Estrogen lowers breast cancer death rate

Another example of marketing wisdom that is counter to the truth. Marketing spiel: estrogen is bad because HRT doesn’t work except for hot flashes, estrogen increases risk of breast cancer and breast-cancer cells that have estrogen receptors (ER) grow faster in the presences of estrogen. All these are false, as demonstrated by the articles below. I have spent one day searching the medical literature at UCSD medical library, searching for proof that ER receptors is associated with aggressive breast cancer, and have not been able to find the kind of independent basic quality research to make me a believer. Important evidence is that in the studies below and others the right formulation of HRT has been found to be protective, both in reducing the risk for metastatic breast cancer, and in when taken subsequent to breast cancer to reduce the probability that early stage breast cancer will become metastatic. The link between breast cancer and HRT is based on Prempro whose progestin is MPA (medroxyprogesterone). MPA blocks most of the positive effects of estrogen, and thereby increases the risk of breast cancer. Unfortunately Prempro, since the 1940s, has been the leading HRT. There was a 24% increase with Prempro, which has medroxyprogesterone (MPA), but a 20% reduction in the risk on just horse estrogen—see Wiki. Prempro is horse estrogen with MPA. That is more evidence the estrogen doesn’t cause promote breast cancer. The articles below are proof that HRT does not causes breast cancer, or cause breast cancer to grow faster but rather the reverse, less aggressive and slower growth (the same is true about testosterone and prostate cancer). For more on the benefits of HRT, and for testosterone.

The hurdle that cancer drugs need to pass for FDA approval is slightly better than nothing at all (a placebo). The norm for a new cancer drug research submitted to the FDA is a phase III studies on terminal (stage IV) younger cancer patients (younger have less side effects). In most cases the AVERAGE survival is increased by 1 to 4 months. With tamoxifen (which blocks estrogen) the increased period of survival is caused by it angiogenesis effect (inhibits new blood vessels) and thus restricts oxygen and nutrients to the cancer. “Tamoxifen alone has been shown to have an anti-angiogenetic effect… appears to be, at least in part, independent of tamoxifen's estrogen receptor antagonist properties.^[23]” Wikipedia. However, promoting tamoxifen as blocking estrogen allowed it to be prescribed long-term for the 70% of women, those with estrogen receptors. This marketing strategy has yielded billions in profits. See Marketing Science on how pharma controls the production of medical information, and BMJ on average positive bias of 32% on published journal articles—all 74 article review were had positive bias. Extrapolating from this, all articles that support a drug’s effectiveness are based on junk science that promotes marketing. The journal’s peer review is a façade, because the raw data is not submitted with the article. The company who funds the clinical trial owns the results and won’t share them. Moreover, the journals depend on pharmaceutical companies for income through both advertising and through the sales of thousands of reprints of articles which pharmaceutical then give to doctors to support their marketing goals (dressed as science). All other branches of science require the raw data.

Below are two more articles with positive results for HRT. This is because natural estrogen (estradiol) is protective. The results for HRT would be even better if the two natural hormones estradiol and progesterone were used. They aren’t because they are natural to the body, and thus cannot be patented by pharma—for more on HRT.

1998 by American Society of Clinical Oncology CO September 1998 vol. 16 no. 9 3115-3120

http://jco.ascopubs.org/content/16/9/3115.short

Low biologic aggressiveness in breast cancer in women using hormone replacement therapy

K Holli, + Author Affiliations: Department of Oncology, University Hospital of Tampere, Institute of Medical Technology, University of Tampere, Finland. kaholli@tays.fi

Abstract

PURPOSE Hormone replacement therapy (HRT) has been associated with an increased risk for breast cancer. Cancers in women who use HRT are often less advanced, and lower mortality has been reported in those who use HRT than in nonusers. We sought to explain this by a comparison of indicators of tumor aggressiveness in patients who received HRT with those in patients who did not.

PATIENTS AND METHODS A population-based cohort of 477 postmenopausal women with breast cancer were interviewed for the use, type, and duration of HRT. Clinical variables and indicators of tumor aggressiveness (histologic grade, hormone receptors, DNA ploidy, S-phase fraction, and c-erbB-2 oncoprotein overexpression) were analyzed.

RESULTS Breast tumors from HRT users were smaller (odds ratio, 0.47; P=.005), had better histologic differentiation (P=.04), and had a lower proliferation rate (S-phase fraction, P=.009) than tumors from nonusers. These differences persisted after adjustments for age and method of diagnosis (mammography screening v self-referral) by multiple logistic regression. No significant differences were observed in the estrogen (ER) or progesterone receptor content, c-erbB-2 oncogene overexpression, or axillary node involvement. A subgroup analysis showed that the tumor proliferation rates among HRT users were significantly lower only if HRT had been used at the time of diagnosis (P=.001). The type of HRT (estrogen v combination of estrogen and progesterone) was not associated with any clinical parameter or tumor phenotype. The association of HRT with lower proliferation rate and smaller tumor size was exclusively caused by ER-positive tumors (P=.0001 and P=.0035 v P > .1, respectively).

CONCLUSION The results indicate that breast cancer in women who receive HRT is biologically less aggressive than those without previous HRT. The lower cell-proliferation rate and smaller tumor size found in ER-positive tumors from current HRT users suggest a direct ER-mediated growth inhibitory effect of HRT on established breast tumors. This may at least partly explain why breast cancer in HRT users has a more favorable clinical course.

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Breast Cancer Survival and Hormone Replacement Therapy: A Cohort Analysis

Abstract: Controversy exists regarding the safety of hormone replacement therapy (HRT) after a diagnosis of breast cancer. The objective of this study is to perform a matched cohort analysis to evaluate the impact of HRT on mortality in breast cancer survivors. Patients with breast cancer who received HRT after diagnosis of breast cancer were identified. Control subjects were identified from the regional cancer registry. Matching criteria included age at diagnosis, stage of breast cancer, and year of diagnosis. Controls were selected only if they were alive at the time of initiation of HRT of the matched case. Only subjects not included in a previously reported matched analysis were selected. One hundred twenty-five cases were matched with 362 controls. Ninety-eight percent (123/125) of the cases received systemic estrogen; 90/125 (72%) also received a progestational agent. The median interval between diagnosis of breast cancer and initiation of HRT was 46 months (range 0-401 months). The median duration of HRT was 22 months (range 1-357 months). The risk of death was lower among the HRT survivors; odds ratio 0.28 (95% confidence interval 0.11-0.71). This analysis does not suggest that HRT after the treatment of breast cancer is associated with an adverse outcome.

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Hormone Replacement Therapy After a Diagnosis of Breast Cancer in Relation to Recurrence and Mortality

Abstract

Background: Hormone replacement therapy (HRT) is typically avoided for women with a history of breast cancer because of concerns that estrogen will stimulate recurrence. In this study, we sought to evaluate the impact of HRT on recurrence and mortality after a diagnosis of breast cancer. Methods: Data were assembled from 2755 women aged 35–74 years who were diagnosed with incident invasive breast cancer while they were enrolled in a large health maintenance organization from 1977 through 1994. Pharmacy data identified 174 users of HRT after diagnosis. Each HRT user was matched to four randomly selected nonusers of HRT with similar age, disease stage, and year of diagnosis. Women in the analysis were recurrence free at HRT initiation or the equivalent time since diagnosis. Rates of recurrence and death through 1996 were calculated. Adjusted relative risks were estimated by use of the Cox regression model. All statistical tests were two-sided. Results: The rate of breast cancer recurrence was 17 per 1000 person-years in women who used HRT after diagnosis and 30 per 1000 person-years in nonusers (adjusted relative risk for users compared with nonusers = 0.50; 95% confidence interval [CI] = 0.30 to 0.85). Breast cancer mortality rates were five per 1000 person-years in HRT users and 15 per 1000 person-years in nonusers (adjusted relative risk = 0.34; 95% CI = 0.13 to 0.91). Total mortality rates were 16 per 1000 person-years in HRT users and 30 per 1000 person-years in nonusers (adjusted relative risk = 0.48; 95% CI = 0.29 to 0.78). The relatively low rates of recurrence and death were observed in women who used any type of HRT (oral only = 41% of HRT users; vaginal only = 43%; both oral and vaginal = 16%). No trend toward lower relative risks was observed with increased dose. Conclusion: We observed lower risks of recurrence and mortality in women who used HRT after breast cancer diagnosis than in women who did not. Although residual confounding may exist, the results suggest that HRT after breast cancer has no adverse impact on recurrence and mortality.