Phytoestrogens are plant-derived dietary compounds with structural similarity to 17-β-oestradiol (E2), the primary female sex hormone. This structural similarity to E2 enables phytoestrogens to cause (anti)oestrogenic effects by binding to the oestrogen receptors. The aim of the present review is to present a state-of-the-art overview of the potential health effects of dietary phytoestrogens. Various beneficial health effects have been ascribed to phytoestrogens, such as a lowered risk of menopausal symptoms like hot flushes and osteoporosis, lowered risks of cardiovascular disease, obesity, metabolic syndrome and type 2 diabetes, brain function disorders, breast cancer, prostate cancer, bowel cancer and other cancers. In contrast to these beneficial health claims, the (anti)oestrogenic properties of phytoestrogens have also raised concerns since they might act as endocrine disruptors, indicating a potential to cause adverse health effects. The literature overview presented in this paper illustrates that several potential health benefits of phytoestrogens have been reported but that, given the data on potential adverse health effects, the current evidence on these beneficial health effects is not so obvious that they clearly outweigh the possible health risks. Furthermore, the data currently available are not sufficient to support a more refined (semi) quantitative risk–benefit analysis. This implies that a definite conclusion on possible beneficial health effects of phytoestrogens cannot be made.

Linked Articles
This article is part of a themed section on Principles of Pharmacological Research of Nutraceuticals. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v174.11/issuetoc

https://bpspubs.onlinelibrary.wiley.com/doi/pdf/10.1111/bph.13622

The potential health effects of dietary phytoestrogens

The treatment of transsexual subjects is a challenging task for the endocrinologist who, in collaboration with the mental health professional and the surgeon, is called upon to confirm the diagnosis and adjust hormonal treatment aimed at suppressing endogenous sex hormones and to develop hormone characteristics of the desired gender. These guidelines are structured to provide evidence-based suggestions or, where evidence is lacking, expert recommendations on diagnostic procedures and hormonal treatment in adolescent and adult transsexuals, including long-term care and eligibility for surgery. The multidisciplinary approach to treatment, the additional diagnostic role of hormone administration and the need to maintain hormone levels within the physiological range are key suggestions stressed in the guidelines which are particularly important for an endocrinologist unfamiliar with this field. The need for psychological assessment before surgery is not common in many countries and should be stressed further in the guidelines. Some important issues such as time and method of hormone withdrawal before surgery together with when and which hormones should be administered after sex reassignment surgery has been completed also remain unclear. These guidelines represent a pivotal document for endocrinologists setting a standard for the care of transsexuals and providing directions for future research.

/pdf/endocrine-treatment-of-transsexual-persons-an-endocrine-rhup567cwi.pdf

Endocrine treatment of transsexual persons: an Endocrine Society Clinical Practice Guideline: commentary from a European perspective.

Ovarian cancer remains the leading cause of mortality due to gynecological tumors. Estrogen receptors (ERs) seem to participate in tumor progression even in the absence of estrogens. Twenty years after the cloning of the second estrogen receptor, a wide spectrum of studies have shown its implication in both physiologic and pathologic pathways. ERβ, being the predominant type of ER in normal ovary tissue, has not only been linked with pathogenesis of ovarian cancer, but also with response to treatment. Unlike ERα, which is primarily linked with cell growth, ERβ presence is prominent in signaling pathways, cell cycle regulation and apoptosis. Literature review of relevant published material (from PubMed, Scopus, and Cochrane databases) was conducted. Polymorphisms in the respective ESR2 gene, epigenetic modifications and isoforms of the receptor have been extensively studied to assess potential correlations with responsiveness to treatment and tumor behavior. Studies on the exact roles of ERβ and its genetic variations in altering effectiveness and toxicity of ovarian cancer treatment regimens are lacking. Clinical utilization of ERβ actions in the management of ovarian cancer is discussed in an up-to-date review.

Estrogen receptor beta and ovarian cancer: a key to pathogenesis and response to therapy

OBJECTIVE To investigate genetic single nucleotide polymorphisms (SNPs) in estrogen receptor-α (ERα) (ESR1, rs2234693, rs1801132, rs7757956 and rs2813544) and ERβ (ESR2, rs3020450, rs7154455 and rs4986938) genes and relate them to the adverse effects lipodystrophy, dyslipidemia and metabolic syndrome as well as to differences in their prevalence between sexes in HIV-infected individuals on HAART. DESIGN Cross-sectional study. METHODS Blood samples and anthropometric measurements were collected from 614 patients at reference services in the cities of Porto Alegre, Pelotas and Rio Grande in Brazil. The SNPs were genotyped by real-time PCR. RESULTS The lipodystrophy subtype frequencies in patients of different sexes showed statistically significant differences; the atrophic pattern was more prevalent in men, and the hypertrophic pattern was more prevalent in women. Furthermore, metabolic syndrome prevalence was higher in women than in men. The ESR1 rs2813544 G-allele was associated with higher measurements of several anthropometric variables in women: BMI, total subcutaneous fat and subcutaneous fat of limbs. Additionally, patients who were AA homozygous for ESR2 rs3020450 presented an increased risk for developing lipoatrophy (prevalence ratio 1.37, 95% confidence interval 1.09-1.73, P = 0.007). CONCLUSION Significant differences in lipodystrophy and metabolic syndrome prevalence were detected between sexes. Moreover, the ESR1 gene (rs2813544) presented significant sex-specific associations with anthropometric variables, and the ESR2 gene (rs3020450) was associated with an increased risk of developing lipoatrophy. Our results suggest that these genes are in part responsible for the sexual dimorphism in fat tissue redistribution and patterns of lipodystrophy.

Genetic polymorphisms in estrogen receptors and sexual dimorphism in fat redistribution in HIV-infected patients on HAART.

Endometriosis is certainly responsible for many instances of infertility although its physiopathological mechanism is not very clear. Tubal endometriosis can lead to occlusion of the tubes ovarian endometriosis can cause adhesions and peritoneal endometriosis can cause adnexitis. Sterility caused by endometriosis is often secondary while amenorrhea menstrual fever and pain are always present. Clinical medical examinations should be completed by hysterography and celioscopy. Endometriosis can be treated with hormonotherapy: lynestrenol and norethindrone atrophy the endometrium block ovulation and cause persistent amenorrhea. Surgical treatment has benefited enormously from the recent progress in microsurgery; it is now possible not only to resect the unwanted tissue but to reconstitute the healthy one. It would be now reasonable to expect a pregnancy in about 50% of treated cases.

Endometriosis and infertility

Estrogen hormones play critical roles in the regulation of many tissue functions. The effects of estrogens are primarily mediated by the estrogen receptors (ER) alpha and beta. ERs are ligand-activated transcription factors that regulate a complex array of genomic events that orchestrate cellular growth, differentiation and death. Although many factors contribute to their etiology, estrogens are thought to be the primary agents for the development and/or progression of target tissue malignancies. Many of the current modalities for the treatment of estrogen target tissue malignancies are based on agents with diverse pharmacology that alter or prevent ER functions by acting as estrogen competitors. Although these compounds have been successfully used in clinical settings, the efficacy of treatment shows variability. An increasing body of evidence implicates ERalpha polymorphisms as one of the contributory factors for differential responses to estrogen competitors. This review aims to highlight the recent findings on polymorphisms of the lately identified ERbeta in order to provide a functional perspective with potential pharmacogenomic implications.

Do Estrogen Receptor beta Polymorphisms Play A Role in the Pharmacogenetics of Estrogen Signaling

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Do Estrogen Receptor beta Polymorphisms Play A Role in the Pharmacogenetics of Estrogen Signaling