Errors in Modern Medicine: The Fear of Estrogen
Rebecca is a 52 year old post menopausal school teacher sitting in my office crying because she knows she needs menopausal hormone replacement if she wants to remain healthy, and yet her primary care doctor and OB/Gyne doctor have both told her estrogen is dangerous, causes breast cancer. Both doctors refused to prescribe hormone replacement for her. In addition, Rebecca’s two closest friends have advised her against it, citing a family member currently diagnosed with breast cancer undergoing chemotherapy. Clearly, Rebecca is torn between two opposing viewpoints, creating mental tension and despair (see left image). This is a recurring scenario all across the country. As is my usual practice, I explained to Rebecca there is no need to make a decision right now, there is plenty of time to study the issue. I even pointed her to reading material on my blogs, my newsletters, and book discussing the safety and efficacy of menopausal hormone replacement. I then told Rebecca that if she gains a greater understanding and feels more comfortable in the future, I would be glad to get her started on the hormone replacement program. There is no pressure, and I respect whatever decision she feels comfortable with. Finally, Rebecca agreed with the plan and left the office in good spirits. This is a recurring scenario in my office, duplicated in countless doctor’s offices across the country.
Left upper image: The Scream by Annemarie Busschers, painting, 250 x 160 cm 2010 private collection Miami, courtesy of Wikimedia Commons.
Errors in Modern Medicine
One of the most glaring errors in conventional medicine is the false idea that Estrogen is somehow bad, and causes breast cancer, blood clots, other adverse effects. Modern medicine falsely says that Estrogen should never be prescribed for the post-menopausal female, and especially never to breast cancer survivors. The resulting mass media propaganda campaign creates fear of estrogen throughout the population. Nothing could be farther from the truth. The reality is Menopausal Hormone Replacement with Estrogen is safe and effective. Not only does Estrogen not cause breast cancer, it is actually preventive of breast cancer. I will show you the studies why this is true. When applied via the transdermal route with topical creams, estrogen does not cause blood clots. That is why we use transdermal creams and avoid oral estrogen tablets (which are associated with blood clots, increased coagulation, deep venous thrombosis and pulmonary embolus).
Premarin-Alone (Estrogen) Users Have 23 percent less Breast Cancer Than Placebo
The second arm of the WHI study included 10,739 post-menopausal women after hysterectomy randomized to Estrogen (Premarin, CEE) or to placebo. In 2004, the data from the second arm of the Women’s Health Initiative (WHI) was published in JAMA 2004. This data included 6.8 years of follow up showing 23% less invasive breast cancer in the Premarin treated group (also called CEE) compared to placebo group. There were 94 breast cancer cases in the estrogen hormone group (CEE) and 124 cases of breast cancer in the placebo group.
Estrogen Group Second Arm of WHI: 45% Reduction in Mortality from Breast Cancer
The 18 year follow up showed a 45 percent reduction in mortality from breast cancer in the estrogen treated group compared to placebo. In 2017, Dr. JoAnn Manson reviewed the 18 year follow up of the Second Arm of the WHI (Premarin-Alone) showing a 45 percent reduction in breast cancer mortality in the Estrogen User Group !! Dr. Manson writes:
After 18 years of cumulative follow-up of the WHI-CEE cohort, breast cancer mortality was statistically significantly reduced by 45% (HR, 0.55; 95% CI, 0.33–0.92). This may well be the most significant and most over-looked finding of the WHI-CEE trial (1).
Breast Cancer Mortality in Both Arms of WHI
Here is the Data on the cumulative 18-year follow-up of 2 randomized clinical trials WHI First and Secoond Arms, between 1993 and 1998 and followed up through December 31, 2014
First Arm CEE plus MPA vs Placebo active=61/ Placebo=40 HR=1.44
Second Arm CEE alone vs Placebo active=22 /Placebo 41 HR 0.55
Premarin Plus Medroxyprogesterone – First Arm of the Women’s Health Initiative 26 percent greater Breast cancer in Hormone Users
Remember there are two arms of the WHI. We discussed the second arm from 2004 above. Now, we will go back two years to 2002 and discuss the first Arm.
In 2002, the first Arm of the Women’s Health Initiative (WHI) was published in JAMA, halted early after 5.2 years because of increased breast cancer in the estrogen treated group. This study created havoc in medical practice and in the general population. Fear of estrogen made women stop requesting and doctors stop prescribing Hormone Replacement Therapy (HRT). Following this 2002 publication in JAMA, the entire previous medical edifice of menopausal hormone replacement was dismantled. Training programs disappeared. New doctors no longer had training or expertise to even practice hormone replacement.
The first arm of the WHI randomized 16,608 post-menopausal women to either Prempro (Premarin plus Medroxyprogesterone) or placebo. After 5.2 years of follow up, there were 290 cases of breast cancer in the Prempro group which is 26% greater than the placebo group. The authors write:
Estimated hazard ratios (HRs) (nominal 95% confidence intervals [CIs]) were as follows: CHD, 1.29 (1.02-1.63) with 286 cases; breast cancer, 1.26 (1.00-1.59) with 290 cases; stroke, 1.41 (1.07-1.85) with 212 cases; PE, 2.13 (1.39-3.25) with 101 cases; colorectal cancer, 0.63 (0.43-0.92) with 112 cases; endometrial cancer, 0.83 (0.47-1.47) with 47 cases; hip fracture, 0.66 (0.45-0.98) with 106 cases; and death due to other causes, 0.92 (0.74-1.14) with 331 cases.
The synthetic progestin, Medroxyprogesterone (MPA), is a known breast cancer carcinogen, and commonly used to induce breast cancer in animal models.
Lanari, Claudia, et al. “The MPA mouse breast cancer model: evidence for a role of progesterone receptors in breast cancer.” Endocrine-related cancer 16.2 (2009): 333.
Re-Analysis of First Arm WHI Data Shows Glaring Error
In 2018, Dr. Howard Hodis and Phillip Sarrel re-analyzed the data from the WHI first and second arms. They found an error in the study. Some of the women in the placebo group had a history of prior HRT use. These women should have been removed from the placebo group, and were not. The prior use of estrogen confers protection from breast cancer, and falsely reduces the incidence of breast cancer in the placebo group. If the women with prior HRT use are removed from the placebo group, the data chart (see Figure 1 below) looks entirely different. There is a null effect, meaning no difference between the Prempro group and the Placebo group in terms of breast cancer incidence. Dr. Howard Hodis writes:
In fact, the increased HR [Hazard Ratio] was not due to an increased breast cancer incidence rate in women randomized to CEE + MPA [Prempro] therapy but rather due to a decreased and unexpectedly low breast cancer rate in the subgroup of women with prior HT [Hormone Therapy] use randomized to placebo. For women who were HT naïve when randomized to the WHI, the breast cancer incidence rate was not affected by CEE + MPA therapy relative to placebo for up to 11 years of follow-up…the data clearly show that CEE+MPA therapy had a null effect on breast cancer risk particularly in the subgroup of women representing the typical population of women treated with HT who are HT naïve before receiving menopausal HT…it is clear that breast outcome data from the WHI-CEE+MPA trial has been misinterpreted and overgeneralized. (2)
SEE Below FIG. 1: There are two different placebo groups. Left Chart shows placebo group with no prior hormone use. Notice Invasive breast cancer trend lines are superimposed. Right Chart shows placebo group with prior hormone use: Notice divergence in trend lines for breast cancer (Red Arrows). This divergence accounts for the false impression of increased cancer risk in the Prempro (Premarin +MPA) Group. This shows that prior hormone use is breast cancer protective! (2)
Above image Fig. 1 Courtesy of Hodis, Howard 2018: It is the divergence (Red Arrow- Right Chart) in the trend line for women with prior hormone therapy use randomized to placebo that accounts for the elevated hazard ratio for breast cancer falsely giving the impression that breast cancer incidence was increased in the trial due to conjugated equine estrogen plus medroxyprogesterone acetate where in fact the elevated hazard ratio was due to a DECREASED breast cancer incidence In the PLACEBO treated group. (2)
Dr. Rowan Chlebowski, December 2019
In 2019, Dr. Rowan Chlebowski reviewed the re-analysis of the data stating that estrogen alone reduces breast cancer, while estrogen plus medroxyprogresgerone has the opposite effect, writing:
Estrogen alone decreased, while adding progestin increased, breast cancer incidence…CEE-alone [Premarin-Alone] and CEE plus MPA [Medroxyprogesterone] use have opposite effects on breast cancer incidence. CEE alone significantly decreases breast cancer incidence which is long term and persists over a decade after discontinuing use. CEE plus MPA use significantly increases breast cancer incidence which is long term and persists over a decade after discontinuing use. (3)
Dr. Lindsay Berkson: Nothing Else Like Estrogen Therapies Has Ever Been Shown to Be So Breast Protective.
On October 2023, Dr Lindsay Berkson discussed this issue on her substack blog, writing:
The WHI 1 authors forgot to ask, and thus did not remove, in the placebo group, any women who had already taken estrogen therapies…Since estrogen was ultimately, on re-analysis found to be “breast protective” , and the synthetic progestins were huge adverse contributing issues, this made the incidence of breast cancer in the placebo group of ladies, lower, as women had already taken the protective estrogen…This made the experimental arm, women taking hormones, falsely appear as though they had more cases of breast cancer…When the data was re-analyzed, thus “righted” by taking out this “confounding issue”, and longer term effects of estrogen looked at with a fine tooth comb, the same original authors, re-published their re-analysis. This is now what I call the WHI 2…Conclusions of WHI 2: Women taking estrogen replacement therapy (ERT) had 23% less incidence or chance of getting breast cancer in the first place. And if you had been on ERT, and got breast cancer, you had a 44% decreased chance of dying from it. Progestins were more the breast damaging issue. Not estrogen. So, stunning as it is, being on ERT put you in a better position, even if you went on to get breast cancer! This is something that is now replicated. Substantiated. But not taught in most med schools or appreciated by most docs and women. Or lawyers!…Estrogen “protects” healthy breast tissue from getting breast cancer in the first place. And, if a women has been on estrogen therapies for an average of 5 years and then gets breast cancer, the estrogen therapies “reduce” her risk of dying from breast cancer by 44%. Nothing else like estrogen therapies has ever been shown to be so breast protective. (4)
Our Breast Cancer Prevention Program
- Use human bioidentical progesterone, avoiding the carcinogenic synthetic progestins such as medroxyprogesterone and norethindrone (see below chart) .
- Include Estriol (E3) which is breast cancer protective.
- Include Progesterone which prevents endometrial hyperplasia, prevents endometrial cancer, and prevents breast cancer.
- Iodine supplementation – decreases breast cancer risk and useful in treatment of breast cancer. (Iodine Treats Breast Cancer)
- Testosterone- decreases breast cancer risk by 40 per cent. (See: Testosterone for Prevention and Treatment of Breast Cancer)
- DIM (Di-Indole-Methane) diverts estrogen metabolism toward favorable metabolic pathways.
- Selenium- low selenium increases cancer risk.
- Vitamin D3 – low D3 increases cancer risk.
- Methyl-Folate – methylation defects increase cancer risk
- We do not perform screening mammography on the healthy population because screening mammography has been shown to have no effect on breast cancer mortality in national data. (see: Laura Esserman Questions Screening Mammography)
Listing of progesterone and synthetic progestins. Progesterone is protective, all other synthetic progestins are carcinogenic:
Above chart courtesy of Siddique, Y. H., and M. Afzal. “A review on the genotoxic effects of some synthetic progestins.” Int J Pharmacol 4.6 (2008): 410-30. (5)
Conclusion: Thanks and credit goes to Dr. Lindsay Berkson for bringing to my attention the above re-analysis of the WHI by Dr. Hodis, who points out the placebo group included women with prior hormone use which confers protection from breast cancer and gives the false impression of increased breast cancer risk in the Premarin+ MPA group compared to placebo. When prior hormone use is removed from the placebo group, trend lines for breast cancer are superimposed for both groups (left chart Fig.1)
Articles with Related Interest
All Bioidentical Hormone Articles by Jeffrey Dach MD
Jeffrey Dach MD
7450 Griffin Road Suite 180/190
Davie, Fl 33314
954-792-4663
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References:
1) Manson, JoAnn E., et al. “Menopausal hormone therapy and long-term all-cause and cause-specific mortality: the Women’s Health Initiative randomized trials.” Jama 318.10 (2017): 927-938.
2) Hodis, Howard N., and P. M. Sarrel. “Menopausal hormone therapy and breast cancer: what is the evidence from randomized trials?.” Climacteric 21.6 (2018): 521-528.
3) Long-term Follow-up Shows Estrogen Alone and Estrogen Plus Progestin Have Opposite Effects on Breast Cancer Incidence in Postmenopausal Women by Rowan Chlebowski, Dec. 13, 2019
4) Substack article by Dr. Lindsay Berkson on Estrogen Hormone Replacement for Menopausal Women, a rebuttal to Mercola. Dr lindsay devaki berkson Oct 24, 2023
estrogen “protects” healthy breast tissue from getting breast cancer in the first place. And, if a women has been on estrogen therapies for an average of 5 years and then gets breast cancer, the estrogen therapies “reduce” her risk of dying from breast cancer by 44%. Nothing else like estrogen therapies has ever been shown to be so breast protective.
5) Siddique, Y. H., and M. Afzal. “A review on the genotoxic effects of some synthetic progestins.” Int J Pharmacol 4.6 (2008): 410-30.
6) The Anticancer Testosterone Metabolite 3β-Adiol. Published in: Townsend Letter By. Dr. Jonathan V. Wright, MD The bad side is that too much 16-OHE1 increases breast and prostate cancer risk.11-14 But like DHT, which also increases cancer risk, 16a-OHE1 s transformed into the anticarcinogenic
7) Warner, Margaret, et al. “25 years of ERβ: a personal journey.” Journal of Molecular Endocrinology 68.1 (2022): R1-R9.
8) Rymbai, Emdormi, et al. “Role of estrogen receptors in cancer: a special emphasis on the therapeutic potential of estrogen receptor ß.” Pharmaceutical Sciences Asia 49.5 (2022).
9) Wu, Wan-fu, et al. “Estrogen receptor β and treatment with a phytoestrogen are associated with inhibition of nuclear translocation of EGFR in the prostate.” Proceedings of the National Academy of Sciences 118.13 (2021): e2011269118.
10) Chimento, Adele, et al. “Estrogen receptors-mediated apoptosis in hormone-dependent cancers.” International journal of molecular sciences 23.3 (2022): 1242.
11) free pdf
Vasconsuelo, Andrea, et al. “Role of 17β-estradiol and testosterone in apoptosis.” Steroids 76.12 (2011): 1223-1231.
17b-Estradiol (E2) and Testosterone (T) exert actions in most animal tissues, in addition to the reproductive system. Thus, both sex steroid hormones affect growth and different cell functions in several organs. Accordingly, the nuclear estrogen (ER) and androgen (AR) receptors are ubiquitously expressed. Moreover, ER and AR may have non-classical intracellular localizations, e.g. plasma membrane, mitochondria and endoplasmic reticulum, raising additional complexity to the functional roles of E2 and T. In addition to the modulation of gene transcription by direct interaction with their cognate nuclear receptors, the steroids can rapidly activate signaling pathways by a non-genomic mechanism mediated by receptors identical to or different from known steroid receptors. Among various functions, E2 and T can regulate apoptosis through those pathways. In mitochondria, the presence of ER and AR and actions of estrogen and androgen have been shown, in keeping with the organelle being a control point of apoptosis. The most recurrent action for each steroid hormone is the protection of mitochondria against different insults, resulting in antiapoptosis. This review summarizes the molecular basis of the modulation of programmed cell death by E2 and T in several tissues.
12) https://www.sciencedirect.com/science/article/abs/pii/S0039128X11002571
Vasconsuelo, Andrea, et al. “Role of 17β-estradiol and testosterone in apoptosis.” Steroids 76.12 (2011): 1223-1231.
However, under some specific conditions E2 could trigger apoptosis in breast cancer cells, opposed to its well studied antiapoptotic role. This peculiar hormone behavior has
been observed in cells from breast cancer which have been longterm estrogen-deprived (LTED) or treated exhaustively with antiestrogens [87]. Curiously, the paradoxical induction of apoptosis by estrogen has been established under several unusual circumstances.
For example, in this case, the pre-conditions of prolonged estrogen depletion or exhaustive treatment with anti-estrogens of the breast cancer cells are mandatory requisites to trigger apoptosis by E2 and could explain the dual action of the steroid to stimulate growth or apoptosis. Thus, the development of antihormone resistance over years of therapy, reprograms the survival mechanism of the breast cancer cell so that estrogen no longer
functions as a survival factor but as a death signal.
13) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3978907/
Rizza, Pietro, et al. “Estrogen receptor beta as a novel target of androgen receptor action in breast cancer cell lines.” Breast cancer research 16 (2014): 1-13.
The two isoforms of estrogen receptor (ER) alpha and beta play opposite roles in regulating proliferation and differentiation of breast cancers, with ER-alpha mediating mitogenic effects and ER-beta acting as a tumor suppressor. Emerging data have reported that androgen receptor (AR) activation inhibits ER-positive breast cancer progression mainly by antagonizing ER-alpha signaling. However, to date no studies have specifically evaluated a potential involvement of ER-beta in the inhibitory effects of androgens.
Collectively, these data provide evidence for a novel mechanism by which activated AR, through an up-regulation of ER-beta gene expression, inhibits breast cancer cell growth.
14) Pietri, Elisabetta, et al. “Androgen receptor signaling pathways as a target for breast cancer treatment.” Endocrine-related cancer 23.10 (2016): R485-R498.
15) https://pubmed.ncbi.nlm.nih.gov/33462444/
Hickey, Theresa E., et al. “The androgen receptor is a tumor suppressor in estrogen receptor–positive breast cancer.” Nature medicine 27.2 (2021): 310-320.
Notably, AR agonists combined with standard-of-care agents enhanced therapeutic responses. Mechanistically, agonist activation of AR altered the genomic distribution of ER and essential co-activators (p300, SRC-3), resulting in repression of ER-regulated cell cycle genes and upregulation of AR target genes, including known tumor suppressors. A gene signature of AR activity positively predicted disease survival in multiple clinical ER-positive breast cancer cohorts. These findings provide unambiguous evidence that AR has a tumor suppressor role in ER-positive breast cancer and support AR agonism as the optimal AR-directed treatment strategy, revealing a rational therapeutic opportunity.
16) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9739178/
You, Chan-Ping, et al. “Modulating the activity of androgen receptor for treating breast cancer.” International Journal of Molecular Sciences 23.23 (2022): 15342.
17) Traphagen, Nicole A., et al. “High estrogen receptor alpha activation confers resistance to estrogen deprivation and is required for therapeutic response to estrogen in breast cancer.” Oncogene 40.19 (2021): 3408-3421.
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18) https://www.sabcs.org/sabcs/2019/pressreleases/3_7gFrcb4gFfda_Estrogen%20Alone%20and%20Estrogen%20Plus%20Progestin%20Have%20Opp.%20Effects%20on%20BC%20Incidence.pdf
presented at the yearly SA TX Breast Cancer Symposium see below including authors at 2019 SABCS.
Long-term Follow-up Shows Estrogen Alone and Estrogen Plus Progestin Have Opposite Effects on Breast Cancer Incidence in Postmenopausal Women by Rowan Chlebowski, Dec. 13, 2019
Estrogen alone decreased, while adding progestin increased, breast cancer incidence
SAN
CEE-alone and CEE plus MPA use have opposite effects on breast cancer incidence. CEE alone significantly decreases breast cancer incidence which is long term and persists over a decade after discontinuing use. CEE plus MPA use significantly increases breast cancer incidence which is long term and persists over a decade after discontinuing use. As a result of the attenuation of subgroup interactions: all postmenopausal women with prior hysterectomy using CEE-alone have the potential benefit of experiencing a reduction in breast cancer incidence while all postmenopausal women using CEE plus MPA have the potential risk of experiencing an increase in breast cancer incidence.
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!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!! BEST !!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!
19 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6386596/
Hodis, Howard N., and P. M. Sarrel. “Menopausal hormone therapy and breast cancer: what is the evidence from randomized trials?.” Climacteric 21.6 (2018): 521-528.
The relationship between menopausal hormone therapy (HT) and breast cancer is complex and further complicated by misinformation, perception, and overgeneralization of data. These issues are addressed in this mini-review through the lens of the Women’s Health Initiative (WHI) that has colored the view of HT and breast cancer. In the WHI, unopposed conjugated equine estrogen (CEE) reduced breast cancer risk and mortality. In the WHI CEE plus continuously combined medroxyprogesterone acetate (MPA) trial, although the hazard ratio (HR) was elevated it was statistically non-significant for an association between CEE + MPA and breast cancer. In fact, the increased HR was not due to an increased breast cancer incidence rate in women randomized to CEE + MPA therapy but rather due to a decreased and unexpectedly low breast cancer rate in the subgroup of women with prior HT use randomized to placebo. For women who were HT naïve when randomized to the WHI, the breast cancer incidence rate was not affected by CEE + MPA therapy relative to placebo for up to 11 years of follow-up. The current state of science indicates that HT may or may not cause breast cancer but the totality of data neither establish nor refute this possibility. Further, any association that may exist between HT and breast cancer appears to be rare and no greater than other medications commonly used in clinical medicine.
any conclusions that HT causes breast cancer has eluded definitive proof for over 5 decades, including WHI.
However, the data clearly show that CEE+MPA therapy had a null effect on breast cancer risk particularly in the subgroup of women representing the typical population of women treated with HT who are HT naïve before receiving menopausal HT.
SEE FIGURE 1 !!!!!!!!!!!!!!!!!!!!!
Although the cause of this outlier low incidence rate of breast cancer in the placebo group of women who had prior HT use is unknown, it is stunning that this unappreciated fact has escaped a more conspicuous and transparent discussion of the important impact that this finding has on interpretation of the breast cancer results from the WHI-CEE+MPA trial.
it is clear that breast outcome data from the WHI-CEE+MPA trial has been misinterpreted and overgeneralized
That is, the WHI-CEE+MPA trial strongly refutes the possibility that CEE+MPA therapy increased the risk of breast cancer in this trial.
50 years of study has failed to conclusively prove cause-and-effect between HT and breast cancer with the preponderance of evidence supporting benefits over risks with amelioration of downstream morbidity and mortality.
!!!!!!!!!!!!!!!!!! ???????? !!!!!!!!
After 18 years of cumulative follow-up of the WHI-CEE cohort, breast cancer mortality was statistically significantly reduced by 45% (HR, 0.55; 95% CI, 0.33–0.92). This may well be the most significant and most over-looked finding of the WHI-CEE trial (7).
20) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5728370/.55
Manson, JoAnn E., et al. “Menopausal hormone therapy and long-term all-cause and cause-specific mortality: the Women’s Health Initiative randomized trials.” Jama 318.10 (2017): 927-938.
cumulative 18-year follow-up,
2 randomized clinical trials between 1993 and 1998 and followed up through December 31,2014
Breast Cancer Mortality
CEE plus MPA vs Placebo active=61/ Placebo=40 HR=1.44
CEE alone vs Placebo
active=22 /Placebo 41 HR 0.55
cumulative 18-year follow-up of WHI
———————————–
Dr. Lindsay Berkson:
The WHI 1 authors forgot to ask, and thus did not remove, in the placebo group, any women who had already taken estrogen therapies.
Since estrogen was ultimately, on re-analysis found to be “breast protective” , and the synthetic progestins were huge adverse contributing issues, this made the incidence of breast cancer in the placebo group of ladies, lower, as women had already taken the protective estrogen.
This made the experimental arm, women taking hormones, falsely appear as though they had more cases of breast cancer.
When the data was re-analyzed, thus “righted” by taking out this “confounding issue”, and longer term effects of estrogen looked at with a fine tooth comb, the same original authors, re-published their re-analysis. This is now what I call the WHI 2.
Conclusions of WHI 2:
Women taking estrogen replacement therapy (ERT) had 23% less incidence or chance of getting breast cancer in the first place.
And if you had been on ERT, and got breast cancer, you had a 44% decreased chance of dying from it.
Progestins were more the breast damaging issue. Not estrogen.
So, stunning as it is, being on ERT put you in a better position, even if you went on to get breast cancer! This is something that is now replicated. Substantiated. But not taught in most med schools or appreciated by most docs and women. Or lawyers!
21) https://www.medrxiv.org/content/10.1101/2022.05.25.22275595.abstract
Baik, Seo H., Fitsum Baye, and Clement J. McDonald. “Effects of Hormone Therapy on survival, cancer, cardiovascular and dementia risks in 7 million menopausal women over age 65: a retrospective observational study.” medRxiv (2022): 2022-05.
The 7 million menopause study
The 7 million NIH study, the largest study ever run on women, with 1.5 million American women on ERT, shows that women 65 and older on estrogen therapies have statistically “less” of all 5 cancers studied (breast, ovarian, uterine, lung and colon). As well as live almost 20% longer, healthier lives. With less heart disease (unless on oral estrogens) and less dementias.
The Arizona insurance study showed that women (almost 400,000) taking natural steroids had 79% less dementias (Association between menopausal hormone therapy and risk of neurodegenerative diseases: Implications for precision hormone therapy. Alzheimers Dement (N Y). 2021 May 13;7(1):e12174.).
22) https://pubmed.ncbi.nlm.nih.gov/34027024/
Kim, Yu Jin, et al. “Association between menopausal hormone therapy and risk of neurodegenerative diseases: Implications for precision hormone therapy.” Alzheimer’s & Dementia: Translational Research & Clinical Interventions 7.1 (2021): e12174.
23) Evaluating Estrogen Detoxification to Understand Breast Cancer Risk
by Debbie Rice, ND, MPH
The most dangerous estrogen metabolite is the 4-OH-E1 metabolite.The 4-OH-E1 metabolite has the potential to become a reactive quinone that causes DNA damage. Thus, if the body is not able to neutralize the 4-OH metabolites well or efficiently, they can wreak havoc on DNA. When DNA is damaged, it disrupts cellular signaling and the body’s ability to repair itself and stop abnormal cell growth. There is correlation between increased 4-OH-E1 metabolites and breast cancer risk. Miao, et al state: “Among many alterations of sex hormone metabolisms, 4-hydroxy estrogen (4-OH-E) metabolite was found to be significantly increased in the urine samples of patients with breast cancer compared with the normal healthy controls. This was the most important risk factor for breast cancer”.
24) Does Estrogen Cause Breast Cancer ? The Answer is –
NO – Estrogen Does NOT Cause Breast Cancer by Jeffrey Dach MD
The results of the 11 year follow up of the Women’s Health Initiative was covered in my previous article.(1) Rather than causing breast cancer, estrogen prevented it. This study found a significant reduction in breast cancer rates for Post-Menopausal women using Estrogen Replacement (Premarin Only Arm)(To be exact, there was a 23% reduction in breast cancer in Premarin Users compared to placebo.)(1)
Rebuttal to Mercola’s Article on Hormone Therapy Lindsey Berkson, DC
Women taking estrogen replacement therapy (ERT) had 23% “less” incidence or chance of getting breast cancer in the first place.
And if you had been on ERT and got breast cancer, you had a “44%” decreased chance of dying from it.
Progestins were the more breast-damaging issue. Not estrogen.
https://price-pottenger.org/journal_article/the-true-power-of-hormones-an-interview-with-devaki-lindsey-berkson-dc/
The True Power of Hormones: An Interview with Devaki Lindsey Berkson, DC by Steven Schindler / October 13, 2023
Price-Pottenger’s former executive director, Steven Schindler, on the important role of hormones in helping us achieve our highest possible levels of health and vitality.
https://drannacabeca.com/blogs/show/hormones-and-breast-cancer-with-dr-devaki-lindsey-berkson
Podcast with Dr Anna Cabeca and Dr. Lindsay Berkson discussing the myths surrounding Estrogen and HRT for women.
The Girlfriend Doctor w/ Dr. Anna Cabeca
Hormones and Breast Cancer with Dr. Devaki Lindsey Berkson
Dr. Anna Cabeca, the girlfriend doctor podcast. Importance of hippocampus volume
20 years after the WHI Trial.
Dr Lindsay Berkson Austin Texas
1977 Rotation in integrative medicine with Dr. Jonathan Wright. In practice for 52 years. My Current Age 75.
Dr Wright taught hormones and gut health were the most important. He had heidelberg capsule anaysis machine to test stomach acid production.
I wrote Hormone Deception about endocrine disruption. Basded on that book, I was invited to an estrogen think tank, and work as a distinuished estrogen scholar at Tulane Med SChool under John Mcclaughlin as my mentor. Worked with the scientists who discovered the first estrogen receptors. Jensen and Gustafson.
Women’s hormones are the most controversial and confusing topic in medicine today.
Most women are terrified of hormones, and really think estrogen is really a bad thing. This term estrogen dominance dominated the airways/ Lets have a conversation to clear some of this up.
very few doctors have heard of the re-analysis of the womens health initiative,
A big part of anti-aging comes from hippocamus volume. This is where memories and emotions, motivation, soul resides in brain. Hippocampus shrinks as we age.
Exercise and meditation does not preserve volume. However, HRT does preserve it.
Yale MedX study tracked volume of hippocampus.
Studies 20 years ago from McGill U by Catherine Lonhartford showed HRT restores hippocampus volume.
re-analysis of whi
peter attia
leon speroff said
Testosterone is Breast Cancer Preventive: Mechanism of Action
There are two estrogen receptors, Alpha and Beta. The Alpha receptor is pro-carcinogenic. The Beta Receptor is protective and suppresses carcinogenesis. Estradiol attached to both receptors 50:50. Estrone (E1) attaches mostly to ER-alpha, while Estriol (E3) attached mosty to ER Beta (protective). The most like likely mechanism for testosterone’s protective effect in breast cancer prevention is the testosterone metabolite 3β-Adiol which attaches to Estrogen Receptor Beta (ER-Beta), thus upregulated ER-Beta expression, thus inhibiting breast cancer cell growth.(38-49)
This is illustrated in 2014 by Dr. Pietro Rizzo who writes:
The two isoforms of estrogen receptor (ER) alpha and beta play opposite roles in regulating proliferation and differentiation of breast cancers, with ER-alpha mediating mitogenic effects and ER-beta acting as a tumor suppressor. …..Collectively, these data provide evidence for a novel mechanism by which activated AR [Androgen Receptor], through an up-regulation of ER-beta gene expression, inhibits breast cancer cell growth.(45) Emphasis Mine.
Jeffrey Dach MD
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