The increase in risk varies depending on a woman’s race, body mass index and breast density
Taking hormones to treat the symptoms of menopause is thought to increase women’s risk of breast cancer, but this risk doesn’t rise equally in all women, a new study finds.
The researchers looked at nearly 1.65 million postmenopausal women ages 45 and older, and found that leaner women, as well as women with denser breasts, were more likely to see the detrimental effects of hormone replacement therapy (HRT) on their breast cancer risk.
Beating the Odds after being diagnosed with Premature Ovarian Failure
” My name is Cole. I’m writing this today because I feel it is important to get my story out there to as many women as possible. To give inspiration to those wanting a family but are suffering from infertility and encourage them to not lose hope. I am 34 years old and had come off of birth control last summer after seventeen years. When I didn’t get my period back after four months my OBGYN recommended I see a reproductive specialist. Upon doing so I was given a battery of blood tests to measure my hormone levels. When the test results came back I was given the shock of my life. The numbers indicated I was POSTmenopausal with diminished ovarian reserve. ”
In utero exposure of women to DES is associated with a high lifetime risk of a broad spectrum of adverse health outcomes
2011 Study Abstract:
BACKGROUND: Before 1971, several million women were exposed in utero to Diethylstilbestrol (DES) given to their mothers to prevent pregnancy complications. Several adverse outcomes have been linked to such exposure, but their cumulative effects are not well understood.
METHODS: We combined data from three studies initiated in the 1970s with continued long-term follow-up of 4653 women exposed in utero to DES and 1927 unexposed controls. We assessed the risks of 12 adverse outcomes linked to DES exposure, including cumulative risks to 45 years of age for reproductive outcomes and to 55 years of age for other outcomes, and their relationships to the baseline presence or absence of vaginal epithelial changes, which are correlated with a higher dose of, and earlier exposure to, DES in utero.
RESULTS: Cumulative risks in women exposed to DES, as compared with those not exposed, were as follows:
for infertility, 33.3% vs. 15.5% (hazard ratio, 2.37; 95% confidence interval [CI], 2.05 to 2.75)
spontaneous abortion, 50.3% vs. 38.6% (hazard ratio, 1.64; 95% CI, 1.42 to 1.88)
preterm delivery, 53.3% vs. 17.8% (hazard ratio, 4.68; 95% CI, 3.74 to 5.86)
loss of second-trimester pregnancy, 16.4% vs. 1.7% (hazard ratio, 3.77; 95% CI, 2.56 to 5.54)
ectopic pregnancy, 14.6% vs. 2.9% (hazard ratio, 3.72; 95% CI, 2.58 to 5.38)
preeclampsia, 26.4% vs. 13.7% (hazard ratio 1.42; 95% CI, 1.07 to 1.89)
stillbirth, 8.9% vs. 2.6% (hazard ratio, 2.45; 95% CI, 1.33 to 4.54)
early menopause, 5.1% vs. 1.7% (hazard ratio, 2.35; 95% CI, 1.67 to 3.31)
grade 2 or higher cervical intraepithelial neoplasia, 6.9% vs. 3.4% (hazard ratio, 2.28; 95% CI, 1.59 to 3.27)
breast cancer at 40 years of age or older, 3.9% vs. 2.2% (hazard ratio, 1.82; 95% CI, 1.04 to 3.18).
For most outcomes, the risks among exposed women were higher for those with vaginal epithelial changes than for those without such changes.
CONCLUSIONS: In utero exposure of women to DES is associated with a high lifetime risk of a broad spectrum of adverse health outcomes. (Funded by the National Cancer Institute).
Read: Adverse health outcomes in women exposed in utero to diethylstilbestrol, NCBI, PMID: 21991952, 2011 Oct 6;365(14):1304-14. doi: 10.1056/NEJMoa1013961.
” Estrogens have important effects on bone turnover in both humans and experimental animals models. Moreover, the decreased level of estrogen after menopause appears to be one of the key factors in determining postmenopausal osteoporosis. The presence of estrogen receptor in both osteoblasts and osteoclasts has suggested a direct role of these steroid hormones on bone tissue. Thus, this tissue is now regarded as a specific estrogen target tissue. Exposure to estrogens during various stages of development has been shown to irreversibly influence responsive target organs. We have recently shown that transient developmental neonatal exposure (days 1-5 of life) of female mice to estrogen resulted in an augmented bone density in the adult animals. The aim of the present study was to evaluate whether short-term modification of maternal estrogen levels during pregnancy would induce changes in the skeleton of the developing fetuses and to identify any long-term alterations that may occur. Pregnant mice were injected with varying doses (0.1-100 micrograms/kg maternal BW) of the synthetic estrogen diethylstilbestrol (DES) from day 9-16 of pregnancy. Offspring were weaned at 21 days of age, and effects on bone tissue of the female mice were evaluated in adulthood (6-9 months of age). Prenatal DES treatment(s) did not significantly affect BW. However, a dose-dependent increase in bone mass, both in the trabecular and cortical compartments, was observed in the prenatal DES-exposed female offspring. Furthermore, long bones of DES-exposed females were shorter than controls. Normal skeletal mineralization accompanied these changes in the bone tissue, as shown by a parallel increase in skeletal calcium content. Double tetracycline labeling performed in 6-month-old DES-exposed animals showed an increase in mineral apposition rate in adult DES-exposed mice as compared with untreated control animals, although no significant difference in the circulating estrogen levels was found in animals of this age. Experiments were then performed to evaluate whether perturbation of the estrogen surge at puberty in these diethylstilbestrol (DES)-exposed mice could reverse the observed changes. Femur length was chosen as a marker of potential estrogenic effect. Prepubertal ovariectomy of the prenatally DES-treated animals could only partially reverse the effects observed in the skeleton of the DES-treated animals. Further experiments were performed to evaluate whether these changes could have occurred in utero. CD-1 pregnant female mice were injected with DES (100 micrograms/kg maternal BW) from days 9-15 of gestation. On day 16 of gestation, fetuses were examined and stained by a standard Alizarin Red S and Alcian Blue procedure to visualize calcified and uncalcified skeletal tissue. Estrogen treatment induced an increase in the amount of calcified skeleton as compared with untreated controls and also a decrease in the length of long bones, strongly suggesting a change in both endochondral ossification and endosteal and periosteal bone formation. In summary, these data show, for the first time, that alterations in the maternal estrogenic levels during pregnancy can influence early phases of fetal bone tissue development and subsequently result in permanent changes in the skeleton. Finally, the effect of this short-term estrogen treatment can be seen in the fetal skeleton, suggesting an estrogen-imprinting effect on bone cell-programming in fetal life because treatment effects on bone cell turnover can be observed later in adult life. ”
Vitamin D may reduce risk of uterine fibroids, according to NIH study
Fibroids, also known as uterine leiomyomata, are noncancerous tumors of the uterus. Fibroids often result in pain and bleeding in premenopausal women, and are the leading cause of hysterectomy in the United States.
Estrogen Plus Progestin and Breast Cancer Incidence and Mortality in the Women’s Health Initiative Observational Study
The use of combined estrogen plus progestin among postmenopausal women was associated with an increased risk of breast cancer, a longer-term analysis of data from the observational Women’s Health Initiative (WHI) suggested.
DES Action USAcommented: “ Most DES Daughters go cautiously when considering HRT-use to avoid additional hormonal exposures. Another study now bolsters the concern. While not specifically about DES it’s a good reminder for all to use the lowest dose for shortest period of time – if absolutely needed. ”
Background In the Women’s Health Initiative (WHI) randomized trial, estrogen plus progestin increased both breast cancer incidence and mortality. In contrast, most observational studies associate estrogen plus progestin with favorable prognosis breast cancers. To address differences, a cohort of WHI observational study participants with characteristics similar to the WHI clinical trial was studied.
Methods We identified 41 449 postmenopausal women with no prior hysterectomy and mammogram negative within 2 years who were either not hormone users (n = 25 328) or estrogen and progestin users (n = 16 121). Multivariable-adjusted Cox proportional hazard regression was used to calculate hazard ratios (HRs) with 95% confidence intervals (CI). All statistical tests were two-sided.
Results After a mean of 11.3 (SD = 3.1) years, with 2236 breast cancers, incidence was higher in estrogen plus progestin users than in nonusers (0.60% vs 0.42%, annualized rate, respectively; HR = 1.55, 95% CI = 1.41 to 1.70, P < .001). Women initiating hormone therapy closer to menopause had higher breast cancer risk with linear diminishing influence as time from menopause increased (P < .001). Survival after breast cancer, measured from diagnosis, was similar in combined hormone therapy users and nonusers (HR = 1.03, 95% CI = 0.79 to 1.35). On a population basis, there were somewhat more deaths from breast cancer, measured from cohort entry (HR = 1.32, 95% CI = 0.90 to 1.93, P = .15), and more all-cause deaths after breast cancer (HR = 1.65, 95% CI = 1.29 to 2.12, P < .001) in estrogen plus progestin users than in nonusers.
Conclusions Consistent with WHI randomized trial findings, estrogen plus progestin use is associated with increased breast cancer incidence. Because prognosis after diagnosis on combined hormone therapy is similar to that of nonusers, increased breast cancer mortality can be expected.
Could it help patients and researchers estimate the time to FMP?
Predicting the final menstrual period (FMP) would help women know when their menopause transition will be completed. A new model using levels of two hormones may help predict when perimenopausal women will have their final period, researchers reported.
Context: Predicting the final menstrual period (FMP) would help women know when their menopause transition will be completed. Additionally, biological changes, such as accelerated bone loss, precede the FMP by at least 1 year.
Objective: Our objective was to assess whether FSH, estradiol, or urinary N-telopeptide predict where an individual is on her timeline to FMP.
Methods: The sample was 554 women from the Study of Women’s Health Across the Nation. We modeled the probability of having crossed specified landmarks: 2 years before, 1 year before, and the FMP. We also modeled the probability of being in narrower intervals: 2 to1 year before FMP, 2 years before FMP and FMP, or 1 year before FMP and FMP. We determined the candidate markers that best predicted having crossed each landmark, with the optimum defined as the greatest area under the receiver-operator curve; created formulas for the probability of having crossed each landmark; and calculated sensitivity and specificity.
Results: Final models included current estradiol and FSH (each as a fraction of 1 previous reference measure), age, menopause transition stage, race/ethnicity, and whether serum was collected during the early follicular phase. Areas under the receiver-operator curves of final models that predicted the probability of a woman having crossed 2 years before, 1 year before, and the FMP itself were 0.902, 0.926, and 0.945, respectively. If we classified women as having crossed the 2 years before the FMP landmark when predicted probability exceeded 0.3, sensitivity was 85% and specificity 77%.
Conclusion: This model could help patients and researchers estimate the time to FMP.