Treating estrogen responsive cancer naturally
Comments
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I have a basic question: Do you moniter your estrogen levels while using alternative methods? If so, how often and what have your experiences been? Thank you! Tammy
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@comingtoterms, I've been wondering about that too, and whether alternative therapies can allow the dose of standard hormone treatments to be reduced, which (hopefully) would reduce the severity of any side effects. But I don't even know whether MOs using standard hormone treatments typically track the estrogen level to adjust dose to the minimum amount that will produce the needed effect on estrogen levels, or if the dose is set by some other means. Is it even known how much the estrogen level has to be reduced in order to prevent recurrence/spread? Does anyone know of any studies along those lines?
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When I was doing progesterone I had the estrogen levels checked every 3 months. They were always <30. Or maybe it was <10. I can't remember. Pretty sure it was 30 though.</p>
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Why did my signature do that?
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I had my estrogen levels checked mid chemo and they indicated I was through menopause, however, I can testify that is not the case. I am still menstruating! Because of this, I am a bit leary about depending on the results of hormone testing. They change. However, if you cannot keep track, then how can you know how well Tamoxifen is working or how well alternative therapies work? No Tamoxifen for this gal! Thanks, Tammy
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Curveball: Hm---I am wondering that too - I have a feeling the medical community doesn't know the answer. Because if they did we would not all be getting the same dosage. My onc didn't even mention estrogen levels, let alone checking them periodically. I also read that the levels vary throughout the day. If that is the case, what good is testing?
Wouldn't it be nice if there was a way to monitor so that if the level was high for instance, we could go off the AI for a while or vice vers
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I am surprised that there is not more discussion about the fact that the big Women's Health Initiative study, which was what disclosed the supposedly irrefutable link between estrogen and BC, did not really show that link at all. It now appears that a greater culprit in many bcs may be progestin and not estrogen.
See this New York Times article about the study:
http://www.nytimes.com/2010/12/14/health/research/14hormone.html?_r=1
Excerpt:
"In 2002, researchers halted a major government study of so-called combination therapy, part of the Women's Health Initiative, when women taking these hormones were shown to have a higher risk of breast cancer, heart attack and stroke.
"....Frightened women abandoned hormones in droves. But now a controversial new review of data suggests some good news: certain women who take estrogen alone, without progestin, to treat menopause symptoms may actually be protected from breast cancer.
"The review, released last week during a poster session at the San Antonio Breast Cancer Symposium, drew immediate criticism from researchers who said it was merely a rehash of old data. But the oncologist behind the report, Dr. Joseph Ragaz, a clinical professor at the University of British Columbia, said the evidence that estrogen can protect against breast cancer had been largely ignored, and that it was time to shine a spotlight on the findings.
"The data were absolutely missed. They weren't emphasized, and they weren't brought to the attention of oncologists," said Dr. Ragaz, who said he had no ties to any drug firms. "These data are nevertheless very much important because they add to the evidence for estrogen being protective."
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Fear really is our worst enemy. Without it, the cancer research and patient world wouldn't be so apt to jump hysterically to conclusions before the evidence is out, and the Women's Health Initiative study would neither have been stopped before completion, nor would the masses have jumped to wrong assumptions.
Why is careful science so often missing from breast cancer? It makes me angry every time. I suppose that is how we come to have a disease, in 2012, that kills 1/4 of those who are diagnosed with it. The sadder part (sadder because it will lead to even more deaths) is that despite this dismal landscape an army of patients, doctors and researchers continues to parrot the mantra of "rah, rah, rah, treatment is great, it works, the SEs are microscopic and rare, and we've made so much progress." None of those expressed sentiments are true, and a big part of me wants to ask for a vomit bag when I hear that.
This article reports on findings that some women (some - not all) may actually benefit from estrogen to protect against BC:
http://www.nytimes.com/2010/12/14/health/research/14hormone.html?pagewanted=print
Excerpt:
"In a finding that challenges the conventional wisdom about the risks of some hormones used in menopause, a major government study has found that years after using estrogen-only therapy, certain women had a markedly reduced risk of breast cancer and heart attack.
The research, part of the landmark Women's Health Initiative study, is likely to surprise women and their doctors, who for years have heard frightening news about the risks of hormone therapy. But most of those fears are related to the use of a combination of two hormones, estrogen and progestin, which are prescribed to relieve hot flashes and other symptoms of menopause, and have been shown to increase a woman's risk of breast cancer."
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And yet most of us have doctors repeating the same mantra of "estrogen is bad for bc."
I can only guess it's because both patients and doctors want to feel they are doing something. They desperately need to feel they can make a difference and that treatment works. There is no big pharma conspiracy to keep a cure secret - there is a societal permission for women to use fear as an excuse for bad behavior and lack of judgement. Both sexes play on that habit, and it's got to stop. I'm not surprised that Act Up was successful in really transforming AIDS policy and the AIDS landscape. It was led by men who, whatever their faults, used the Molotov cocktail approach over the hairspray-addled, smiling, obliging Nancy Brinker approach.
Look where AIDS is, and look where BC is....and to think that AIDS has only been a kinown epidemic since the 80s.
I know I can't survive on a community's psychological need. I can only survive on the science. And what it tells me is that I have no convincing evidence that either a conventional method (Tamox) or an alternative method of controlling estrogen are going to help me regarding bc.
Having a quiet day at home, with time to rant. Thank you for listening!
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Hi Athena,
Your post brings-up a couple issues:
1. I think the disputed studies you reference were with regard HRT (hormone replacement therapy) and breast cancer (?) I won't go into this ... but the below video I can't recommend enough as explaining how to test estrogen levels in a lab and the complex interplay between estrogen and other chemicals in the body. She is talking about testing which is more detailed than what mainstream / corporate doctors normally do. She emphaizes the FULL picture of hormones - not just estrogen.
http://www.youtube.com/watch?v=HSOPTO6cwxg&feature=channel&list=UL
http://www.youtube.com/watch?v=hw4inaJEISgHaven't read it all ... but the book What your Doctor may not tell you about Breast Cancer looks promising (although it doesn't seem to address progesterone positive cancers?).
These doctors do NOT demonize estrogen but focus on the complex relationship of ALL hormones - not just the simplistic "estrogen = bad" model. http://www.amazon.com/What-Doctor-About-Breast-Cancer/dp/044652686XYour rant? I agree! My philosophy is the estrogen is NOT the enemy - cancer is. My personal research indicates that making sure the body can metabolize and excrete estrogen correctly is the correct treatment. I LIKE my estrogen and don't want to kill it. I just want to make sure it leaves my body like its supposed to when I'm done with it.
The shoddy science in breast cancer research? All I can say is that breasts are considered "expendable" and "rebuildable" so surgeons amputate them rather than use advanced modern surgical techniques to save them. As for why the mainstream seems to want every woman in USA on a 5 year programme of Tamox or similar corporate drug ... you can read my rant here if you care to. I will stop now as I don't want to go off topic.
http://breastcancercult.wordpress.com/2012/08/18/polio-vs-breast-cancer/0 -
NatKat - I find this especially interesting. My Estrogen response was 90-100% positive , but my progesterone (sp?) response was only 10-15% positive. If it's not estrogen driven, than the dire warnings of my recurrence rate should be looked at in a whole different light rather than "proof" of my need for Rx drugs. A wise PA once told me when I mentioned that my doctor wanted to do surgery on my shoulder that well, when you're a hammer, everything looks like a nail. We all have breast cancer so we must all need the same treatment. The study wasn't taken seriously because the doc wasn't financed by big pharma.They are looking out for their wallet not our health.
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Hi - happened on this thread, I have been looking for people to talk this through with after making a decision to begin my natural progesterone cream again. Here are the studies and will post the others in next one. I had this on bioidentical hormone thread but no one there. Have a multitude of threads open for Bcl-2 gene an natural progesterone info.
So.... posting a bomb here on most current thread of them all.
February, I was told by my integrative MD not to use my natural progesterone cream, which I had stopped using when I found the mass, then used a few wks then stopped again for good, then surgery and history.... But all my kinesiology and bioenergetic testing, including his, point to me using the bioidentical natural progesterone cream, vaginally (in this way, doctors are now saying that the body utilizes it more like if it were presented by ovaries, Mercola comes to mind but there are many more who say Dr. Lee would update his recommendations to this course verses on the skin and breasts, wish I had time and energy to find this for you.....) so I am doing research today after finding in the book Outsmart Your Cancer the following paragraph...... Had not thought more about it until finding this statement in book and now deciding to use the natural progesterone cream or not. Studies below also brings to light that there are indeed studies in Europe and worldwide on natural progesterone.
"It is extremely unfortunate that the medical community has resorted to using .... studies such as those mentioned above to warn women against any use of hormones - even bioidentical ones. In fact, the misunderstanding has gone so far as to terrify women if their breast cancerr cells are not only estrogen receptor positive, but also progesterone receptor positive. Once again, conventional medicine has now adopted the erroneous idea that natural progesterone is bad, when the studies that have been scaring them have only been done on non-bioidentical progestins. Given that natural progesterone promotes apotosis and down-regulates the Bcl-2 gene, it would appear to be a good thing if a woman's cancer cells are progesterone positive."
Yes, I was almost blaming my natural progesterone cream that I had used off and on for about two years. but perhaps it was keeping the cancer under control? Then I stopped and whammo? I don't know about then, but now I need to make decisions. I do know that during timee I was dealing with mass prior to surgery, there was a period when the mass became smaller, larger, smaller, larger and I decided to just get it oout but no mx like the surgeon wanted for me.
I am open for input, certainly, please share. Thank you.
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I found this post on another thread too, very informative studies and details. Just moving facts here, but a huge thank you to the woman who posted it who was helping her mom. Link, edited to add community.breastcancer.org/forum/79/topic/696430?page=1#post_787148
now a skunk is rubbing her little face on my toes bcz she wants breakfast, : ) better go.
Research
Campagnoli C, Abba C, Ambroggio S, Peris C. Pregnancy, progesterone and progestins in relation to breast cancer risk. J Steroid Biochem Mol Biol 2005; 97(5):441-50.
The authors review recent findings that show that the production of progesterone during pregnancy and the use of bioidentical progesterone in hormone therapy do not increase breast cancer risk, and can even protect against the development of breast cancer.
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Kaaks R, Berrino F, Key T, Rinaldi S, Dossus L, Biessy C, Secreto G, Amiano P, Bingham S, Boeing H, Bueno de Mesquita HB, Chang-Claude J, Clavel-Chapelon F, Fournier A, van Gils CH, Gonzalez CA, Barricarte Gurrea A, Critselis E, Khaw KT, Krogh V, Lahmann PH, Nagel G, Olsen A, Onland-Moret NC, Overvad K, Palli D, Panico S, Peeters P, Quirós JR, Roddam A, Thiebaut A, Tjønneland A, Chirlaque MD, Trichopoulou A, Trichopoulos D, Tumino R, Vineis P, Norat T, Ferrari P, Slimani N, Riboli E. Serum sex steroids in premenopausal women and breast cancer risk within the European Prospective Investigation into Cancer and Nutrition (EPIC). J Natl Cancer Inst 2005; 97:755-65.
In this large multicenter study, higher serum progesterone levels were associated with a significant reduction in breast cancer risk.
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Fournier A, Berrino F, Riboli E, Avenel V, Clavel-Chapelon F. Breast cancer risk in relation to different types of hormone replacement therapy in the E3N-EPIC cohort. Int J Cancer 2005; 114(3):448-54.
Combined HRT with estrogen (either oral or transdermal) and synthetic progestins was found to carry a significantly increased risk of breast cancer compared with estrogens plus oral micronized progesterone. In fact, no increase in breast cancer risk was seen in the estrogen plus oral micronized progesterone group compared with estrogen alone. This large multicenter study therefore suggests that there is a dramatic difference between the effects of bioidentical progesterone versus synthetic progestins on breast cancer risk.
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Missmer SA, Eliassen AH, Barbieri RL, Hankinson SE. Endogenous estrogen, androgen, and progesterone concentrations and breast cancer risk among postmenopausal women. J Natl Cancer Inst 2004; 96(24):1856-65.
Blood progesterone levels were found not to be related to breast cancer risk in this first study to investigate this in postmenopausal women. The occurrence of progesterone receptor positive tumors was the tumor type most strongly affected by all the circulating steroid hormones measured except for progesterone. Higher levels of endogenous estrogens and androgens were significantly correlated with increasing breast cancer incidence. This suggests that circulating natural progesterone does not increase breast cancer risk.
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Malet C, Spritzer P, Guillaumin D, Kuttenn F. Progesterone effect on cell growth, ultrastructural aspect and estradiol receptors of normal human breast epithelial (HBE) cells in culture. J Ster Biochem Mol Biol 2002; 73: 171-181.
In a culture system, progesterone was found to have an inhibitory effect on breast cell growth. When given following estradiol (E2), it limited the stimulatory effect of E2 on cell growth.
---------Desreux J, Kebers F, Noel A, Francart D, Van Cauwenberge H, Heinen V, Thomas JL, Bernard AM, Paris J, Delansorne R, Foidart JM. Progesterone receptor activation- an alternative to SERMs in breast cancer. Eur J Cancer 2000 Sep;36 Suppl 4:S90-1.
This review emphasizes progesterone's role in supporting healthy breast homeostasis and opposing the proliferative effects of estradiol in the breast, unlike synthetic progestins.
Plu-Bureau G, Le MG, Thalabard JC, Sitruk-Ware R, Mauvais-Jarvis P. Percutaneous progesterone use and risk of breast cancer: results from a French cohort study of premenopausal women with benign breast disease. Cancer Detect Prev 1999;23(4):290-6.This cohort study followed 1150 premenopausal French women diagnosed with benign breast disease. Topical progesterone cream, a common treatment for mastalgia in Europe, had been prescribed to 58% of the women. Follow-up accumulated 12,462 person-years. There was no association noted between progesterone cream use and breast cancer risk. Furthermore, women who had used both progesterone cream and an oral progestogen had a significant decrease in breast cancer risk (RR= 0.5) as compared to women who did not use progesterone cream. There was no significant difference in the risk of breast cancer in percutaneous progesterone users versus nonusers among oral progestogen users. These results suggest there are no deleterious effects caused by percutaneous progesterone use in women with benign breast disease.
-------Formby B, Wiley TS. Bcl-2, survivin and variant CD44 v7-v10 are downregulated and p53 is upregulated in breast cancer cells by progesterone: inhibition of cell growth and induction of apoptosis. Mol Cell Biochem 1999 Dec;202(1-2):53-61.
This study sought to elucidate the mechanism by which progesterone inhibits the proliferation of breast cancer cells. Utilizing breast cancer cell lines with and without progesterone receptors (T47-D and MDA-231, respectively) in vitro, the authors looked at apoptosis (programmed cell death) in response to progesterone exposure as a possible mechanism. The genetic markers for apoptosis - p53, bcl-2 and surviving, were utilized to determine whether or not the cells underwent apoptosis. The results demonstrated that progesterone does produce a strong antiproliferative effect on breast cancer cell lines containing progesterone receptors, and induced apoptosis. The relatively high levels of progesterone utilized were similar to those seen during the third trimester of human pregnancy.
--------Lin VC, Ng EH, Aw SE, Tan MG, Ng EH, Chan VS, Ho GH. Progestins inhibit the growth of MDA-MB-231 cells transfected with progesterone receptor complementary DNA. Clin Cancer Res 1999 Feb;5(2):395-403.
Progesterone is mainly thought to exert its effects via the estrogen-dependent progesterone receptor (PR), the effects of which may be overshadowed by the presence of estrogen. In order to study the independent effects of progesterone on breast cancer cell lines, PR expression vectors were transfected into a PR and ER negative cell line (MDA-MB-231). The growth of these cells was then studied in response to progesterone and several progestins. Progesterone was found to significantly inhibit DNA synthesis and cell growth in a dose-dependant fashion. The results of this study indicate that progesterone and progestins independent of estrogen have an antiproliferative effect on breast cancer cells via the progesterone receptor. This suggests a possible role in the treatment of PR negative breast cancer via re-activation of the PR receptor.
------------Formby B, Wiley TS. Progesterone inhibits growth and induces apoptosis in breast cancer cells: inverse effects on Bcl-2 and p53. Ann Clin Lab Sci 1998 Nov-Dec;28(6):360-9.
This study explored the mechanism by which progesterone inhibits breast cancer cell proliferation (growth). In progesterone receptor positive T47-D breast cancer cells, the mechanism of apoptosis appeared to be through the regulation of the genes p53 and bcl-2 by progesterone. These genes control the apoptotic process. It was demonstrated that at progesterone levels that approximate the third trimester of pregnancy, there was a strong antiproliferative effect in at least 2 breast cancer cell lines.
---------Foidart JM, Colin C, Denoo X, Desreux J, Beliard A, Fournier S, de Lignieres B. Estradiol and progesterone regulate the proliferation of human breast epithelial cells. Fertil Steril 1998 May;69(5):963-9.
In this double-blind randomized study, to evaluate the effects of estrogen and progesterone on normal breast cells, 40 postmenopausal women received daily topical application of a gel containing either placebo, estradiol, progesterone, or estradiol + progesterone for two weeks prior to esthetic breast surgery or the excision of a benign breast lesion. The results showed that increased estrogen concentration increased the number of cycling epithelial cells, whereas exposure to progesterone for 14 days reduced the estrogen-induced proliferation of normal breast epithelial cells.
----------Pasqualini JR, Paris J, Sitruk-Ware R, Chetrite G, Botella J. Progestins and breast cancer. J Steroid Biochem Mol Biol 1998 Apr;65(1-6):225-35.
This review article outlines the many functions of progestogens in hormone-dependent and independent breast cancer and suggests new clinical applications for their use in the treatment of breast cancer.
--------Mohr PE, Wang DY, Gregory WM, Richards MA, Fentiman IS. Serum progesterone and prognosis in operable breast cancer. British Journal of Cancer 1996;73:1532-1533.
Higher blood levels of progesterone measured during surgical treatment of breast cancers were associated with significantly better survival, especially in women who were node-positive (P<0.01). There was no significant relationship between estradiol levels and survival. This study demonstrated that a higher level of progesterone at time of excision is associated with improved prognosis in women with operable breast cancer.
-------Chang KJ, et al. Influences of percutaneous administration of estradiol and progesterone on human breast epithelial cell cycle in vivo. Fertil Steril 1995; 63(4):785-91.
The effect of transdermal estradiol (1.5 mg), transdermal progesterone (25 mg), and combined transdermal estradiol and progesterone (1.5 mg and 25 mg) on human breast epithelial cell cycles was evaluated in vivo. Results demonstrated that estradiol significantly increases cell proliferation, while progesterone significantly decreases cell replication below that observed with placebo. Transdermal progesterone was also shown to reduce estradiol-induced proliferation.
-------Laidlaw IJ, Clarke RB. The proliferation of normal breast tissue implanted into athymic nude mice is stimulated by estrogen, but not by progesterone. Endocrinology Jan 1995;136(1):164-71.
Normal human breast tissue was implanted subcutaneously into athymic nude mice. The mice were then treated with estradiol or progesterone such that serum levels approximated those seen in normal menstruating women.
Immunocytochemical measures were made of proliferative activity and steroid receptor expression of the tissue implants. It was found that physiologic levels of estradiol significantly stimulated the proliferation of human breast epithelial cells and increased progesterone receptor expression 10-20-fold. Progesterone failed to affect proliferation alone or after estradiol priming.-----
Nappi C, Affinito P. Double-blind controlled trial of progesterone vaginal cream treatment for cyclical mastodynia in women with benign breast disease. J Endocrin Invest 1994;15(11):801-6.
Eighty regularly menstruating women with mastodynia were studied to evaluate the clinical effectiveness of vaginally administered micronized progesterone. Subjects were randomly assigned to one of two groups, with all participating in a control cycle prior to treatment. One group received 4 grams of vaginal cream containing 2.5% natural progesterone for six cycles from day 19 to day 25 of the cycle. The other group was similarly treated with placebo. Both subjective reporting on a daily basis and clinical examination revealed a significant reduction in breast pain, defined as 50% reduction, in 64.9% of subjects receiving progesterone and 22.2% of subjects receiving placebo. Effects of breast nodularity were not significant. No side effects were detected.
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Mauvais-Jarvis P, Kuttenn F, Gompel A. Antiestrogen action of progesterone in breast tissue. Horm Res 1987;28(2-4):212-8.
In a review of international literature on the cellular effects of progesterone on both normal breast cells and breast cancer cell lines, the authors conclude that most data indicate progesterone and progestins have an antiestrogenic effect on the breast, as reflected in the decrease in estradiol receptor content, the decrease in cell proliferation, and an increase in a marker of cell differentiation, 17 beta-hydroxysteroid activity, which is mediated by the progesterone receptor.
-------Cowan LD, Gordis L, Tonascia JA, et al. Breast cancer incidence in women with a history of progesterone deficiency. American Journal of Epidemiology 1981; 114:209. ,083.
Infertile women were followed for 14-34 years. Those who were deficient in progesterone showed a fivefold greater incidence of premenopausal breast cancer.
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MORE RESEARCH explains how synthetic progesterone would block natural progessterone from occupying the receptor space that would decrease the cell proliferation rate by >400% if allowed.
LIVE LINK http://www.health-science.com/breast_cancer.html
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Molecular biologist, Dr. Ben Formby of Copenhagen, Denmark and Dr. T.S. Wiley at the University of California in Santa Barbara have researched two genes, BCL2 and P53, and their effect on female-specific cancers and prostate cancer.
Cells of breast, endometrium, ovary and prostate, were grown in the laboratory. Estrogen (estradiol) was added to the cells. This hormone turned on the BCL2 gene, causing the cells to grow rapidly and not die. Then, progesterone was added to the cell cultures. Cell reproduction stopped and the cells died on time (apoptosis).
This methodology was applied to all the above types of cancer. The BCL2 gene, therefore, stimulates the growth of these cells and the risk of cancer. On the other hand, the P53 gene promotes apoptosis or programmed cell death and thereby, reduces the risk of cancer. Estradiol upregulates or stimulates the production of the BCL2 gene, while progesterone upregulates or stimulates the production of the P53 gene.
Transdermal estradiol increased the cell proliferation rate by 230%, while transdermal progesterone decreased the cell proliferation rate by >400%. A combination estradiol/progesterone cream maintained the normal proliferation rate. This is direct evidence that estradiol (a potent estrogen) stimulates hyper-proliferation of breast tissue cells and progesterone mediates hyper-proliferation.
A second study by noted researcher Bent Formby, Ph.D. was just published with more insightful results. To determine the biologic mechanism of why progesterone inhibits the proliferation of breast cancer cells, a variety of cancer cell lines with different receptors and different expression of genes were exposed to progesterone. Exposure to progesterone induced a maximal 90% inhibition of cell proliferation in T47-D breast cancer cells and no measurable response to MDA-231 progesterone-receptor negative breast cancer cells. An impressive 43% of the T47-D cancer cells had undergone apoptosis (programmed cell death) within 24 hours after exposure to progesterone. Further analysis showed that the genetic expression by T47-D cancer cells of the bcl-2 gene was down regulated, and that of the p53 gene (tumor suppressor gene) was up regulated. Since the p53 gene expression induces cell apoptosis and the bcl-2 gene when expressed inhibits apoptosis, if one's cancer cells are progesterone-receptor positive, then progesterone as part of one's therapy appears to be very important. However, 50% of breast cancer cell lines have mutant or no p53 oncogene expression, so in this instance, genistein therapy might be helpful.Therefore unopposed estradiol causes these same types of cancer. Since Breast cancer is considered to be a hormone dependent cancer it is critically important to avoid the factors that would promote too much estradiol.
Birth ControlIn order for natural progesterone to stimulate the production of the P53 gene it must attach itself to progesterone receptors found in abundance in breast, ovarian, and endometrial cells. If a woman is taking birth control pills or any other form of synthetic progesterones (progestins, progesterone acetate, medroxy-progesterone acetate) these synthetic progesterones will occupy progesterone receptors and prevent natural progesterone from occupying the receptor site. Synthetic progesterones not only fail to produce the P53 gene but prevent it's production by blocking natural progesterone from occupying the progesterone receptor and in the presence of excess estradiol, dramatically increase a woman's risk for female-specific cancers.
There are 12 references to tests on BCL2 and P53, and how they are affected by progesterone & estrogen. This information has been published, in part, in the following journals:
The American Cancer Society Journal
The Journal of Clinical Endocrinology
The American Journal of Pathology
International Journal of Cancer
The Journal of the American Medical Association (JAMA)
Fertility and Sterility - Journal of the American Society For Reproductive Medicine
Clearly some of the underlying causes of breast cancer are too much estrogen relative to too little of the helpful benefits of the P53 gene. This is especially so in the presence of trans fatty acids (hydrogenated fats).
Anyway, will be reading this thread tip to tail - need all the info I can get and sharing waht I know so far. This has been a difficult decision for me and start stop in use, but I think it is a chance to not pass by for me.
I also use black beans as an estrogen soaker-upper. That post is around here somewhere.
Diane Essa
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Natkat
Thx very much for that! For whatever reason, I did not realize the turmeric was specifically for the ER PR pos. ( just thought of it as ' good for cancer' spice :>)
Not sure how I missed all the deatils, but is it akin to DIM?
Does anyone have more info on the mechanism of turmeric as well as a suggested dosage /SEs ?
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Purple - Wow you've been busy. Lots of good information. I will definitely be starting a new line of research. I never thought about progesterone alone. This is very timely as I see my onco doc this week so he can try to talk me into Tamox. I will have new questions on my list now and some new thoughts on how approach this disease from a away from the norm approach.
Nice to start the day off on a positive note!
HAPPY MONDAY!
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THX mini1, but I am not the one who did the research. Guess this thread is so chock fuill of info it is tough to see who's who !
ALSO----- I was told my ER score was 8 and my PR an 7. Has anyone else ever had their scores read in that fashion?
I am wondering if it means ER 80% and PR 70-% ...or if its just a screw up or ??????0 -
Mine was by percentage.
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thank you , mini
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Purple:
You bring up the issue of degree of er positivity. That is another problematic area. Usually, so the story goes, the most reliable measure of one's degree of hormone responsiveness is via the pathologists report following surgery. But new findings say it appears that different areas of a tumor may have different degrees of receptivity. At first glance, this might not seem problematic, but I think it is. In my needle biopsy, the report said 95 percent er-pos. That would argue for a treatment plan with heavy emphasis on estrogen receptor suppression. But my post-surgical pathology report later put my positivity at only 10 percent, and only 1 percent er-pos. All of a sudden, I become very close to triple neg. Pathologists simply take a sample of the tumor and analyze it, but it appears that tumors have many stripes and that different sections may yield different results.
To me, this may partly (not completely) explain why so many stage IV sisters report that their receptor status has changed in mid-course. It seems that it can indeed change, but it's also believed that in multiple tumors there can be native differences.
Conclusion: It's so hard to figure out how to do targeted therapy for cancer, and this is regardless of whether you used prescription drugs or OTC products.
Again, though, as my previous post suggests, estrogen may not be the bc enemy it is made out to be.
ASIDE:
Mods, something happened to the formatting here - is it possible to fix? thx!
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1Athena1- you mention that a post-surgical path report gave you differing numbers. Was this testing something your oncologist ordered? What kind of testing was it?, if you don't mind my asking. I see my onco doc tomorrow to argue my case against taking Tamox and I'm sure that he will use my path report - 90-100% ER+ 10-15%-PR+ - as the reason I need to take the Tamox. I'm not going to, but I want to discuss this with him armed with as much info as I can. Also, I would like to know, as you mentioned above, if my path has changed. Knowing specifically what to ask for would be very helpful to me.
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athena
That is really interesting!
I cannot seem to get reliable numbers from my reports which is upsetting. I had my surgery at MGH in Boston and when I asked my MO what % I was she said : " We dont quanitify it."
I DO! That just might factor in to how I make *my* decision !0 -
I don't like to think of estrogen as the enemy either -after all we need it to protect our bones, hearts and who knows what else.
Today I saw my ob/gyn and mentioned I had gone off the Aromasin. He was so understanding and didn't seem that concerned at all. But that is probably due to my age 76 and maybe he is familiar with the Danish study of 70 plus women not needing AIs.
Anyway, it was refreshing not to be scolded for not following the usual protocol!
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Mini - No, it was nothing out of the ordinary. My official cancer dx came from a needle biopsy. In that report, which was delivered to my breast surgeon, it noted 95 percent for er-pos. But those measurements are known for not necessarily being accurate. The most important thing the needle biopsy physician really wants to convey is whether it's cancer. Then, the 10 percent figure came after the pathologist examined my tumor sample excised in surgery. That is considered the more reliable piece of data and the one to go by when planning adjuvant treatment. If you have a needle biopsy and sugery, then, both reports will automatically follow.
I am anything BUT knowledgeable about hormones, but I think blood tests are not the way to go, because overall hormone presence is not what conventional cancer hormone therapies seek to target. TAMOX is an selective estrogen receptor modulator, so it is more subtle than, say, getting rid of your ovaries. That is why I finally consented to it. I have no knowledge of OTC products in this regard.
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Purple - it's a tough call. IMO - this is only an opinion - it matters whether you are on the very high or the very low end, as it offers some guidance on both prognosis and recommended treatments. Exact percentage would probably require a more detailed tumor examination by a pathologist than is currently the standard of care.
If I knew then what I know now, I would have set up a pre-surgery meeting with the pathologist and questioned him closely about what receptors could be tested for. I probably would have requested extra testing and examination of samples from various locations in the tumor.
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Jumping in here to say, I think this might be where the Oncotype dx score can help if you were able to have it done. I had my ER+/PR+ results from the biopsy, but then they sent off a sample of the tumor from the lumpectomy to Oncotype folks. Those results were also ER+/PR+ so that gave me the feeling my numbers might be more correct than just relying on the core biopsy result.
Purple, were you able to get an Oncoscore?
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All good to read, I just don't understand all this. But tomorrow I am going to the endocrinologist for initial appt and bloodwork. I know he is very much into alternatives and the bioidentical HRT, so we will be on same page, but am nervous. Dealing w the medical professionals as an alternative choice 'patient' brings me great stress.
My path report from lumpectomy and surgery that removed 25% of breast, that report was 90 % ER+ and PR+. The lymph node biopsy in July was 90% ER+ and 70% PR+
I am the one who posted the sheets of research which was actually from long ago on another thread, plus my own. I am still reading that and doing what I think best for th etime being.
The page is stretched who knows why? On one thread it stretched out due to an image too large even though it had been pulled in to a good size it didn't hold the new size. Hopefully the next page for this thread will be fine and wehn ther eis a new page this one will go back to template.
Diane Essa or LOVEssa
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MadBluebird - I am right there with you. I have my appt. tomorrow for the same conversation. I am 90-100% ER+ and 10-15% PR+. My oncotype score is 18. I looked it up and "low risk" is 0-18 and "intermediate risk" is 18-to 30 something, so I am right on the cusp, making it even harder for me. If you learn anything that might be helpful to me, feel free to pass it on. :-) Good Luck
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Hello. I am investigating naturapaths in my area and see that an initial appt. is approx. $150.00, subsequent $75.00, saliva testing done through a lab $180.00. Wow! I didn't realize that the monetary output would be so high! That's not including supplements, etc. My question: Did you 'shop around' for your naturapth? How did you decide whom to use? Do these figures seem reasonable? Thank you! Tammy
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I had my BMX in February of this year and am doing all alternative medicine and let me tell you, it is costing a fortune - both for dr. appts. and supplements - I can only hope and pray that this works. My alt. dr. still feels I should be monitored by an oncologist to be sure it doesn't recur - so now I am looking for one who will only monitor - I am 66 years old and my ER+ was 97% and my PR- zero - the alt. M.D. has me on estrogen balancing supplements - I feel like I am running blind here but just don't know what else to do - the conventional treatments are brutal - who knows, I don't know if I am making the right decision or not - scary!!! Good Luck to all my sisters here!!! Barbie
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That is ridiculous that it is so expensive. No way can I afford that on Soc. Sec. I think I'll just do a lot of research on my own - try some supplements that are recommended, keep eating healthy foods and exercising.
And hope for the best!
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I am having difficulty just finding a legit one around me. I also am torn as to if it's the right things to do and how long I will be able to afford it even doing it on my own. It is frustrating that docs won't work with us, but given the already high malpractice costs they face from so many people that are sue crazy, I guess I can understand their perspective. And they are MO's and as they say, when you're a hammer, everything looks like a nail. I'm sure that most genuinely believe that the the best course of treatment is conventional medicine. And for some, I'm sure it is. I'm just not sure that at this stage of the game it should be my first choice of treatment.
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Great thread! I've been reading through this thread and didn't see any mention of mushrooms. Lately I've been hearing about mushrooms being a powerful food in preventing cancer. It seems that initial studies indicate that mushrooms are aromatase-inhibiting and overall great at reducing cancer risk or slowing tumor growth.
Mushrooms have never been my thing, mostly because I don't like how they are grown. Now I'm trying to incorporate them into my diet, and they're really not that bad. They seem to take on the flavor or whatever they're cooked with. Most days I have one big anti-cancer meal of mushrooms and red onion heated in olive oil then mixed with steamed broccoli and squash or other veggies to create a sort of stir fry.
I'm on Tamoxifen but am always looking for more natural ways to be healthy. Plus, I'm thinking ahead to when my five years are up with the Tamoxifen (knocking on wood that all will be well then). I know when I eventually go off of it, I'm gonna freak without a backup plan for controlling estrogen.
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