Impact Of Estrogen Therapy Research Articles

Impact of Estrogen Therapy on BRCA1-Associated Breast Cancer Progression in Transgender Women

The combination of hormone treatment and genetic liabilities in transgender women leads to a complicated situation for breast cancer growth particularly linked to BRCA1 mutations. Gender-affirming treatment relies heavily on estrogen and causes intense cell growth and differentiation in breast tissue driven by estrogen receptor mechanisms. Mutations in BRCA1 lead to weak DNA repair processes which enhance an individual's vulnerability to cancerous changes. Rodestrogens enhance the functioning of proliferative pathways like PI3K/AKT and MAPK pathways in cells with dysfunctional BRCA1. This collaborative action elevates the threats posed by benign growths such as fibroadenomas leading to invasive breast cancer. By affecting the expression of vital regulatory proteins linked to cell proliferation estrogen further compromises the genomic integrity in cells harboring BRCA1 mutations. The hormone environment influenced by exogenous estrogen therapy can shape the tumor microenvironment for better cancer progression and metastasis. Comprehending the relationship between estrogen signaling and pathways related to BRCA1 is important for identifying the enhanced risk of cancer in transgender women using hormone therapy. This detailed study aligns recent discoveries regarding genetic vulnerability and hormonal impacts with cell mechanisms to reveal a detailed insight into breast cancer progression in these individuals. The study emphasizes the necessity for custom-designed cancer screening methods and targeted treatments to help mitigate risks and support transgender care. Understanding these pathways greatly enriches our knowledge of hormone-induced carcinogenesis among those who carry certain genetic markers while also guiding the creation of personalized care for transgender women at enhanced risk of breast cancer.

A prospective controlled study of sexual function and sexually related personal distress up to 12 months after premenopausal risk-reducing bilateral salpingo-oophorectomy.

Premenopausal risk-reducing bilateral salpingo-oophorectomy (RRBSO) may impair sexual function, but the nature and degree of impairment and impact of estrogen therapy on sexual function and sexually related personal distress after RRBSO are uncertain. Prospective observational study of 73 premenopausal women at elevated risk of ovarian cancer planning RRBSO and 68 premenopausal controls at population risk of ovarian cancer. Participants completed the Female Sexual Function Index and the Female Sexual Distress Scale-Revised. Change from baseline in sexual function following RRBSO was compared with controls at 12 months according to estrogen therapy use. Baseline sexual function domains did not differ between controls and those who underwent RRBSO and subsequently initiated (56.2%) or did not initiate (43.8%) estrogen therapy. At 12 months, sexual desire and satisfaction were unchanged in the RRBSO group compared with controls. After RRBSO, nonestrogen therapy users demonstrated significant impairment in sexual arousal (β-coefficient (95% confidence interval) -2.53 (-4.86 to -0.19), P < 0.03), lubrication (-3.40 (-5.84 to -0.96), P < 0.006), orgasm (-1.64 (-3.23 to -0.06), P < 0.04), and pain (-2.70 (-4.59 to 0.82), P < 0.005) compared with controls. Although sexually related personal distress may have been more likely after RRBSO, irrespective of estrogen therapy use, there was insufficient data to formally test this effect. The findings suggest premenopausal RRBSO adversely affects several aspects of sexual function which may be mitigated by the use of estrogen therapy. Further research is needed to understand the effects of RRBSO on sexual function and sexually related personal distress, and the potential for estrogen therapy to mitigate against any adverse effects.

Impact of estrogen therapy on temporomandibular joints of rats: Histological and hormone analytical study

ObjectivesThis research aims to evaluate the effects of estrogen deficiency and replacement on the TMJ structures of rats. The considerable similarities in the anatomical features of rats and humans make rats a suitable model for human scientific studies. MethodsA clinical trial was conducted on 18 female Sprague-Dawley rats grouped into three categories. The GI group included 6 female rats labelled as the control group, the GII group consisted of 6 females that received ovariectomies, and the GIII group had 6 ovariectomised females that were injected with estrogen replacement therapy in a science laboratory at King Abdulaziz University. ANOVA and Tukey HSD post hoc tests were used to determine any significant differences between the levels of estrogen among the three groups. ResultsThe results indicate that some TMJ structures, including the articular disc and condylar cartilaginous layer, were degraded after estrogen deficiency. However, there was a slight improvement in the cartilaginous layer thickness and proliferation of chondroid cells after estrogen replacement therapy. Estrogen level was reduced in the ovariectomized rats, and while estrogen injections increased blood hormone levels, the levels did not reach those of the control group. ConclusionEstrogen deficiency degraded some TMJ structures, and there is only a slight recovery after estrogen replacement therapy.

Influence of estrogen therapy on immune markers in postmenopausal women

Objective: To evaluate the impact of estrogen therapy on cellular and humoral immune markers in postmenopausal women.Methods: This prospective, controlled cohort study included 30 patients who used oral estradiol (1 mg) for 14–17 weeks and 28 patients who served as controls. Total leukocytes and leukocyte subtypes were counted and immunophenotyped by flow cytometry. The concentrations of immunoglobulins and pro- and anti-inflammatory cytokines were also measured in the peripheral blood before and after estrogen therapy. Immunoglobulin E level was measured by electrochemiluminescence, and levels of immunoglobulins A, G, and M were measured by nephelometry. Simultaneous quantification of multiple cytokines was performed by chemiluminescence to measure the serum concentrations of interferon gamma, interleukin (IL)-4, IL-6, IL-10, and IL-17.Results: Hematological cellular components were not significantly different before and after the use of estradiol (p = 0.332–0.984). Serum concentrations of immunoglobulins G, M, E, and A also remained stable (p = 0.248–0.845). Finally, cytokines were not modified throughout the 14–17 weeks of follow-up (p = 0.407–0.873).Conclusion: Isolated estrogen therapy with 1 mg of estradiol for 14–17 weeks in postmenopausal women did not modify any of the cellular or humoral immune markers analyzed in this study.

Impact of Estrogen Therapy on Lymphocyte Homeostasis and the Response to Seasonal Influenza Vaccine in Post-Menopausal Women

It is widely recognized that changes in levels of ovarian steroids modulate severity of autoimmune disease and immune function in young adult women. These observations suggest that the loss of ovarian steroids associated with menopause could affect the age-related decline in immune function, known as immune senescence. Therefore, in this study, we determined the impact of menopause and estrogen therapy (ET) on lymphocyte subset frequency as well as the immune response to seasonal influenza vaccine in three different groups: 1) young adult women (regular menstrual cycles, not on hormonal contraception); 2) post-menopausal (at least 2 years) women who are not receiving any form of hormone therapy (HT) and 3) post-menopausal hysterectomized women receiving ET. Although the numbers of circulating CD4 and CD20 B cells were reduced in the post-menopausal group receiving ET, we also detected a better preservation of naïve B cells, decreased CD4 T cell inflammatory cytokine production, and slightly lower circulating levels of the pro-inflammatory cytokine IL-6. Following vaccination, young adult women generated more robust antibody and T cell responses than both post-menopausal groups. Despite similar vaccine responses between the two post-menopausal groups, we observed a direct correlation between plasma 17β estradiol (E2) levels and fold increase in IgG titers within the ET group. These findings suggest that ET affects immune homeostasis and that higher plasma E2 levels may enhance humoral responses in post-menopausal women.

Effects of estrogen therapy on microalbuminuria in healthy post-menopausal women

Objective. To evaluate the impact of estrogen therapy on microalbuminuria levels in healthy post-menopausal women.Methods. Sixty post-menopausal women were evaluated in a prospective, randomised, double-blind, placebo-controlled study. The patients were randomly allocated to one of two groups to take one pill orally per day containing either 1 mg of 17β-estradiol (E2 group) or placebo (placebo group). Prior to initiating treatment and at the end of the sixth treatment month, microalbumin was measured in a 12-h urine sample, and lipid profile (total cholesterol, HDL, LDL and triglycerides) and fasting glucose were evaluated. Comparative intra- and inter-group analyses between the initial and final laboratory parameters were performed using the t-test for paired samples and for independent samples, respectively.Results. Microalbuminuria levels remained within normal limits throughout the study and no statistically significant differences were found in the intra- or inter-group analyses. With respect to lipid profile, alterations characteristically encountered during use of estrogen replacement therapy were found. No statistically significant variation in glucose levels occurred during the study period.Conclusion. Estrogen replacement therapy had no significant effect on microalbuminuria levels in healthy post-menopausal patients.

Impact of estrogen therapy on Alzheimer's disease: a fork in the road?

The results of recent clinical studies have challenged our previously held view that estrogen therapy promotes neurological health and prevents or ameliorates Alzheimer's disease. A major question emerging from these studies is: how can there be such disparity between the basic science and epidemiological data that show that estrogen can protect neurons against degenerative insults and reduce the risk of Alzheimer's disease and the recent data (from the Women's Health Initiative Memory Study [WHIMS] trial and the trial of estrogen treatment for Alzheimer's disease), which show that hormone replacement therapy (HRT) showed no benefit and even a potential deleterious effect? Which set of data is correct? The proposition put forth in this review is that both sets of data are correct and that two major factors determine the efficacy of estrogen or HRT. First is the time at which estrogen therapy is initiated. The data indicate that initiation of therapy early in menopause and when neurons are in a healthy state, reduces the risk of Alzheimer's disease; whereas, estrogen therapy initiated after the disease has developed or decades following menopause is without benefit. Second, estrogen therapy is not the same as HRT and the type of progestogen used determines the outcome of the therapeutic intervention. Insights into the mechanisms of action of estrogen and progestogen in the brain provide a framework for understanding the paradox of the benefit of estrogen in the prevention of Alzheimer's disease versus the lack of benefit in treatment trials and in trials when HRT is instituted many years after menopause. Based on estrogen-inducible mechanisms, which have been elucidated in healthy neuron model systems, it would be predicted that estrogen therapy could be highly effective in preventing neurodegenerative disease by promoting neuronal defence and memory mechanisms. The mechanisms of action of estrogen also predict that estrogen therapy would be an ineffective strategy for reversing the pathology of Alzheimer's disease. In summary, the time at which estrogen therapy is initiated, the neurological status of the brain at the time of estrogen therapy initiation and the type of progestogen used all contribute to the efficacy of estrogen in preventing neurodegenerative disease and to sustaining neurological health and function. An estrogen advantage hypothesis is put forth that provides a unifying mechanism of estrogen action with implications for both the benefits and risks of estrogen therapy.