggest offender. Common sources of EMFs include:
- Cellphones
- Wi-Fi
- Wi-Fi dependent devices
- TVs
- Radios
- Power lines
- Microwave ovens
- Computers
Our home environment can no longer be simply defined by the walls and roof of our house/apartment/Condo… but these home sources of Wi-Fi exposure even travel with us in our personal cellphones, car Wi-Fi… In fact, with the 4G and the coming 5G wave, EMFs are essentially becoming another element in our atmosphere home: Oxygen—check, CO2–check, EMFs—check.
Yet, we really don’t know what the long-term impact will be. The same mistakes are repeated time and time again. The new definition of our home environment must now include the immediate environment of our body wherever it goes.
EMFs have their own set of carcinogenic risk issues, such as leukemia [53]. The International Agency for Research on Cancer labeled EMFs as potentially carcinogenic in 2011. Research also shows, that in addition to isolated EMF exposure risk, EMFs can actually stimulate fungal growth [54] [55].
This post is not about EMFs specifically, but about their synergistic activity with fungi which can have significant implications in the increase in mycotoxin production and mycotoxin release. Whatever the mycotoxin source exposure is (food, water-damaged houses, vaping pens…), add EMF exposure, which is all around us, and the mycotoxin production, mycotoxin exposure and resultant risk i.e. estrogenic, carcinogenic risk, will increase.
It is the Consistent Exposure to Mycotoxins on a Daily Basis That Presents a Threat To Our Health
When it comes to potential environmental toxins, in this case, mycotoxins, everybody is looking for the 1 hit phenomenon or the 1 giant bomb that definitively results in disease. That is a pie in the sky view and won’t be found except in very rare cases of exposure.
In fact, it is a basic misunderstanding of what and how toxicity can occur. In this day of 30-second commercials, sound bites, and attention, if the cause and effects are instantaneous, then they don’t exist.
This lack of patience has even permeated science. The reality is that environmental toxins can also work via what I like to call the rain of 1000 bullets. This mechanism is the regular, often unrecognized, smaller spray of hits of accumulative toxic effects will cause disease given adequate time.
It is like a shotgun versus a bomb. Odds are much better that you will survive the acute spray of a gunshot from the shotgun, compared to the direct hit by a bomb, but eventually, that spray of gunshots will do its damage and get the same job done given time.
These toxins were never approved based on long-term studies that detailed their long-term risk to the general public; except in the case of the long-term exposure tests ongoing of which we are the unwilling test subjects without our approval. Time will tell the final numbers that will be written in some future scientific publication and our unknowing participation will be a mere afterthought.
My purpose here is not to create fear, but enhance knowledge, because knowledge is power. Knowledge is the power to act. Knowledge is the power to make a difference.
39 Steyn PS. Mycotoxins, general view, chemistry, and structure. Toxicol Lett. Dec 1995;82–83: 843–851.
40 Wallace Hayes A. Mycotoxins: A review of biological effects and their role in human diseases. Clinical Toxicology.1983;17(1):45–83.
41 Bennett J.W. Mycotoxins, mycotoxicoses, mycotoxicology and mycopathologia. Mycopathologia. 1987;100:3–5. doi: 10.1007/BF00769561.
42 Alshannaq A, Yu JH. Occurrence, Toxicity, and Analysis of Major Mycotoxins in Food. Int J Environ Res Public Health. 2017;14(6):632. Published 2017 Jun 13. doi:10.3390/ijerph14060632.
43 Bennett JW, Klich M. Mycotoxins. Clin Microbiol Rev. 2003;16(3):497–516. doi:10.1128/CMR.16.3.497-516.2003.
44 Brera C., Debegnach F., De S.B., Di I.S., Gregori E., Neuhold S., Valitutti F. Exposure assessment to mycotoxins in gluten-free diet for celiac patients. Food Chem. Toxicol. 2014;69:13–17. doi: 10.1016/j.fct.2014.03.030.
45 Hueza IM, Raspantini PC, Raspantini LE, Latorre AO, Górniak SL. Zearalenone, an estrogenic mycotoxin, is an immunotoxic compound. Toxins (Basel). 2014;6(3):1080–1095. Published 2014 Mar 13. doi:10.3390/toxins6031080.
46 Kowalska K, Habrowska-Górczyńska DE, Urbanek KA, Domińska K, Piastowska-Ciesielska AW. Estrogen Receptor α Is Crucial in Zearalenone-Induced Invasion and Migration of Prostate Cancer Cells. Toxins (Basel). 2018;10(3):98. Published 2018 Feb 28. doi:10.3390/toxins10030098.
47 Pluciennik E. The role of WWOX tumor suppressor gene in the regulation of EMT process via regulation of CDH1-ZEB1-VIM expression in endometrial cancer. Int. J. Oncol. 2015;46:2639–2648. doi:10.3892/ijo.2015.2964.
48 Pitt J.I. Toxigenic fungi and mycotoxins. Br. Med. Bull. 2000;56:184–192. doi: 10.1258/0007142001902888.
49 Kwon O, Soung NK, Thimmegowda NR, et al. Patulin induces colorectal cancer cells apoptosis through EGR-1 dependent ATF3 up-regulation. Cell Signal. 2011;24(4):943–950. doi:10.1016/j.cellsig.2011.12.017.
50 Kowalska K., Habrowska-Gorczynska D.E., Dominska K., Piastowska-Ciesielska A.W. The dose-dependent effect of zearalenone on mitochondrial metabolism, plasma membrane permeabilization and cell cycle in human prostate cancer cell lines. Chemosphere. 2017;180:455–466. doi: 10.1016/j.chemosphere.2017.04.027.
51 Liu Q., Wang Y., Gu J., Yuan Y., Liu X., Zheng W., Huang Q., Liu Z., Bian J. Zearalenone inhibits testosterone biosynthesis in mouse Leydig cells via the crosstalk of estrogen receptor signaling and orphan nuclear receptor Nur77 expression. Toxicol. In Vitro. 2014;28:647–656. doi: 10.1016/j.tiv.2014.01.013.
52 Ayed-Boussema I., Bouaziz C., Rjiba K., Valenti K., Laporte F., Bacha H., Hassen W. The mycotoxin Zearalenone induces apoptosis in human hepatocytes (HepG2) via p53-dependent mitochondrial signaling pathway. Toxicol. In Vitro. 2008;22:1671–1680. doi: 10.1016/j.tiv.2008.06.016.
53 Calvente I., Fernandez M. F., Villalba J., Olea N., Nuñez M. I. (2010). Exposure to electromagnetic fields (non-ionizing radiation) and its relationship with childhood leukemia: a systematic review. Sci. Total Environ. 408, 3062–3069.10.1016/j.scitotenv.2010.03.039
54 Voichuk SI, Podgorskii VS, Gromozova EN. Effect of radio-frequency electromagnetic radiation on physiological features of Saccharomyces cerevisiae strain UCM Y-517. Mikrobiol Z. 2004 May-Jun;66(3):51-7.
55 Hadjiloucas S, Chahal MS, Bowen JW. Preliminary results on the non-thermal effects of 200-350 GHz radiation on the growth rate of S. cerevisiae cells in microcolonies. Phys Med Biol. 2002 Nov 7;47(21):3831-9.
Friday, August 23, 2019
Monday, August 19, 2019
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
Monday, August 12, 2019
Xenoestrogens And Cancer Connection
Xenoestrogens and cancer understanding the estrogenic effects in the body.
Xenoestrogens and other toxins that affect estrogen signaling. Estrogen signaling is not just confined to estradiol, estrone, and estriol. I want to take it deeper than the visible surface by stepping outside the estrogen that is produced within the body and look at estrogenic signaling that comes from environmental toxins.
You may know them as xenoestrogens. Xenoestrogens are compounds in our environment that have estrogenic effects in the body. The official definition is “man-made non-steroidal organic chemicals which have been released into the environment from agricultural spraying, industrial processes, urban waste or consumer products” [25].
Common, well-known xenoestrogens include polycyclic aromatic hydrocarbons (PAH), pesticides, polychlorinated biphenyl (PCB), dichloro diphenyl-trichloroethane (DDT), some drugs (e.g., antiepileptic drugs), fungicides, cotinine, phytoestrogens, mycotoxins, bisphenol A (a plastics additive), phthalates, alkylphenols [26]. Even heavy metals have been labeled as metalloestrogens due to their estrogenic activity [25]. All of these xenoestrogens mimic estrogen effect in estrogen signaling via the binding to estrogen receptors and through non-estrogen receptor pathways.
Dr. Nathan Goodyear Explains The Xenoestrogens and Cancer Link
What does the future hold for environmental toxins such as xenoestrogens? What does the future hold for our children and their children’s exposure? Look to the research. A 2004 Environmental Working Group study in collaboration with outside labs found 287 chemicals in the umbilical cord blood of 10 randomly selected births of which 180 are known carcinogens.
Toxins such as Mercury, Lead, Organochlorine pesticides (OCP), Polychlorinated biphenyls (PCB) and many others were among the identified. This Environmental Work Group study was repeated in 2009 in collaboration with 5 independent labs in the U.S., Canada, and Europe and found 232 chemicals in the umbilical cord blood of babies born from 2007-2009. The toxins identified were similar and included Mercury, methylMercury, Lead, Polychlorinated biphenyls, Phalates, Bisphenol A, and Perchlorates.
BPA – bisphenol A is a Xenoestrogen
The perfect example of a xenoestrogen is bisphenol A (BPA). Bisphenol A is a xenoestrogen commonly found in plastics and is definitely one of the more ubiquitous and well-recognized xenoestrogens. BPA, as a xenoestrogen, is a very weak estrogen receptor stimulator [27].
Many discount the impact of BPA due to its weak estrogenic activity. That would be a mistake. As weak as BPA is in potency, it is strong in its ubiquitous presence in the environment. Prolonged exposure of a low potency toxin is just as dangerous as a short exposure of a high potency toxin. One could argue that it is perhaps more dangerous due to it’s indolent, gradual accumulation and effect.
What the body does with BPA is worse than the BPA itself. Scientists are discovering that the metabolites of BPA are equally prevalent and maybe even more toxic. One such metabolite, 4-methyl-2,4-bis(4-hydroxyphenyl) pent-1-ene or MBP for short, is found to have 1,000 times the estrogenic activity of BPA alone [28] which makes up for the weak estrogenic activity of BPA.
Additionally, bisphenol A has been shown to cause a shift of the estrogen receptors from an ER-beta dominance to an ER alpha dominance by increasing the genetic encoding of ER-alpha [29] [30]. This shift to ER-alpha dominance favors inflammation and growth. All this in the low-level blood concentrations commonly found in humans. Most alarming, these low levels are found in our children and are changing our children’s response to hormones (estrogen receptors) even before they are even born [31].
25 Darbre PD. Metalloestrogens: an emerging class of inorganic xenoestrogens with potential to add to the oestrogenic burden of the human breast. J. Appl. Toxicol. 2006; 26: 191–197.
26 Fucic A, Gamulin M, Ferencic Z, et al. Environmental exposure to xenoestrogens and oestrogen related cancers: reproductive system, breast, lung, kidney, pancreas, and brain. Environ Health. 2012;11 Suppl 1(Suppl 1):S8. Published 2012 Jun 28. doi:10.1186/1476-069X-11-S1-S8.
27 Timms BG et al. Estrogenic chemicals in plastic and oral contraceptives disrupt the development of the fetal mouse prostate and urethra. Proceedings of the National Academy of Sciences. 2005.
28 Okuda, T, Takiguchi M, Yoshihara S. In vivo estrogenic potential of 4-methyl-2,4-bis(4- hydroxyphenyl)pent-1-ene, an active metabolite of bisphenol A, in uterus of ovariectomized rats. Toxicol Lett. 2010;197:7-11.
29 Monje L, Varayoud J, Luque EH, Ramos JG. Neonatal exposure to bisphenol A modifies the abundance of estrogen receptor alpha transcripts with alternative 5-untranslated regions in the femal rat preoptic area. J Endocrinol. July 1st, 2007;194:201-212.
30 Takao T et al. Exposure to the environmental estrogen bisphenol A differentially modulated estrogen receptor-alpha and beta immunoreactivity and mRNA in male mouse testis. Life Sci. Jan 24 2004;72(10):1159-69.
31 Schonfelder G, Flick B, Malsness C, Paul M, Chahoud I. In Utero Exposure to low doses of Bisphenol A lead to Long-term deleterious effects in the Vagina. Neoplasia. March 2002;4(2): 98-102.
Thursday, August 8, 2019
Three Types Of Estrogen
There are three types of estrogen that have cancer implications that must be understood while treating someone with cancer. Not all hormones are created equally and that s no more evident than in the estrogens. There are three primary estrogens that a woman or a man can make. Estradiol is the most potent estrogen Estrone is the second most potent estrogen Estriol is the weakest of the three and in a woman, dominates during pregnancy Now the complexity of these hormones is found in how they interact with the estrogen receptors. Estrone is the estrogen that has a very significant inflammatory signal. Read the entire post here for full details - https://anoasisofhealing.blogspot.com/2019/08/three-types-of-estrogen-and-cancer.html
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Three Types Of Estrogen And The Cancer Implications Explained
The three types of estrogen; estradiol, estrone, and estriol have different effects in the body especially relating to cancer.
All estrogens are not created equally. Whether it is the three types of estrogen we’ll discuss in this article or the many other types and their effects of the different estrogens in men as well as in women, there is much confusion regarding estrogens.
It would appear that the majority of people believe that there is only 1 important estrogen and for women, estrogen production stops after menopause or after a total hysterectomy.
The body never stops producing estrogens. That applies to perimenopausal and postmenopausal women. That applies to men and women.
Estrogens are produced by various tissues in the body. Most know that the ovaries are the primary production site of estrogens in cycling women.
But, did you know that the adrenal glands and fat cells produce estrogens as well. In fact, beyond menopause and in men, abdominal and visceral fat is the primary site of estrogen production.
The three types of estrogen produced in the body are:
- estradiol
- estrone
- estriol
These 3 estrogens, though similar, have very different estrogenic effects which have significant cancer implications.
Estriol (E3) is the weakest of the estrogens. Estriol dominates during pregnancy and is produced in very large amounts from the placenta during pregnancy. However, estriol production is not confined to the placenta during pregnancy.
Estriol is also produced from the liver in smaller amounts. Estriol’s activity is focused on hair, nails, skin, and the vaginal lining. Studies also suggest estriol has potential in breast cancer prevention secondary to its higher affinity for the beta estrogen receptors (ER-beta).
Estriol binds to the ER-beta in the breast to inhibit breast cell growth. Estriol has a 3:1 higher affinity for ER-beta versus ER-alpha which promotes a more anti-inflammatory signal [1] [2]. It is important to remember that the ER-beta receptor regulates the ER-alpha receptor. Thus, estriol’s affinity for ER-beta will counter any ER-alpha signaling. In contrast, estradiol and estrone will increase breast cell growth (cancer) because of their higher affinity for the alpha estrogen receptors (ER-alpha).
Estrone (E1) is the second most potent estrogen produced in the body. In women, premenopausal estrone production predominantly comes from the adrenal glands and fat.
Estrone is produced predominately from fat cells beyond menopause. Overweight and obese women and men have high circulating estrone levels. The enzyme aromatase, that converts DHEA into estrone, is upregulated in fat.
Dr. Nathan Goodyear Explains The 3 Main Types Of Estrogen
Approximately 67% of adult Americans are either overweight or obese which translates to a lot of estrone production. Regardless of age and sex, excess abdominal fat will result in an increase in estrone production. The postmenopausal increase in estrone production has been implicated in breast tumors in animal studies.
In stark contrast to estriol, estrone has a 5:1 higher affinity for ER-alpha versus ER-beta in the breast and other tissues 23 24. This ER-alpha preference will preferentially promote breast growth. Estrone increases inflammation due to its higher affinity for the ER-alpha receptors.
Estradiol is the most potent and dominant estrogen for a woman who is cycling. Estradiol is produced predominately from the ovaries and declines after menopause with the decline in ovarian function.
Estradiol is the main stimulus for the lining of the uterus during the first 2 weeks of a woman’s monthly cycle and is also involved in triggering ovulation. Estradiol has an equal affinity for ER-alpha and ER-beta alpha receptors 23 24. However, estradiol has a very high affinity for the estrogen receptors which promote breast growth and inflammation.
[1] Zhu BT, Han GZ, Shim JY, Wen Y, Jiang XR. Quantitative structure-activity relationship of various endogenous estrogen metabolites for human estrogen receptor alpha and beta subtypes: Insights into the structural determinants favoring a differential subtype binding.
Endocrinology. 2006;147(9):4132–4150.
[2] Rich RL, Hoth LR, Geoghegan KF, et al. Kinetic analysis of estrogen receptor/ligand interactions. Proc Natl Acad Sci U S A.2002;99(13):8562–8567.
23 Zhu BT, Han GZ, Shim JY, Wen Y, Jiang XR. Quantitative structure-activity relationship of various endogenous estrogen metabolites for human estrogen receptor alpha and beta subtypes: Insights into the structural determinants favoring a differential subtype binding.
Endocrinology. 2006;147(9):4132–4150.
24 Rich RL, Hoth LR, Geoghegan KF, et al. Kinetic analysis of estrogen receptor/ligand interactions. Proc Natl Acad Sci U S A.2002;99(13):8562–8567.
Tuesday, August 6, 2019
Alternative Cancer Treatments
An Oasis of Healing is a center for advanced integrative medicine who treats the whole body and not just the symptoms of cancer. We administer alternative cancer treatments using intravenous treatments and adjunct therapies that target cancer and boost and strengthen the immune system doing no harm to the human body. We use a holistic approach to helping people heal from cancer. Our cancer care program challenges it at a metabolic level where it is unable to respond to and where normal cells are unaffected. Give our healing center a call today and learn more about how we can help you or a loved one dealing with cancer. An Oasis of Healing 210 N Center St #102 Mesa, AZ 85201 480-834-5414 https://anoasisofhealing.business.site
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Tuesday, July 23, 2019
Hodgkin’s Lymphoma Alternative Treatment Leads To Full Recovery
Eric’s Hodgkin’s Lymphoma alternative treatment is a truly wonderful story of complete health restoration.
Eric R. was kind enough to share his Hodgkin’s Lymphoma alternative treatment triumph as a result of our comprehensive cancer care program at An Oasis of Healing. Watch the video below in its entirety to hear his story of how he was able to recover his health from the direst of circumstances!
We wanted to share a little of what Eric spoke about in his testimonial video below. We invite you to view the entire video as it is truly inspiring. It could help you or a loved one who may be dealing with cancer.
Eric and his wife Kristy travel across the US in an RV. Eric shared that he had been a healthy person up until his diagnosis of Hodgkin’s Lymphoma. He was having a constant cough that wouldn’t go away and decided to go to Urgent Care and check it out.
Urgent Care told him to get to an Emergency Center immediately. The reason for this was his blood count was extremely low at a 5.1. For men, an average blood count is 13. Following these tests, Eric was admitted to a hospital spending a week there.
The hospital ran tests and they showed that Eric had Hodgkin’s Lymphoma. He and his wife were shocked. Eric did not have the best experience while in the hospital. At that time they happened to be in Tucson, AZ, and Kristy while searching on the internet found An Oasis of Healing located in Mesa, AZ.
They got on the phone and made an appointment to meet Dr. Goodyear at An Oasis of Healing. Eric and Kristy meet some staff members and took a tour of our healing center. He said the center’s environment was amazing as soon as they walked in and completely different than the hospital and laying in bed all day.
Alternative Treatment For Hodgkin’s Lymphoma Helped Provide Eric R. With A Full Recovery As Told In This Video
Eric stated that he was treated like family at Oasis. He said the biggest blessing for him was when he met other patients going through the same types of challenges for their own situation. We all worked together having a common goal; helping and supporting one and other.
Eric suggests for those who are dealing with cancer or have a loved one dealing with it to come and visit An Oasis of Healing, meet Dr. Goodyear and staff and see firsthand for yourself why this place is like never you have ever seen before.
Dr. Nathan Goodyear, unfortunately, had to admit Eric to a hospital as a result of his kidney function. He had to spend six weeks there and another three weeks doing the rehabilitation. The hospital Eric was staying in told him that he would not get his kidney function back and it was probable that he wasn’t going to survive.
When the hospital released Eric, he met with Dr. Goodyear again and was afraid he would not take him back into the center for treatment of his Hodgkin’s Lymphoma as a result of his dire condition. Dr. Goodyear and An Oasis of Healing welcomed him back and immediately began a unique program developed specifically for him.
“Everyone at An Oasis of Healing is treated for their individual circumstances and I’m a great example of that”, said Eric. The program Dr. Goodyear had me on worked incredibly well and I got my kidney’s back! This enabled me to get off the dialysis machine sometime thereafter.
The doctor at the hospital treating Eric on the dialysis machine said that for people in his same condition receiving treatment for only three months would never come off it. Eric was not going to be one of them and got off dialysis from the Hodgkin’s Lymphoma alternative treatment and integrated therapies under the care of Dr. Goodyear and An Oasis of Healing.
Eric ended by saying, “He got his life back”. He was given his final Pet Scan and it showed no evidence of any disease! Seven months after his diagnosis in December of 2018 there was no longer any evidence of disease.
Treatment For Hodgkin s Lymphoma
Eric R. recently shared how his treatment for Hodgkin s Lymphoma was a success while at An Oasis of Healing. Hearing his personal story of recovery was both emotional and inspiring! The tests came back that showed Eric he had Hodgkin s Lymphoma in December 2018. It was a shock to him and his wife. He was not having the best experience in the Hospital. As fate would have it, they were in Tucson, Az at the time and found An Oasis of Healing in Mesa, AZ. Eric said, you are treated like family here . He continued that the biggest blessing he received was meeting the other patients who were going through the same types of situations. Everyone works together with a common goal to help and support each other. Everyone here at this amazing center is treated individually and as a result of Dr. Goodyear s program, we got my kidney s back. I was able to get off of having dialysis after a certain number of weeks and had my port removed. Eric stated, he got his life back . He received his final Pet Scan and there is no evidence no disease! Eric was diagnosed in December of 2018 and seven months later there is no evidence of any disease. An Oasis of Healing 210 N Center St #102 Mesa, AZ 85201 480-834-5414 https://anoasisofhealing.business.site
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Monday, July 22, 2019
Saturday, July 20, 2019
Monday, July 15, 2019
Estrogen Receptors And Cancer
When we get into the estrogen receptors and cancer, the complexity evident in hormones really increases.
The discussion of estrogen has to begin with the estrogen receptors because the estrogen receptors are critical in determining the signal that is transmitted from the different estrogens. Estrogen receptors and cancer is a complex subject that needs to be broken down and explained so a thorough understanding can be attained.
For the men in the audience, I can hear their collective: “I could have told you that…” But, for the women in the audience, at least it takes 2 because in men it only takes 1 hormone receptor to drive the show. The majority of the current research around estrogen receptors is in breast and prostate cancer. However, estrogen receptors are ubiquitous in the body and play a significant role in normal physiology [1].
The current understanding is that there are 2 estrogen receptors: estrogen receptor alpha (ER-alpha) and estrogen receptor beta (ER-beta). These two different estrogen receptor types appear to have some specific tissue-specific expression [2] and can produce profoundly different results when stimulated. As it relates to a wide variety of diseases, including cancer, ER-alpha has been shown to produce a pro-inflammatory [3] and pro-growth [4] signal from estrogen stimulation.
Inflammation is a prerequisite for cancer initiation and pro-growth signaling will favor cancer growth and progression.
After all, cancer is synonymous with unregulated growth. The often-mentioned ER+ in some cancer types is, in fact, a reference to ER-alpha. One cannot say all ER-alpha expression is associated with cancer, but the scientific literature does point to an increased cancer risk with increased ER-alpha expression and signaling.
ER-alpha expression and stimulation has been shown to play roles in breast cancer [5] and prostate cancer [6] to name a few. In fact, the loss of ER-beta expression and increase in ER-alpha expression has been shown to play a significant role in the initiation, growth, and invasion of prostate cancer [7], breast cancer [8], ovarian cancer and colorectal cancer [9]. Kind of important!
In contrast to ER-alpha, ER-beta has been shown to produce an anti-inflammatory [10] and anti-growth [11] signal from estrogen stimulation. ER-beta stimulation has even been shown to benefit asthma [12] and the excitotoxic diseases [13] MS, Parkinson’s disease, Alzheimer’s, and ALS. It doesn’t take a rocket scientist to see the potential positive impact on many diseases, including cancer, through ER-beta stimulated inflammation reduction and growth restriction to increase healthy and disease-free living potential.
Does ER-alpha always produce a pro-inflammatory signal? Does ER-beta always produce an anti-growth response? Are these receptors tissue specific? Can the expression of ER-alpha and ER-beta change? These are some of the questions that have yet to be answered by current science.
Similar to genetic expression and hormone expression, estrogen receptor expression can change. Maybe this can explain some of the variations in hormone response between individuals?
Or maybe this can explain the response difference and cancer risk in women to Hormone Replacement Therapy (HRT) in the years of pre-menopause, perimenopause and those that are post-menopause. The perfect example of the changes that can occur in ER expression and their effects on cancer risk can actually be found in men.
Estrogen receptors are an equal opportunity offender and in the case of men with low testosterone, there is a shift from ER-beta dominance to ER-alpha dominance in the prostate [14]. Remember, ER-alpha produces a pro-inflammatory and a pro-growth signal. In addition, inflammation up-regulates aromatase activity which increases testosterone to estrogen production to further increase estrogen production and stimulation of ER-alpha. What a vicious cycle!
The simple and linear thinking is that estrogen equals cancer in women and testosterone equals cancer in men.
No linear thinking here. The slogan is to keep it simple stupid. The problem is that ignorance of the complex for the purpose of the simple is more than stupid, it is dangerous. Accepting the complex as complex makes it simple. Moving on.
Keeping the focus on estrogen receptors in male cancer, the loss of ER-beta expression in the prostate has been shown to increase prostate cancer. In a recent study in mice, loss of ER-beta expression was found to increase abnormal prostate cell growth [15].
Another study in mice, found ER-beta stimulation lead to a decrease in prostate size and triggered programmed cell death through a process called apoptosis [16]. Apoptosis is a critical cancer control mechanism that is often lost early in cancer development.
However, we are talking about humans here. In human studies, ER-beta expression has been shown to reduce the incidence of prostate cancer [17] [18]. Looks pretty promising that ER-beta expression in the male prostate is protective against prostate cancer and prostate disease.
Dr. Nathan Goodyear Explains The Complexity of Estrogen Receptors and Cancer in This Video
Just to stir things up a little more and to show the insane yet beautiful complexity that really exists in hormone receptors, I present Estrogen-Related Receptors (ERR). Estrogen-Related Receptors exist in 3 forms: alpha, beta, and gamma [19].
These receptors are nuclear receptors just like the regular estrogen receptors. These ERR have significant similarity to estrogen receptors however, they do not respond to estrogen as do estrogen receptors [20] [21].
The exact specific substances that bind and stimulate the ERR are yet to be determined. This is a common theme in science: the body is beautifully and wonderfully made, yet we only know a fraction of it.
The implication of estrogen receptors and cancer is that it is not the hormone levels alone that poise the sole cancer risk for the individual as it is so often misunderstood and presented. It is the combination of the type of hormone present and its interaction with the type of estrogen receptors present plays a significant part in what signal the estrogen transmits: pro-inflammatory and pro-carcinogenic or not pro-inflammatory and not pro-carcinogenic.
[1] Tiwari-Woodruff S, Morales LB, Lee R, Voskuhl RR. Differential neuroprotective and anti-inflammatory effects of estrogen receptor (ER)alpha and ERbeta ligand treatment. Proc Natl Acad Sci U S A. Sep 11 2007;104(37):14813-8.
[2] Mueller SO, Korach KS. Estrogen receptors and endocrine diseases: lessons from estrogen receptor knockout mice. Curr Opin Pharmacol. 2001 Dec;1(6):613-9.
[3] Vegeto E, Cuzzocrea S, Crisafulli C, et al. Estrogen receptor-alpha as a drug target candidate for preventing lung inflammation. Endocrinology. 2009;151(1):174–184. doi:10.1210/en.2009-0876.
[4] Stephanie J Ellison-Zelski and Elaine T Alarid. Maximum growth and survival of estrogen receptor-alpha positive breast cancer cells requires the Sin3A transcriptional repressor. Molecular Cancer20109:263. Https://doi.org/10.1186/1476-4598-9-263.
[5] Ali S and Coombes RC. Estrogen receptor alpha in human breast cancer: occurrence and significance. J Mammary Gland Biol Neoplasia. 2000 Jul;5(3):271-81.
[6] William A. Ricke, Stephen J. McPherson, Joseph J. Bianco, Gerald R. Cunha, Yuzhuo Wang, and Gail P. Risbridger. Prostatic hormonal carcinogenesis is mediated by in situ estrogen production and estrogen receptor alpha signaling.The FASEB Journal 2008 22:5, 1512-1520.
[7] Weihua Z, Makela S, Andersson LC, et al. A role for estrogen receptor beta in the regulation of growth of the ventral prostate. Proc Natl Acad Sci U S A. 2001;98(11):6330–6335. doi:10.1073/pnas.111150898.
[8] Lazennec G, Bresson D, Lucas A, Chauveau C, Vignon F. ER beta inhibits proliferation and invasion of breast cancer cells. Endocrinology. 2001;142(9):4120–4130. doi:10.1210/endo.142.9.8395.
[9] Bardin A, Boulle N, Lazennec G, Vignon F, Pujol P. Loss of ERb expression as a common step in estrogen-dependent tumor progression. Endocrine-Related Cancer (2004) 11 537–551.
[10] Matthew C. Catley, Mark A. Birrell, Elizabeth L. Hardaker, Jorge de Alba, Stuart Farrow, Saleem Haj-Yahia and Maria G. Belvisi. Journal of Pharmacology and Experimental Therapeutics July 2008, 326 (1) 83-88; DOI: https://doi.org/10.1124/jpet.108.136275.
[11] Zhang J, Tu Y and Smith-Schneider S. Activation of p53, inhibition of telomerase activity and induction of estrogen receptor beta are associated with the anti-growth effects of combination of ovarian hormones and retinoids in immortalized human mammary epithelial cells. Cancer Cell Int. 2005 Mar 8;5(1):6.
[12] Matthew C. Catley, Mark A. Birrell, Elizabeth L. Hardaker, Jorge de Alba, Stuart Farrow, Saleem Haj-Yahia and Maria G. Belvisi. Estrogen Receptor β: Expression Profile and Possible Anti-Inflammatory Role in Disease. Journal of Pharmacology and Experimental Therapeutics July 2008, 326 (1) 83-88; DOI: https://doi.org/10.1124/jpet.108.136275.
[13] Tiwari-Woodruff S, Morales LB, Lee R, Voskuhl RR. Differential neuroprotective and antiinflammatory effects of estrogen receptor (ER)alpha and ERbeta ligand treatment. Proc Natl Acad Sci U S A. 2007;104(37):14813–14818. doi:10.1073/pnas.0703783104.
[14] Cohen PG. Obesity in men: the hypogonadal-estrogen receptor relationship and its effect on glucose homeostasis. Med Hypotheses. 2008;70(2):358-60.
[15] Imamov O et al. Estrogen receptor beta regulates epithelial cellular differentiation in the mouse ventral prostate. Proc Natl Acad Sci U S A. 2004;101:9375-9380.
[16] Krishnana G et al. Novel ER beta selective agonists induce prostate atrophy in rodents without affecting the hypothalamo-pituitary-gonadal axis. In the Endocrine Society Annual Meeting 2004. 2004. The Endocrine Society Press. Chase, Maryland, USA. 180-181.
[17] Leav I et al. Comparative studies of the estrogen receptors beta and alpha and the androgen receptor in normal human prostate glands, dysplasia, and in primary and metastatic carcinoma. Am J Pathol. 2001;159:79-92.
[18] Horvath LG et al. Frequent loss of estrogen receptor-beta expression in prostate cancer. Cancer Res. 2001;61:5331-5335.
[19] Coward P, Lee D, Hull MV, Lehmann JM. 4-Hydroxytamoxifen binds to and deactivates the estrogen-related receptor gamma. Proc Natl Acad Sci U S A. July 17 2001;98(15):8880-8884.
[20] Heard DJ, Norby PL, Holloway J, Vissing H. Human ERRgamma, a third member of the estrogen receptor-related receptor (ERR) subfamily of orphan nuclear receptors: tissue-specific isoforms are expressed during development and in the audit. Mol Endocrinol. Mar 2000;14(3): 382-92.
[21] Vanacker JM. Pettersson K, Gustafsson JA, Laudet V. Transcriptional targets shared by estrogen receptor-related receptors (ERRs) and estrogen receptor (ER) alpha, but not by ER beta. EMBO J. Aug 2 1999;18(15):4270-4279.
Monday, July 8, 2019
Hormonal Regulation Of Metabolism
How the body processes hormones is called hormone metabolism.
Metabolism is presented as simply the means to gain or lose weight. Metabolism goes far beyond this simple definition. Metabolism is the mass production of day to day cellular processes that help the cell survive and thrive or not.
In reality, metabolism is a measure of optimal cellular and thus body homeostasis. Thus, metabolism can correctly be defined and applied to all cellular and body functions that result in day to day cellular homeostasis.
Hormone metabolites are just as important as the individual hormone levels and the hormone balance themselves. In fact, it may be more important as they reflect the flow, the trend of hormone movement which is so important in the assessment of function. We need to look at function, not static values. The body functions. The body is by no means static.
Hormone metabolites are just as they sound—the breakdown products that are the result of hormone metabolism. Whether hormones are endogenously made by the body or whether they are exogenously administered through hormone therapy, hormone metabolism manages the breakdown of these hormones to help the body survive, thrive or not.
The error is to think that hormone metabolites are merely waste products without any activity or physiologic significance. This has been the long-held thought. The truth is that hormone metabolites are very much active in hormone signaling.
In fact, hormone metabolites provide much of the risk and side effects equated to hormones and hormone therapy in cancer that is often overlooked. Not all hormone metabolites are bad. Some of these hormone metabolites can also provide significant protection.
Hormone Receptors
Hormone receptors are just what the words imply. They are the receptors that the individual hormones bind too. Once the hormones bind to the respective receptors, the signal of the hormone is then internalized inside the cell through a series of secondary messengers.
Hormone receptors are the doorway to the cell. Most of these signals then interact with DNA to turn genes off and/or on. There are, however, non-DNA and non-hormone receptor signaling that occurs as well.
Again, simple need not apply. As important as hormone receptors are to the signal transmission of hormones to the cell, they are impossible to assess except in the case of physical tissue specimens in biopsies.
Hormonal Regulation of Metabolism And Outside Influences
We are all products of our genetics (DNA) and our environment. The DNA that we have inherited from our parents is hard-wired. In contrast, the expression of DNA is not hard-wired but is in fact quite fluid.
The lifestyle choices we make and/or the environment we expose our DNA to influences the very expression of our DNA. Let this settle in for a moment. Though our DNA is fixed, we have the ability to determine whether genes are turned on or genes are turned off.
These effects can be good, or they can be bad. This is called the study of epigenetics or the study of things “above genetics”. Above genetics includes things i.e. diet, stress, sleep… that are above genetics, yet influence the expression of genetics. For example, studies have shown that our diet can affect our genetic expression to increase or decrease cancer risk [1]. Sorry, when your mom told you to eat your broccoli, she knew something that researchers are just now discovering. Broccoli anyone?
The same “environment” that can influence genetics can also influence the expression of hormones. One might call it the study of epihormones or “above hormones” if such a study actually existed. Based on the current dogma and outcomes of conventional medicine in hormones and cancer, it clearly should exist.
Physiologic Hormone Therapy When Treatment Is Required
The classic approach to most things these days is that more is better: super-size that drink, supersize those fries… Unfortunately, the same super-size logic applies to medicine today. This is no more apparent than in hormones. Just look at how conventional medicine handles low hormones: More is good, and a lot is even better.
The conventional approach to hormones is the same approach to chemotherapy: more is better; when the ole testosterone levels in men or estrogen levels in women are running on empty, you just stop off at your local doc station to filler up with more testosterone or estrogen.
The overdosing of these hormones is evident in the testing of these patients as well as the complications of these dosing strategies. If testosterone therapy causes cancer or thickens the blood (polycythemia) or causes aggressiveness/rage/anger issues, then why doesn’t endogenous testosterone production cause the same at age 24 when peak testosterone production occurs in men?
The point is that is doesn’t. These symptoms are simply the result of overdosing. If testosterone doesn’t cause these symptoms at the peak age of production of 24, then it shouldn’t with optimal physiologic dosing.
It only does with overdosing. The exact same can be said of estrogen and breast cancer. If testosterone caused prostate cancer and if estrogen caused breast cancer, then every young man and every young woman would have breast cancer.
They clearly don’t. The more is better philosophy, or the super-size logic need not apply to hormone therapy. That is if your goal is health and healing.
[1] Liu YC, Chen WL, Kung WH, Huang HD. Plant miRNAs found in the human circulating system provide evidence of cross-kingdom RNAi. BMC Genomics. 2017;18(Suppl 2):112. Published 2017 Mar 14. doi:10.1186/s12864-017-3502-3.
Tuesday, July 2, 2019
Monday, July 1, 2019
Hormonal Imbalance And Cancer
We are going to explore hormonal imbalance and cancer and why the body must be in homeostasis.
It only takes a pill. It just needs to be cut out. It is all about Estrogen. It is all about Testosterone. Disease is the normal outcome of life built into our genetic code without the means for change… Simple isn’t it.
When it comes to conventional medicine, when it comes to the conventional medicine marketing mantra, simple is the modus operandi. Simple would be nice. Simple, would be… well, simple. If only simple existed.
No matter how much we may want, the body just does not work on simple. The perfect example of this simple modus operandi can be found in the relationship between hormones and cancer.
Simple would have you believe men are nothing more than testosterone-fueled erections and women are simply estrogen-fueled hot flashes. Just look at the conventional medical marketing mantra: testosterone causes prostate cancer and estrogen causes breast cancer.
If a man is diagnosed with prostate cancer or a woman with breast cancer, testosterone or estrogen is the culprit and these hormones must be eliminated. It is almost a modern-day Wizard of Oz Lions and Tigers and Bears oh my… fear mongering.
Though our bodies may seem simple enough, they really are a beautiful, complex biochemical machine maintaining an intricate, delicate, balance designed for healing potential. Thank goodness for that complexity! Though advocated as simple, the body is anything but simple.
Dr. Nathan Goodyear Discusses Hormonal Imbalance And Cancer Goes In-Depth On The Important Subject Of Homeostasis
If it is not simple, then the opposite is true: complexity rules the day. Hormones, especially in reference to cancer, are a perfect example of this complexity. Hormones are just one piece of a very complex puzzle when it comes to hormones and cancer. For scientific, safe and effective hormone knowledge and therapy in patients with cancer it takes all the following:
- Re-evaluate definition of normal
- proper hormone evaluation
- knowledge of hormone levels
- hormone balance
- hormone metabolites
- hormone receptors
- outside influences
- physiologic hormone therapy
Re-evaluate Normal
The first question that often comes up in the discussion of hormones is are they normal. But what is normal after all? Who is normal? That discussion could go on for days.
Normal is defined as what falls within the statistical reference range of normal. Normal is then determined as a percentage of the population as a whole. This is why the definition of normal can change based on a shift in the population as a whole.
As the population becomes more abnormal, then a shift occurs as normal is re-defined. What was once abnormal is now normal and what is now normal is abnormal. Statistically speaking, the top 2.5% and the bottom 2.5% are determined to be statistically abnormal and all other 95% are deemed normal.
If I used that logic with my kids, a 65 on a test at school would be considered statistically normal right? From my perspective and my child’s, a 65 would not be considered normal. A 65 clearly falls far closer to failing than succeeding, yet it is statistically normal.
This highlights the limitations of this simple definition of normal when discussing anything, but especially hormone levels in people with cancer. This approach may work for disease medicine (though I highly doubt it), but it is not the best for the pursuit of healing from cancer.
Proper Hormone Testing And Evaluation
In the past, hormone evaluation was limited to blood. Today, hormone evaluations can come in all shapes and sizes: from blood to saliva, to urine. Even blood spot and urine spot hormone evaluation are available today.
People like my good friend, Dr. Zava, have pioneered these new hormone evaluation techniques. When it comes to different methods to evaluate hormones, no method is better than another, but it is all about perspective.
Each hormone evaluation is a different perspective or different window into the room of hormone physiology. No one window is better than the other, but each provides a different window with a different perspective.
The different windows provide different clinical perspectives that help to provide a more complete evaluation of hormone physiology of the individual. It also provides a more complete hormone treatment regimen for the specific environment of the individual with cancer.
The question simply becomes what perspective or what window provides the most useful information for the clinical question at hand. Is a single image good enough, or is a panoramic view better?
For me, I like the complete hormone panoramic view. In the treatment and healing of cancer, no questions should be left unanswered; or in this perspective, in viewed.
Hormone Levels
What is your number? The conventional medicine marketing mantra is full of this. Just look at the Testosterone marketing for men. What is your number is a common marketing cry for low Testosterone clinics around the country?
For this reason, I call testosterone clinics the 21st-century version of the methadone clinic. Contrary to most thought today, hormones are not just about the individual numbers.
Hormones are a means of communication throughout the body; a language if you will. I am always amazed at the answers I get when I ask post-menopausal women if they still make hormones or men older than 65 if they make testosterone.
Most will say no. Because of what they are exposed to in marketing, I am not surprised by their responses. Of course, the answer to both questions is yes.
The body must have these hormones to communicate, to live and to survive. Even after menopause, women need some estrogen.
It can be about the numbers if the numbers are exceedingly low or exceedingly high. However, that is a rare finding and usually occurs as a result of hormone therapy. Hormone impacts on individuals with cancer are rarely about the levels, but more about the balance.
Hormone Balance
Hormones must exist in balance. Balance is the source of health and wellness. Just look at the body for the importance of balance.
The human body is created in balance: 2 eyes, 2 ears, 2 legs…Just trying to lose a leg and see how the rest of your body is affected by the imbalance. Bumps, bruises, and even worse are definitely in the future.
The loss of balance is often the precipitating cause of symptoms short term and contribution to disease risk in the long-term. The most well-publicized hormone imbalance is that of the Estrogens and Progesterone in women. However, the imbalances of hormones are widespread in the body and have a significant impact on cancer risk and cancer healing.
Imbalances are not just isolated to hormones, but also apply to neurotransmitters and the immune system. The body must exist in balance.
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