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The cyclical changes in sex hormones across the menstrual cycle (MC) are associated with various biological changes that may alter resting metabolic rate (RMR) and body composition estimates. Hormonal contraceptive (HC) use must also be considered given their impact on endogenous sex hormone concentrations and synchronous exogenous profiles. The purpose of this study was to determine if RMR and dual-energy X-ray absorptiometry body composition estimates change across the MC and differ compared with HC users. This was accomplished during a 5-week training camp involving naturally cycling athletes (n = 11) and HC users (n = 7 subdermal progestin implant, n = 4 combined monophasic oral contraceptive pill, n = 1 injection) from the National Rugby League Indigenous Women's Academy. MC phase was retrospectively confirmed via serum estradiol and progesterone concentrations and a positive ovulation test. HC users had serum estradiol and progesterone concentrations assessed at the time point of testing. Results were analyzed using general linear mixed model. There was no effect of MC phase on absolute RMR (p =.877), relative RMR (p =.957), or dual-energy X-ray absorptiometry body composition estimates (p >.05). There was no effect of HC use on absolute RMR (p =.069), relative RMR (p =.679), or fat mass estimates (p =.766), but HC users had a greater fat-free mass and lean body mass than naturally cycling athletes (p =.028). Our findings suggest that RMR and dual-energy X-ray absorptiometry body composition estimates do not significantly differ due to changes in sex hormones in a group of athletes, and measurements can be compared between MC phases or with HC usage without variations in sex hormones causing additional noise. [ABSTRACT FROM AUTHOR]

Background: Sex differences exist in type 2 diabetes (T2D), and androgens have been implicated in the etiology of T2D in a sex-specific manner. We therefore aimed to investigate whether androgens play a role in explaining sex differences in glucose homeostasis and incidence of T2D. Methods: We used observational data from the German population-based KORA F4 study (n = 1975, mean age: 54 years, 41% women) and its follow-up examination KORA FF4 (median follow-up 6.5 years, n = 1412). T2D was determined through self-reporting and confirmed by contacting the physicians and/or reviewing the medical charts. Multivariable linear and logistic regression models were employed to explore associations. Mediation analyses were performed to assess direct effects (DE) and indirect effects (IE), and the mediating role of androgens (total testosterone (TT), dehydroepiandrosterone (DHEA), dehydroepiandrosterone-sulfate (DHEAs)) in the association between sex (women vs. men) and glucose- and insulin-related traits (cross-sectional analysis) and incidence of T2D (longitudinal analysis). Results: After adjustment for confounders, (model 1: adjusted for age; model 2: model 1 + smoking + alcohol consumption + physical activity), women had lower levels of TT, DHEAs, fasting glucose levels, fasting insulin levels, 2 h-glucose levels and HOMA-IR, compared to men. An inverse association was observed for TT and glucose- and insulin-related traits in men, while a positive association was observed for TT and fasting glucose levels in women. We found a mediatory role of TT on the association of sex with fasting glucose levels (IE: β = 3.08, 95% CI: 2.04, 4.30), fasting insulin levels (IE: β = 0.39, 95% CI:0.30, 0.47), 2 h-glucose levels (IE: β = 12.77, 95% CI: 9.01, 16.03) and HOMA-IR (IE: β = 0.41, 95% CI: 0.33, 0.50). Also, the inconsistent mediatory role of TT was seen on the association of sex with incidence of T2D (DE: 0.12, 95% CI: 0.06, 0.20 and IE: OR = 7.60, 95% CI: 3.43, 24.54). The opposing DE and IE estimates suggest that the association between sex and either glucose homeostasis or the incidence of T2D may differ when TT is considered as a potential mediator, with higher TT levels being beneficial for glucose metabolism or incidence of T2D in men, while in women, detrimental. No mediatory role was observed for either DHEA or DHEAs on glucose homeostasis or the incidence of T2D. Conclusions: The dimorphic mediatory role of TT highlights its complex role in metabolic health, contributing differently to the glucose dysregulation and risk of T2D in men and women. [ABSTRACT FROM AUTHOR]

ABSTRACT Introduction Methods Results Conclusion There is evidence that alcohol consumption is influenced by prenatal sex steroids (as measured by digit ratio [2D:4D]). Here, we clarify the effect size of the relationship in a student (rather than a patient) population.There were 258 (169 women) participants. Digit length was measured directly with calipers. Alcohol use was evaluated by the Polish version of Alcohol Use Disorders Identification Test (AUDIT) and operationalized as total AUDIT scores and grams of alcohol/week.Digit ratios were sexually dimorphic (males < females). There were negative correlations between right 2D:4D and Dr‐l (right 2D:4D minus left 2D:4D) and AUDIT scores and grams of alcohol/week in both sexes. Relationships varied from small (r = −0.29) to large (r = −0.69) and they were stronger in males in comparison to females and for right 2D:4D in comparison to Dr‐l. In males only, there were small (r = 0.21) to moderate (r = 0.31) positive associations with body size (height, weight, and mean right digit length) and alcohol consumption. Multiple regression analyses showed relationships between digit ratios remained significant but those for body size did not.Alcohol consumption was negatively related to 2D:4D, suggesting high prenatal testosterone and low prenatal estrogen are linked to its consumption. Correlations varied in strength from small to large with the strongest found for right 2D:4D and for males. Positive relationships between body size and alcohol were small to moderate, confined to males, and were not independent of digit ratios. Prenatal androgenization may influence alcohol drinking patterns in non‐clinical individuals. [ABSTRACT FROM AUTHOR]

Vascular dysfunction, marked by lower endothelial function and increased aortic stiffness, is a nontraditional risk factor that precedes the development of cardiovascular disease (CVD). However, the age at which these changes in vascular function occur in women and the degree to which reproductive hormones mediate these changes has not been characterized. Women free from major disease were enrolled across the adult life span (aged 18–70 yr, n = 140). Endothelial function was assessed as flow-mediated dilation (FMD) of the brachial artery during reactive hyperemia using duplex ultrasound and expressed as percent dilation. Aortic stiffness was measured by carotid-femoral pulse wave velocity (cfPWV). Blood samples were obtained to quantify reproductive hormone concentration. Regression models determined age-related breakpoints and mediating factors between age and vascular outcomes. FMD declined with age with a breakpoint and steeper decline occurring at 47 yr of age. Thereafter, age was independently associated with lower FMD (B = −0.13, P < 0.001). cfPWV was relatively stable until a breakpoint at age 48, and age was independently associated with higher cfPWV thereafter (B = 0.10, P < 0.001). Path analysis revealed that the association between age and FMD was partially mediated by follicle-stimulating hormone (abind = 0.051, P = 0.01) and progesterone (abind = 0.513, P < 0.001) but not estradiol (abind = −0.004, P = 0.08). No mediation was present for cfPWV. Age was associated with endothelial dysfunction and aortic stiffness in women beginning at 47 and 48 yr old, respectively, 3 to 4 yr before the average age of menopause. The association between age and endothelial dysfunction was explained in part by elevations in follicle-stimulating hormone and progesterone, but not declining estradiol. NEW & NOTEWORTHY: We demonstrate that the age at which endothelial function declines and aortic stiffness increases in healthy women is 47 and 48, respectively. The inflection point in flow-mediated dilation (FMD) is 6 yr earlier than previously reported, and the association between age and FMD was mediated by follicle-stimulating hormone (FSH) and progesterone (P4) but not estradiol (E2). [ABSTRACT FROM AUTHOR]

The determination of age‐related transcriptional changes may contribute to the understanding of health and life expectancy. The broad application of results from age cohorts may have limitations. Altering sample sizes per time point or sex, using a single mouse strain or tissue, a limited number of replicates, or omitting the middle of life can bias the surveys. To achieve higher general validity and to identify less distinctive players, bulk RNA sequencing of a mouse cohort, including seven organs of two strains from both sexes of 5 ages, was performed. Machine learning by bootstrapped variable importance and selection methodology (Boruta) was used to identify common aging features where the circadian rhythms (CiR) transcripts appear as promising age markers in an unsupervised analysis. Pathways of 11 numerically analyzed local network clusters were affected and classified into four major gene expression profiles, whereby CiR and proteostasis candidates were particularly conspicuous with partially opposing changes. In a data‐based interaction association network, the CiR‐proteostasis axis occupies an exposed central position, highlighting its relevance. The computation of 11,830 individual transcript associations provides potential superordinate contributors, such as hormones, to age‐related changes, as in CiR. In hormone‐sensitive LNCaP cells, short‐term supraphysiologic levels of the sex hormones dihydrotestosterone or estradiol increase the expression of the CiR transcript Bhlhe40 and the associated senescence regulator Cdkn2b (p15). According to these findings, the bilateral dysregulation of CiR appears as a fundamental protagonist of aging, whose transcripts could serve as a biological marker and its restoration as a therapeutic opportunity. [ABSTRACT FROM AUTHOR]

Objectives: People with HIV are at increased risk for metabolic dysfunction‐associated steatohepatitis (MASH). Although sex differences are documented in the general population, their role in the context of HIV is less understood. Methods: This was a multicentre cohort study including people with HIV without viral hepatitis coinfection. A FibroScan‐AST (FAST) score >0.35 was used to diagnose MASH with significant liver fibrosis (stage F2–F4). We investigated sex‐based differences in MASH trends as a function of age using a segmented linear mixed‐effects model. Random effects accounted for clustering by the four sites. Adjusted models included ethnicity, diabetes, hypertension, and detectable HIV viral load. Results: We included 1472 people with HIV (25% women). At baseline, the prevalence of MASH with fibrosis by FAST score was lower in women than in men (4.8% vs. 9.2%, p = 0.008). Based on the adjusted model, male sex (+0.034; p = 0.04), age per year (+0.003; p = 0.05), detectable HIV viral load (+0.034; p = 0.02), and hypertension (+0.03; p = 0.01) were positively associated with MASH with fibrosis. Although men exhibited generally higher FAST scores, FAST scores increased in women during the critical biological age of presumed perimenopause to menopause (between 40 and 50 years), reaching levels similar to those in men by the age of 55 years. Conclusion: Despite women with HIV having a lower prevalence of MASH with fibrosis than men, they exhibit an acceleration in FAST score increase around the perimenopausal age. Future studies should target adequate consideration of sex differences in clinical investigation of metabolic dysfunction‐associated steatotic liver disease to fill current gaps and implement precision medicine for people with HIV. [ABSTRACT FROM AUTHOR]

Neurotensin (NT) is a peptide involved in digestion, neuromodulation, and cancer progression. NT and its receptors (NTR1 and SORT1 mainly) have been widely studied in oncology. Data show that NT expression is under the control of sex steroid hormones, in particular estradiol. We focused on its involvement in three main female hormone-sensitive cancers, breast, ovarian, and endometrial cancer, in a narrative review. NT, NTR1, and SORT1 are mostly expressed in these three cancers, and their involvement in oncologic processes such as proliferation and invasion seems to match, as does their impact on prognosis for most. The development of NT receptor-targeted therapies, including theranostics and radioligand treatments, presents a promising avenue for personalized cancer treatment. [ABSTRACT FROM AUTHOR]

Objectives: Second to fourth digit ratio is widely known indicator of prenatal sex hormones proportion. Higher prenatal androgenization results in longer fourth finger and lower 2D:4D index. The aim of this study was to determine whether the 2D:4D digit ratio is associated with DNA methylation (DNAm) age dependently on sex. Material and Methods: The study included 182 adults (106 females and 76 males) with a mean age of 51.5 ± 13 years. The investigation consisted of three main parts: a survey, anthropometric dimensions measurements (fingers length) and methylome analysis using collected blood samples. Genome‐wide methylation was analyzed using EPIC microarray technology. Epigenetic age and epigenetic age acceleration were calculated using several widely applied algorithms. Results: Males with the female left hand pattern had more accelerated epigenetic age than those with the male pattern as calculated with PhenoAge and DNAmTL clocks. Conclusions: Finger female pattern 2D:4D above or equal to 1 in males is associated with epigenetic age acceleration, indicating that prenatal exposure to estrogens in males may be related to aging process in the later ontogenesis. [ABSTRACT FROM AUTHOR]

Introduction: Despite the growing awareness of sexual dimorphism between males and females under pathological and physiological conditions, sex bias in biomedical research in animal models and patients is still present nowadays. The main objective of this work was to investigate sex differences in constitutive long non‐coding RNA expression in spinal cord and skeletal muscle from wild‐type mice. Materials and Methods: To assess the influence of gender on long non‐coding RNAs, we extracted RNA from tissues of male and female mice and analyzed the expression on nine long non‐coding RNAs, selected for being among the most commonly studied or exerting an important role in muscle, at 50, 60, and 120 days of age. Results and Discussion: We observed age‐ and tissue‐dependent significant sex differences, being more prominent in skeletal muscle. We also studied the effect of sex steroid hormones on long non‐coding RNA expression in vitro, noticing a modulation of long non‐coding RNA levels upon estradiol and dihydrotestosterone treatment in muscle. Conclusions: Taken together, results obtained evidenced sex differences on constitutive long non‐coding RNA expression and suggested an influence of steroid hormones complementary to other possible factors. These findings emphasize the importance of including both sexes in experimental design to minimize any potential sex bias. [ABSTRACT FROM AUTHOR]

Background: Erectile dysfunction has been associated with leisure sedentary behavior in several epidemiological and observational studies. However, the interpretation of these findings is difficult due to residual confounding or reverse causality. Objectives: To explore the causal association between leisure sedentary behavior and erectile dysfunction, and to explore the underlying mechanism using Mendelian randomization. Materials and methods: In the present study, publicly available large‐scale genome‐wide association studies of leisure sedentary behaviors (television watching, computer use, and driving), erectile dysfunction, sex hormones (total testosterone, bioactive testosterone, estradiol, follicle‐stimulating hormone, luteinizing hormone, prolactin, and sex hormone binding globulin), biomarkers of endothelial function (C reactive protein, E‐selectin, and matrix metalloproteinase 7), and psychiatric symptoms (depression and anxiety) were used to perform two‐sample Mendelian randomization analyses. The inverse variance weighting method was the main method used to estimate the association, and sensitivity analyses were also performed. Results: A greater risk of erectile dysfunction was significantly associated with a higher genetic susceptibility to leisure computer usage (odds ratio = 3.57; 95% confidence interval = 1.78–7.16; p < 0.001). No evidence was obtained to suggest that watching television or driving for leisure increased the risk of erectile dysfunction. No association was found between computer use and depression, anxiety, C reactive protein, E‐selectin, matrix metalloproteinase 7, or other sex hormones, with the exception of follicle‐stimulating hormone levels (odds ratio = 0.29; 95% confidence interval = 0.12–0.69; p = 0.01). No indication of heterogeneity or pleiotropy was identified by sensitivity analysis. Discussion: Extended computer usage for leisure raised the likelihood of developing erectile dysfunction, which may be associated to lower follicle‐stimulating hormone levels; however, the role of endothelial dysfunction and psychological disorders in the development of erectile dysfunction should not be underestimated. Moderate physical activity may help to correct the dysfunction. Conclusion: The present study offered substantial evidence for a positive causal association between computer use and the risk of erectile dysfunction. However, a definitive causal association needs to be established by further research. [ABSTRACT FROM AUTHOR]

Background: Testosterone plays a vital role in maintaining tissue homeostasis, and testosterone deficiency may potentially influence the likelihood of urethral stricture recurrence. Objectives: To evaluate the prognostic value of testosterone levels in the recurrence after direct visual internal urethrotomy in primary short segment bulbar urethral strictures and its clinical reflections. Materials and methods: A total of 723 patients who underwent direct vision internal urethrotomy between January 2000 and October 2022 were retrospectively analyzed. After implying exclusion criteria, 116 patients with available data were enrolled. Patients were divided into two groups as recurrence and no recurrence. Age, stricture length, etiology, time of recurrence, diagnosis of previous diabetes mellitus, hypertension, smoking, body mass index, and total testosterone levels were recorded. Free testosterone and bioavailable testosterone values were calculated using total testosterone, albumin, and sex hormone binding globulin values. Hypogonadism was considered as a total testosterone level less than 300 ng/dL. Demographic characteristics and total testosterone, free testosterone, and bioavailable testosterone levels were compared between the two groups for statistical significance. The recurrence rates of patients with and without hypogonadism were compared. Results: Recurrence was observed in 41.4% of the cases (n = 48). There was no statistically significant difference between the groups in terms of age, body mass index values, diabetes mellitus, hypertension, smoking status, presence of hypogonadism, and etiology (p = 0.745, 0.863, 0.621, 0.622, 0.168, 0.051, and 0.232). In terms of total testosterone levels and bioavailable testosterone levels, the recurrence group had significantly lower values (p = 0.018 and 0.04). There was no significant difference between the two groups in terms of stricture length (p = 0.071). Sixteen of 28 patients with hypogonadism had recurrence, whereas 32 of 88 patients without hypogonadism had recurrence (p = 0.051). Discussion: Testosterone levels have potential to predict recurrence in primary short‐segment bulbar urethral strictures. This study represents the inaugural analysis of the impact of testosterone deficiency on recurrence within the cohort of patients with primary short‐segment bulbar urethral strictures. Conclusion: Testosterone levels and ratios may serve as predictive factors for identifying recurrent cases in primary short‐segment bulbar strictures. For patients at a higher risk of recurrence, urethroplasty may be considered as an initial treatment option, even in cases of primary and short‐segment strictures. [ABSTRACT FROM AUTHOR]

Protogyny, being capable of changing from female to male during their lifetime, is prevalent in 20 families of teleosts but is believed to have evolved within specific evolutionary lineages. Therefore, shared regulatory factors governing the sex change process are expected to be conserved across protogynous fishes. However, a comprehensive understanding of this mechanism remains elusive. To identify these factors, we conducted a meta‐analysis using gonadal transcriptome data from seven species. We curated data pairs of ovarian tissue and transitional gonad, and employed ratios of expression level as a unified criterion for differential expression, enabling a meta‐analysis across species. Our approach revealed that classical sex change‐related genes exhibited differential expression levels between the ovary and transitional gonads, consistent with previous reports. These results validate our methodology's robustness. Additionally, we identified novel genes not previously linked to gonadal sex change in fish. Notably, changes in the expression levels of acetoacetyl‐CoA synthetase and apolipoprotein Eb, which are involved in cholesterol synthesis and transport, respectively, suggest that the levels of cholesterol, a precursor of steroid hormones crucial for sex change, are decreased upon sex change onset in the gonads. This implies a potential universal influence of cholesterol dynamics on gonadal transformation in protogyny. [ABSTRACT FROM AUTHOR]

The effects of androgens on women's bone health are not fully understood. Mendelian randomization (MR) studies using sex-combined data suggest that sex hormone-binding globulin (SHBG) and bioavailable testosterone (BioT) causally affect bone traits. Given significant sex differences in hormone regulation and effects, female-specific MR studies are necessary. In the current study, we explored the causal relationships of SHBG, BioT, and total testosterone (TT) with forearm fracture (FAFx) risk in women using two-sample MR analyses. We utilized a unique female-specific FAFx outcome dataset from three European biobanks (UFO, HUNT, Estonian Biobank) comprising 111,351 women and 8823 FAFx cases, along with female-specific genetic instruments of SHBG, BioT, and TT identified in the UK Biobank. We also assessed bone mineral density (BMD) at the forearm (FA), femoral neck (FN), and lumbar spine (LS) using female-specific GWAS data from the GEFOS consortium. High SHBG (odds ratio per standard deviation increase (OR/SD): 1.53, 95% confidence intervals (CIs): 1.34–1.75), low BioT (OR/SD: 0.77, 0.71–0.84) and low TT (OR/SD 0.90, 0.83–0.98) were causally associated with increased FAFx risk. BioT was positively, and SHBG inversely, causally associated with especially FA-BMD, but also LS-BMD and FN-BMD, while TT was only significantly positively associated with FA-BMD and LS-BMD. We propose that endogenous androgens and SHBG are important for women's bone health at distal trabecular-rich bone sites such as the distal forearm and may serve as predictors for FAFx risk. [ABSTRACT FROM AUTHOR]

Objective: To investigate the correlations of cognitive function with serum levels of homocysteine (Hcy), sex hormone binding globulin (SHBG), and leptin in patients with schizophrenia. Methods: This was retrospective study. This study included 58 patients with schizophrenia (SCZ) as observation group and 60 clinically healthy individuals as control group admitted to Xiangshan County Hospital of Traditional Chinese Medicine Medical and Health Group Third Hospital from March 2022 to June 2023. Serum levels of Hcy, SHBG, and leptin in the two groups were measured, and Pearson correlation analysis was conducted to investigate the correlations between the Hcy, SHBG, and leptin levels and the psychiatric symptoms and cognitive function in the observation group. Results: The Hcy and SHBG levels in the observation group were significantly higher than those in the control group (p<0.05, respectively), and the leptin level was lower than that in the control group (p<0.05). The observation group scored significantly lower than the control group for each dimension of the MCCB (p<0.05, respectively). In the observation group, Hcy was positively correlated with negative symptoms and the PANSS total score (p<0.05, respectively) and was negatively correlated with scores for the leptin was negatively correlated with negative symptoms and the PANSS total score (p<0.05, respectively) and was positively correlated with scores for speed of processing (SOP), WMS-III, BVMT, and MSCEIT (p<0.05, respectively). Conclusions: Increased levels of Hcy and SHBG and decreased leptin are strongly associated with the occurrence of cognitive impairment in SCZ cases. Therefore, clinical observation and monitoring of these markers can help identify changes in patient conditions. [ABSTRACT FROM AUTHOR]

This series of three articles will explore the fundamentals related to anatomy, physiology and pathophysiology in relation to three important topics: the cardiac system, the respiratory system and the endocrine system. The series is intended to provide an informative and evidence-based summary of each topic for both students and clinicians. This third and final paper explores the maternal endocrine system, outlining the key physiological adaptations in pregnancy and summarising the key pathophysiological conditions that may occur. [ABSTRACT FROM AUTHOR]

Introduction: Female hormones and obesity have an impact on women with asthma. We aimed to describe how these components affect asthma inflammatory processes. Methods: Sex hormones [FSH, LH, estradiol (E2), estrone (E1), testosterone and Δ4 androstenedione (A4)] and serum IL1β, IL13, IL17a, IL-5, IL6, TNF-a were measured from 11 to18 pre- and postmenopausal women with asthma. Results: Premenopausal normal weight women revealed higher levels of IL5 and IL17a than obese women on both days of the menstrual cycle (IL5: D1: 6.4 vs 1.4 pg/ml, p =.036 and D14: 3 vs 1.4 pg/ml, p =.045 and IL17a: D1: 13.7 pg/ml vs 10.6 pg/ml and D14: 12.4 pg/ml vs 10.6 pg/ml, p =.009, respectively). In premenopausal women on D1, Δ4 Androstenedione was positively correlated with IL1β (p =.016, r = 0.733), whereas on D14, Estradiol with IL1β (p =.009, r = −.768) and TNF-a with Testosterone (p =.004, r = −0.816), and Δ4 Androstenedione (p =.002, r = −0.841) negatively. In postmenopausal women, TNF-a was negatively associated with FSH (p =.004, r = −0.638), but positively with Testosterone (p =.025, r = 0.526) and IL10 also positively with Estradiol (p =.007, r = 0.610). Conclusion: Obesity shows a protective role in asthma through the suppression of IL5 and IL17. Estrogens seem to inhibit Th1 and Th2 inflammation, while androgens have a dual role with negative and positive correlations with neutrophilic biomarkers. [ABSTRACT FROM AUTHOR]

A unique interplay between body and environment embeds and reflects host–microbiome interactions that contribute to sex‐differential disease susceptibility, symptomatology, and treatment outcomes. These differences derive from individual biological factors, such as sex hormone action, sex‐divergent immune processes, X‐linked gene dosage effects, and epigenetics, as well as from their interaction across the lifespan. The gut microbiome is increasingly recognized as a moderator of several body systems that are thus impacted by its function and composition. In humans, biological sex components further interact with gender‐specific exposures such as dietary preferences, stressors, and life experiences to form a complex whole, requiring innovative methodologies to disentangle. Here, we summarize current knowledge of the interactions among sex hormones, gut microbiota, immune system, and vascular health and their relevance for sex‐differential epidemiology of cardiovascular diseases. We outline clinical implications, identify knowledge gaps, and place emphasis on required future studies to address these gaps. In addition, we provide an overview of the caveats associated with conducting cardiovascular research that require consideration of sex/gender differences. While previous work has inspected several of these components separately, here we call attention to further translational utility of a combined perspective from cardiovascular translational research, gender medicine, and microbiome systems biology. [ABSTRACT FROM AUTHOR]

Sustained release microspheres loaded with goserelin are regarded as a promising candidate for treating prostate cancer and other sex hormone diseases. However, their widespread adoption has been hindered by issues such as wide particle size distribution and unstable release characteristics. To address these challenges, we employed a combination of the solid-in-oil-in-water microspheres preparation approach (S/O/W) and innovative premix membrane emulsification technology and deeply investigated the effects of four key parameters on the loaded performance of microspheres and the microscopic mechanisms behind them. With this approach, we successfully produced goserelin-loaded sustained release microspheres of narrow particle size distribution (Span 0.642), remarkable encapsulation efficiency (DL = 4.23 %, EE = 93.98 %), low initial burst release (about 0.50 % within 2 h), and compatibility with small injection needles (23-G, inner diameter 0.33 mm, outer diameter 0.64 mm, maximal force 59 N). In the animal model(administered dose, 2.4 mg·Kg−1), goserelin long-acting sustained release microspheres sustained release for over 32 days, maintaining effective concentrations above 2 ng·mL−1, and effectively reduced serum testosterone concentrations to castration levels (<1.0 ng·mL−1) by day 4, maintaining this inhibition for up to 21 days, exhibiting comparable efficacy to the positive control group. In vivo release kinetics analysis revealed that goserelin-loaded sustained release microspheres exhibited a release pattern dominated by diffusion with corrosion assistance in vivo. In summary, the systematic and comprehensive evaluation of uniform-sized goserelin-loaded sustained release microspheres has highlighted their excellent translational potential, and the study herein may provide new strategies and ideas for the development of microsphere dosage forms. [Display omitted] • Developed uniform-sized goserelin microspheres (GOS-M) with high encapsulation efficiency. • Achieved low initial burst release and sustained release for over 32 days in vivo. • Uniform-sized GOS-M adapted to 23-G needles, ideal for low-pain administration. • Offers New strategies for microsphere release regulation and prescription screening. [ABSTRACT FROM AUTHOR]

Background: Burning mouth syndrome (BMS) is a chronic pain condition affecting the oral cavity. This condition mostly affects peri‐ or postmenopausal women; for this reason, sexual hormonal changes have been implicated in BMS pathogenesis. Methods: A systematic review was performed in MEDLINE/PubMed, Scopus, Web of Science, Cochrane Library and EMBASE without restriction for language or year. Eligibility criteria were controlled studies addressing the PICO question: (P) patients with BMS; (I) detection of the sex hormones; (C) patients without BMS; (O) changes on sexual hormones as a risk factor for BMS severity. Risk of bias was performed with Newcastle‐Ottawa Quality Assessment Scale. Results: Four studies were included. Salivary levels were evaluated in three studies and serum blood was used in one. Three studies analysed oestradiol and/or dehydroepiandrosterone (DHEA), two assessed progesterone and one evaluated follicle‐stimulating hormone (FSH). Oestradiol results were contradictory, with two studies reporting lower levels in BMS patients compared to controls and one finding the opposite. DHEA was statistically lower in the BMS group in one study. Progesterone showed opposite results in two studies, although none with statistical significance. FSH was statistically higher in the BMS group compared to controls. Correlation of hormones with quality of life was performed in three studies and there was no significant correlation with self‐perceived symptoms severity. Conclusion: Sexual hormones can be altered in BMS, especially oestradiol. Despite these changes, we did not find correlation between hormone fluctuation and BMS symptoms intensity affecting quality of life. These findings suggested the need for further investigation on hormonal alterations, which may be a promising target on BMS management. [ABSTRACT FROM AUTHOR]

The article examines the unnecessary routine endocrinologic evaluations for adolescent boys with gynecomastia. Topics discussed include the various causes of gynecomastia in this age group, the low incidence of pathological conditions underlying the condition, and the potential benefits of reducing healthcare costs and alleviating patient and parental anxiety by minimizing unnecessary referrals and testing.

Air pollution exposure is ranked as a leading environmental risk factor for not only cardiopulmonary diseases but also for systemic health ailments including diabetes, reproductive abnormalities, and neuropsychiatric disorders, likely mediated by central neural stress mechanisms. Current experimental evidence links many air pollution health outcomes with activation of neuroendocrine sympathetic-adrenal-medullary and hypothalamic–pituitary–adrenal (HPA) stress axes associated with resultant increases in adrenal-derived hormone levels acting as circulating mediators of multi-organ stress reactions. Epidemiological and experimental investigations also demonstrated sex-specific responses to air pollutant inhalation, which may be attributed to hormonal interactions within the stress and reproductive axes. Sex hormones (androgens and estrogens) interact with neuroendocrine functions to influence hypothalamic responses, subsequently augmenting stress-mediated metabolic and immune changes. These neurohormonal interactions may contribute to innate sex-specific responses to inhaled irritants, inducing differing individual susceptibility. The aim of this review was to: (1) examine neuroendocrine co-regulation of the HPA axis by gonadal hormones, (2) provide experimental evidence demonstrating sex-specific respiratory and systemic effects attributed to air pollutant inhalation exposure, and (3) postulate proposed mechanisms of stress and sex hormone interactions during air pollution-related stress. Highlights: Air pollution exposure responses are co-regulated by stress and sex hormones Hypothalamic and CNS stress reactions are sensitive to sex hormones Estrogen and testosterone influence HPA axis induction and glucocorticoid dynamics Neuroendocrine axes interactions mediate sex-specific air pollutant health effects [ABSTRACT FROM AUTHOR]

Polycystic Ovary Syndrome (PCOS) is a complex endocrine disorder that affects women at various stages of life, presenting a wide range of symptoms and health implications. The term "Polycystic Ovary Syndrome" can be misleading, prompting many within the medical community and advocacy groups to advocate for a name change. Critics argue that this terminology can complicate understanding and awareness of the disease among patients. The primary concern is that PCOS emphasizes the ovarian aspect, fostering the misconception that PCOS is merely a gynecological disorder. In reality, PCOS impacts multiple organ systems, particularly metabolic health. Patients frequently experience insulin resistance, weight gain, irregular menstrual cycles, and hirsutism—symptoms that extend beyond ovarian dysfunction. In light of these issues, there is increasing support for renaming PCOS to better reflect its systemic implications and minimize confusion. The current name may hinder understanding and potentially lead to inadequate disease management. Alternative names have been proposed, including "Ovarian Dysmetabolic Syndrome," which our team supports, as well as "Metabolic Reproductive Syndrome" and "Hyperandrogenic Persistent Ovulatory Dysfunction Syndrome." These alternatives aim to highlight the hormonal imbalances and metabolic disturbances associated with the condition, fostering inclusivity and reducing stigma for all affected individuals. This narrative review provides a historical overview of PCOS, tracing its recognition from early descriptions to contemporary guidelines. We discuss the evolving understanding of its pathophysiology and the rationale behind the proposed name change. By adopting a new nomenclature, we can enhance understanding among healthcare professionals, increase inclusivity for affected women, reduce the stigma and anxiety linked to the diagnosis, and offer a more accurate representation of the condition's complex pathophysiology. Plain Language Summary: Changing the name "Polycystic Ovary Syndrome" to better reflect the underlying biological mechanisms of the condition Polycystic Ovary Syndrome (PCOS) is a complicated hormone disorder that causes a variety of symptoms and health problems. However, the name "Polycystic Ovary Syndrome" has been criticized by doctors and advocacy groups for being misleading. They argue that the name focuses too much on the ovaries, which might make people think PCOS is only a gynecological issue. The main reason for considering a name change is to better represent the full range of health issues associated with PCOS. For example, "Hyperandrogenic Anovulation" or "Metabolic Reproductive Syndrome" have been suggested as new names. These alternatives aim to highlight the hormonal and metabolic aspects of PCOS, helping to reduce stigma and making the condition easier to understand for everyone affected. In this review, we look at the history of PCOS, how our understanding of its causes has changed over time, and the reasons for wanting to change its name. We also discuss different new names that have been suggested. Changing the name could help doctors and patients better understand the condition and make it more inclusive for all women who have it. [ABSTRACT FROM AUTHOR]

ABSTRACT Objective Design Patients Measurements Results Conclusion Basal metabolic rate (BMR) is an important factor in weight management and is influenced by fat‐free mass (FFM), fat mass (FM) and age. Current knowledge of the influence of hormonal levels on BMR is based on studies with small populations, studies that investigate exogenous administration and studies frequently lacking correction for body composition.Cross‐sectional study.All men (n = 457) who were referred to our centre for a metabolic work‐up were eligible for inclusion. Median age was 47 (18–78) years and the vast majority had obesity (BMI ≥ 30 kg/m², 90.9%).All men had a measurement of BMR, body composition and measurement of testosterone, sex hormone binding globulin (SHBG), dehydroepiandrosterone sulphate (DHEAS), insulin‐like growth factor 1 (IGF‐1), thyroid‐stimulating hormone (TSH) and free thyroxine (fT4). Men with low, normal and/or high levels of each of these hormones were compared. The association between hormone levels and BMR was assessed through linear regression models. All analyses were controlled for FFM, FM and age.In men with obesity, testosterone (total or free) was not associated with BMR. Linear regression analysis showed that DHEAS was positively associated with BMR in a sample of men with obesity and normal endogenous DHEAS levels, with the following equation: BMR (adjusted R² = 0.72): (BMR [kcal/d] = 513.402 + 18.940 × FFM [kg] + 9.507 × FM [kg] − 3.362 × age [years] + 0.307 × DHEAS [µg/dL]) (p < 0.01). TSH, fT4 and IGF‐1 were not associated with BMR.In men with obesity, endogenous DHEAS is positively associated with BMR. Testosterone, TSH, fT4 and IGF‐1 were not associated with BMR in men with obesity. Since we examined the specific population of men with obesity and only examined endogenous hormone levels, no extrapolation of results to other populations or the overall population can be made. [ABSTRACT FROM AUTHOR]

Background: Male sex has been identified as a risk factor for worse COVID-19 outcomes. This sex difference has been mostly attributed to the complex role of sex hormones. Cell surface entry of SARS-CoV-2 is mediated by the transmembrane protease serine 2 (TMPRSS2) which is under transcriptional regulation by androgens. P450 aromatase enzyme converts androgens to estrogens. This study measured concentrations of aromatase enzyme, testosterone, estradiol, and TMPRSS-2 in plasma of hospitalized COVID-19 patients to elucidate the dynamics of sex-linked disparity in COVID-19 and correlate them with disease severity and mortality. Methods: In this prospective cohort study, a total of 265 patients (41% women), age 18 years and older, who had a positive COVID-19 PCR test and were hospitalized for COVID-19 at Memorial Hermann Hospital in Houston, (between May 2020 and May 2021) were enrolled in the study if met inclusion criteria. Plasma concentrations of Testosterone, aromatase, TMPRSS-2, and estradiol were measured by ELISA. COVID-19 patients were dichotomized based on disease severity into moderate-severe (n = 146) or critical (n = 119). Mann Whitney U and logistic regression were used to correlate the analytes with disease severity and mortality. Results: TMPRSS2 (2.5 ± 0.31 vs. 1.73 ± 0.21 ng/mL, p < 0.01) and testosterone (1.2 ± 0.1 vs. 0.44 ± 0.12 ng/mL, p < 0.01) were significantly higher in men as compared to women with COVID-19 after adjusting for age in a multivariate model. There was no sex difference seen in the level of estradiol and aromatase in COVID-19 patients. TMPRSS2 and aromatase were higher, while testosterone was lower in patients with increased COVID-19 severity. They were independently associated with COVID-19 severity, after adjusting for several baseline risk factors in a multivariate logistic regression model. In terms of mortality, TMPRRS2 and aromatase levels were significantly higher in non-survivors. Conclusions: Our study demonstrates that testosterone, aromatase, and TMPRSS2 are markers of COVID-19 severity. Estradiol levels do not change with disease severity in COVID-19. In terms of mortality prediction, higher aromatase and TMPRSS-2 levels can be used to predict mortality from COVID-19 in hospitalized patients. Plain English Summary: COVID-19 has caused over a million deaths in the U.S., with men often getting sicker than women. Testosterone, a male hormone, helps control a protein called TMPRSS-2, which allows the COVID-19 virus to spread more easily in the body. A protein called aromatase converts the male hormone testosterone into the female hormone estrogen. It is thought that female hormone estrogen helps protect women from getting seriously ill from COVID-19. To understand the role of these hormones in COVID-19 and sex differences, we measured levels of testosterone, estrogen, aromatase (which turns testosterone into estrogen), and TMPRSS-2 in hospitalized COVID-19 patients. We also checked how this level might reflect the severity of the disease. We found that critically ill COVID-19 patients (the ones in ICU) had higher levels of TMPRSS-2 and aromatase, and lower testosterone levels. When we used these hormone levels to predict death in hospitalized COVID-19 patients, higher levels of TMPRSS-2 and aromatase were linked to a lower chance of survival. Highlights: COVID-19 Disease Severity: In hospitalized patients with COVID-19, higher TMPRSS-2, aromatase and lower total testosterone are markers of disease severity. COVID-19 Mortality: In hospitalized patients with COVID-19, TMPRSS2 and aromatase levels are significantly increased in COVID-19 non survivors. [ABSTRACT FROM AUTHOR]

With the National Institutes of Health's mandate to consider sex as a biological variable (SABV), there has been a significant increase of studies utilizing both sexes. Historically, we have known that biological sex and hormones influence immunological processes and now studies focusing on interactions between the immune, endocrine, and nervous systems are revealing sex differences that influence pain behavior and various molecular and biochemical processes. Neuroendocrine-immune interactions represent a key integrative discipline that will reveal critical processes in each field as it pertains to novel mechanisms in sex differences and necessary therapeutics. Here we appraise preclinical and clinical literature to discuss these interactions and key pathways that drive cell- and sex-specific differences in immunity, pain, and physiology. Plain English summary: In the last decade, NIH-funded basic and clinical research studies have been mandated to include sex as a biological variable, and this has resulted in a boom of studies discovering sex differences. We know that females are more likely than males to develop chronic pain conditions and experience higher levels of pain for longer periods of time. Conditions that demonstrate this include migraine, arthritis, and peripheral neuropathy. Furthermore, these sex differences extend to surgical outcomes and are observable at the molecular, cellular, and systemic levels. Although pain perception pathways differ by sex, studies are also focusing on differences in the "conversation" between the immune system and the nervous system while addressing implications of sex hormones to gain a better understanding of the impact on pain, physiology, and behavior. Lifestyle factors such as diet and alcohol consumption also play a role in affecting the perception and impact of pain conditions. As this area of research continues to grow, the development and availability of sex-specific treatment options will grow and lead to improved patient outcomes and more effective pain management strategies. Highlights: Immune cell types and molecular pathways drive sex specific differences in inflammatory and neuropathic pain. TLR4 involvement in pain pathways show contextual sex-specific variations and its interaction with TRPV1 channels adds complexity to nociceptor physiology. Female mice tend to exhibit stronger TRPV1-mediated pain responses compared to males due to estrogen enhancement of TRPV1 expression levels. The interplay between nuclear receptors (PPARγ, PPARα) and prolactin receptors influences sex-specific neuroimmune interactions. In males, PPARα impacts immune responses and neuroinflammation. In females, PPARγ activity influences pain perception and PRL influences pain sensitivity. Personalized approaches are needed for pain management in males and females due to sex differences in pain perception and treatment outcomes driven by variations in hormone levels, adiposity, and neuroimmune mechanisms of inflammation. [ABSTRACT FROM AUTHOR]

Researchers have proposed that variation in sex hormones across the menstrual cycle modulate the ability to recognize emotions in others. Existing research suggests that accuracy is higher during the follicular phase and ovulation compared to the luteal phase, but findings are inconsistent. Using a repeated measures design with a sample of healthy naturally cycling women (N = 63), we investigated whether emotion recognition accuracy varied between the follicular and luteal phases, and whether accuracy related to levels of estrogen (estradiol) and progesterone. Two tasks assessed recognition of a range of positive and negative emotions via brief video recordings presented in visual, auditory, and multimodal blocks, and non-linguistic vocalizations (e.g., laughter, sobs, and sighs). Multilevel models did not show differences in emotion recognition between cycle phases. However, coefficients for estrogen were significant for both emotion recognition tasks. Higher within-person levels of estrogen predicted lower accuracy, whereas higher between-person estrogen levels predicted greater accuracy. This suggests that in general having higher estrogen levels increases accuracy, but that higher-than-usual estrogen at a given time decreases it. Within-person estrogen further interacted with cycle phase for both tasks and showed a quadratic relationship with accuracy for the multimodal task. In particular, women with higher levels of estrogen were more accurate in the follicular phase and middle of the menstrual cycle. We propose that the differing role of within- and between-person hormone levels could explain some of the inconsistency in previous findings. [ABSTRACT FROM AUTHOR]

From adolescence, women become more likely to experience fear dysregulation. Oral contraceptives (OCs) can modulate the brain regions involved in fear processes. OCs are generally used for years and often initiated during adolescence, a sensitive period where certain brain regions involved in the fear circuitry are still undergoing important reorganization. It remains unknown whether OC use during adolescence may induce long‐lasting changes in the fear circuitry. This study aimed to examine whether age of onset moderated the relationship between duration of use and fear‐related brain structures. We collected structural MRI data in 98 healthy adult women (61 current users, 37 past users) and extracted grey matter volumes (GMV) and cortical thickness (CT) of key regions of the fear circuitry. Non‐linear multiple regressions revealed interaction effects between age of onset and quadratic duration of use on GMV of the right hippocampus and right ventromedial prefrontal cortex (vmPFC). Among women who initiated OCs earlier in adolescence, a short duration of use was associated with smaller hippocampal GMV and thicker vmPFC compared to a longer duration of use. For both GMV and CT of the right vmPFC, women with an early OC onset had more grey matter at a short duration of use than those with a later onset. Our results suggest that OC use earlier in adolescence may induce lasting effects on structural correlates of fear learning and its regulation. These findings support further investigation into the timing of OC use to better comprehend how OCs could disrupt normal brain development processes. [ABSTRACT FROM AUTHOR]

The roles of sex hormones such as estradiol, testosterone, and sex hormone-binding globulin (SHBG) in the etiology of lung and colorectal cancers in women, among the most common cancers after breast cancer, are unclear. This Mendelian randomization (MR) study evaluated such potential causal associations in women of European ancestry. We used summary statistics data from genome-wide association studies on sex hormones and from the Trøndelag Health Study (HUNT) and large consortia on cancers. There was suggestive evidence of 1-standard deviation increase in total testosterone levels being associated with a lower risk of lung non-adenocarcinoma (hazard ratio 0.60, 95% confidence interval 0.37–0.98) in the HUNT Study. However, this was not confirmed by using data from a larger consortium. In general, we did not find convincing evidence to support a causal role of sex hormones on risk of lung and colorectal cancers in women of European ancestry. [ABSTRACT FROM AUTHOR]

Background: Polycystic ovary syndrome (PCOS) is a unity of endocrine and metabolic disorders, associated with PI3K/AKT/mTOR, autophagy, and gut microbiota. Quinoa is a valuable food source, which contains rich minerals, unsaturated fatty acids, and has a positive modulating effect on metabolic diseases. However, its effects and potential mechanisms on PCOS have not been reported yet. Therefore, the purpose of this study is to investigate the effect of quinoa on PCOS rats by regulating PI3K/AKT/mTOR, autophagy, and gut microbiota. Methods: Ten–week-old female Sprague-Dawley (SD) rats have received letrozole for 24 days for induction of PCOS and subsequently were treated with a quinoa diet for 8 weeks. Vaginal smears were used to analyze the estrous cycle of rats. Hormone and biochemical indexes were analyzed by kit assays and glucometer. The pathological changes of ovary, pancreas, duodenum and colon were observed by HE staining. PI3K, AKT, mTOR and autophagy-related proteins in the ovary and colon were measured by western blot and immunohistochemistry staining. Tight junction proteins in colon were measured by immunohistochemistry staining. 16 s rDNA sequencing was used to detect the changes of intestinal microbiota in rats. Network pharmacology and molecular docking were used to study the possible targets and mechanisms of quinoa on PCOS. Spearman correlation analysis was used to study the relationship between intestinal microbial abundance and hormone levels of PCOS rats at the phylum and genus level. Results: Quinoa significantly improved estrous cycle and biochemical parameters of PCOS-like rats, and the pathological state of ovary, pancreas, duodenum and colon tissues. Especially, quinoa significantly regulated the expression of PI3K, AKT, mTOR and autophagy-related proteins in the ovary. Quinoa may repair the intestinal barrier by upregulating the expression of tight junction proteins in the colon, and regulate autophagy-related factors in colon. Additionally, quinoa increased the abundance of Lactobacillu, Bacteroides and Oscillospira, and decreased the Firmicutes/Bacteroidetes ratio and the Blautia, and Prevotella, reversing the dysregulation of the gut microbiota. Correlation analysis showed that there is a strong correlation between gut microbiota with significant changes in abundance and hormone related to PCOS. Conclusion: Our result indicated that effect of quinoa on PCOS maybe associated with activation of the PI3K/AKT/mTOR signaling pathway, inhibition of autophagy, and regulation of intestinal flora. [ABSTRACT FROM AUTHOR]

In this review, we have amalgamated the literature, taking a multimodal neuroimaging approach to quantify the relationship between neuronal firing and haemodynamics during a task paradigm (i.e., neurovascular coupling response), while considering confounding physiological influences. Original research articles that used concurrent neuronal and haemodynamic quantification in humans (n ≥ 10) during a task paradigm were included from PubMed, Scopus, Web of Science, EMBASE and PsychINFO. Articles published before 31 July 2023 were considered for eligibility. Rapid screening was completed by the first author. Two authors completed the title/abstract and full‐text screening. Article quality was assessed using a modified version of the National Institutes of Health Quality Assessment Tool for Observational Cohort and Cross‐Sectional Studies. A total of 364 articles were included following title/abstract and full‐text screening. The most common combination was EEG/functional MRI (68.7%), with cognitive (48.1%) and visual (27.5%) tasks being the most common. The majority of studies displayed an absence/minimal control of blood pressure, arterial gas concentrations and/or heart rate (92.9%), and only 1.3% monitored these factors. A minority of studies restricted or collected data pertaining to caffeine (7.4%), exercise (0.8%), food (0.5%), nicotine (2.7%), the menstrual cycle (0.3%) or cardiorespiratory fitness levels (0.5%). The cerebrovasculature is sensitive to numerous factors; thus, to understand the neurovascular coupling response fully, better control for confounding physiological influences of blood pressure and respiratory metrics is imperative during study‐design formulation. Moreover, further work should continue to examine sex‐based differences, the influence of sex steroid hormone concentrations and cardiorespiratory fitness. [ABSTRACT FROM AUTHOR]

Key points Testosterone, the major androgen, influences the reproductive and non‐reproductive systems in males and females via binding to the androgen receptor (AR). Both circulating endogenous testosterone and muscle AR protein content are positively associated with muscle mass and strength in males, but there is no such evidence in females. Here, we tested whether circulating testosterone levels were associated with muscle mass, function, or the muscle anabolic response to resistance training in pre‐menopausal females. Twenty‐seven pre‐menopausal, untrained females (aged 23.5 ± 4.8 years) underwent a 12‐week resistance training programme. Muscle strength, size, power, and plasma and urine androgen hormone levels were measured. Skeletal muscle biopsies were collected before and after the training programme to quantify the effect of resistance training on AR content and nuclear localisation. Primary muscle cell lines were cultured from a subset (n = 6) of the participants’ biopsies and treated with testosterone to investigate its effect on myotube diameter, markers of muscle protein synthesis and AR cellular localisation. Physiological levels of total testosterone were not associated with muscle mass or strength at baseline or with the changes in muscle mass and strength that occurred in response to resistance training in our cohort of pre‐menopausal females. In contrast, bioavailable testosterone and the proportion of nuclear‐localised AR were positively associated with skeletal muscle mass and strength in pre‐menopausal females. In vitro, supra‐physiological doses of testosterone increased myocyte diameter, but this did not occur via the Akt/mTOR pathway as previously suggested. Instead, we show a marked increase in AR nuclear localisation with testosterone administration in vitro. Total circulating testosterone was not related to muscle mass or strength before or after resistance training in pre‐menopausal females. Bioavailable testosterone was positively related to exercise‐induced muscle hypertrophy in pre‐menopausal females. In vivo nuclear localisation of the androgen receptor was positively related to muscle mass in pre‐menopausal females at baseline, but not to resistance training‐induced hypertrophy. Testosterone treatment induced androgen receptor nuclear translocation but did not induce mTOR signalling in primary skeletal myocytes cultured from pre‐menopausal female muscle. [ABSTRACT FROM AUTHOR]

ABSTRACT Objectives Methods Results Conclusions Anaemia is a key cause of morbidity in chronic kidney disease (CKD). Androgen deficiency (AD) in males can contribute to anaemia of all causes, including in CKD. We sought to examine the prevalence of AD in men with CKD, the extent to which it contributed to anaemia and whether it was independently associated with long‐term survival.This cross‐sectional observational study was conducted among males aged 18 years and over with CKD stages 4 and 5. The study analysed morning blood samples with regard to their full blood count, urea and electrolytes, albumin, lipids, testosterone (T) and sex hormone binding globulin, with calculation of free testosterone by mass action equation. Mortality data were obtained 15 years later for survival analysis.Among 322 patients with a mean age of 63 years, the overall prevalence of AD was 68.9%. There was a statistically significant negative correlation between erythropoiesis stimulating agent (ESA) dose and testosterone concentrations (Pearson correlation −0.193, p = 0.05). There was a positive correlation between haemoglobin (Hb) and free testosterone level among patients not on ESA therapy (Pearson correlation 0.331, p < 0.001). Kaplan‐Meier plots showed p < 0.001 on log‐rank analysis, indicating that AD was significantly associated with worse survival. However, in Cox regression analysis, free testosterone was not associated with survival (95% CI for free testosterone 0.997–1.000).AD is highly prevalent among this population, and increases further with older age and more severe CKD warranting haemodialysis. Association of lower Hb and higher ESA dose with lower T concentration might be causative, which has important pharmaco‐economic as well as clinical implications. Lower survival in men with low T, more likely reflects overall poor health rather than causation. A properly constituted randomised controlled study evaluating the effect of native T replacement is warranted in men with CKD and AD. [ABSTRACT FROM AUTHOR]

Gonadal steroid hormones are critical regulatory substances involved in various developmental and physiological processes from fetal development through adulthood. These hormones, derived from cholesterol, are synthesized primarily by the gonads, adrenal cortex, and placenta. The synthesis of these hormones involves a series of enzymatic steps starting in the mitochondria and includes enzymes such as cytochrome P450 and aromatase. Beyond their genomic actions, which involve altering gene transcription over hours, gonadal steroids also exhibit rapid, nongenomic effects through receptors located on the cell membrane. Additionally, recent research has highlighted the role of these hormones in the central nervous system (CNS). However, the interactions between gonadal steroid hormones and the retina have received limited attention, though it has been suggested that they may play a protective role in retinal diseases. This review explores the synthesis of gonadal hormones, their mechanisms of action, and their potential implications in various retinal and optic nerve diseases, such as glaucoma, age-related macular degeneration (AMD), diabetic retinopathy (DR), or retinitis pigmentosa (RP), discussing both protective and risk factors associated with hormone levels and their therapeutic potential. [ABSTRACT FROM AUTHOR]

Simple Summary: Skeletal muscle is an endocrine organ capable of responding to and releasing hormones and hormonally active molecules. In particular, sex hormones (e.g., testosterone) specifically regulate metabolic activity, growth, and tissue differentiation. However, the biological and clinical responses to the same type of hormone treatment differ between subjects with male and female karyotypes. Characterization of the biomolecular mechanisms underlying the sexual dimorphism in response to sex hormones is crucial for the design of new methodological approaches aimed at highlighting sex differences in the patho/physiological aspects caused by the use (and abuse) of sex hormones. To date, in vivo and ex vivo studies are very limited, mainly for ethical reasons; it is therefore of fundamental importance to use experimental approaches based on cellular models at the preclinical level. On the other hand, most in vitro studies do not take into account the chromosomal structure of the cell models used, with the result that 'sex' is often a 'confounding factor'. This highlights the need for basic research to develop preclinical models that take into account chromosomal sex differences to ensure the transferability of the data obtained in vivo and to adequately design relevant experimental studies. Therefore, given the role of skeletal muscle in biological responses to testosterone, the aim of this project is to assess the presence of sex differences in endocrine–metabolic cellular responses to increasing doses of testosterone by simulating functional modifications of skeletal muscle cells in vitro. Muscle tissue is an important target of sex steroids, and particularly, testosterone plays essential roles in muscle cell metabolism. Wide ranges of studies have reported sex differences in basal muscle steroidogenesis, and recently several genes have been identified to be regulated by androgen response elements that show innate sex differences in muscle. However, studies accounting for and demonstrating cell sexual dimorphism in vitro are still scarce and not well characterized. Here, we demonstrated the ability of 46XX and 46XY human primary skeletal muscle cells to differently activate steroidogenesis in vitro, likely related to sex-chromosome onset, and to differently induce hormone release after increasing doses of testosterone exposure. Cells were treated with testosterone at concentrations of 0.5, 2, 5, 10, 32, and 100 nmol/L for 24 h. Variations in 17β-HSD, 5α-R2, CYP-19 expression, DHT, estradiol, and androstenedione release, as well as IL6 and IL8 release, were analyzed, respectively, by RT-PCR, ELISA, and luminex-assay. Following testosterone treatments, and potentially at any concentration level, an increase in the expression of 17β-HSD, 5α-R2, and CYP-19 was observed in 46XY cells, accompanied by elevated levels of DHT, androstenedione, and IL6/IL8 release. Following the same treatment, 46XX cells exhibited an increase in 5α-R2 and CYP-19 expression, a conversion of androgens to estrogens, and a reduction in IL6 and IL8 release. In conclusion, this study demonstrated that sex-chromosome differences may influence in vitro muscle cell steroidogenesis and hormone homeostasis, which are pivotal for skeletal muscle metabolism. [ABSTRACT FROM AUTHOR]

Key Clinical Message: This case underscores the importance of recognizing the potential link between hormonal fluctuations during the menstrual cycle and idiopathic intracranial hypertension (IIH), which could lead to spontaneous cerebrospinal fluid (CSF) rhinorrhea. Eliciting a history of intermittent clear rhinorrhea with the onset of menstrual cycle if presenting with menstrual migraines could allow for a more prompt diagnosis and treatment of IIH and CSF leak. Early diagnosis and intervention are crucial to prevent serious complications. [ABSTRACT FROM AUTHOR]

Objective: This study aims to examine the expression of androgen receptor (AR) and estrogen receptor (ER) in patients with classic Kaposi's sarcoma (CKS) in Xinjiang, as well as to assess the serum levels of sex hormones in these patients. The objective is to explore potential new directions and targets for diagnosing and treating CKS in Xinjiang. Methods: The case group comprised 35 patients diagnosed with CKS who presented at our hospital from 2014 to 2021. The control group consisted of 35 patients with pyogenic granuloma (PG) who visited the hospital during the same period, selected using propensity score matching (PSM). Immunohistochemistry was used to detect AR, human herpesvirus type 8 (HHV‐8), and ER in paraffin‐embedded tissue samples from patients diagnosed with CKS and PG. Additionally, enzyme‐linked immunosorbent assay (ELISA) was used to quantitatively measure serum sex hormone levels in the 35 patients with CKS and 35 patients with PG. Results: AR expression was relatively weak in both the CKS and PG groups, with the PG group exhibiting a slightly stronger expression than the CKS group. Conversely, the expression of ER was significantly higher in the CKS group compared to the PG group (p < 0.05). Additionally, serum testosterone (T) levels were elevated in the CKS group, while serum estradiol (E2) levels were higher in the PG group (p < 0.05). Conclusion: Sex hormones and their receptors are implicated in the pathogenesis of CKS in Xinjiang. The use of ER antagonists may represent a novel avenue for research and treatment of CKS. [ABSTRACT FROM AUTHOR]

Colorectal cancer (CRC) ranks as the third most prevalent cancer worldwide and is a leading cause of cancer-related mortality. Since many colon cancers present no significant clinical symptoms, identifying new biomarkers or a set of biological indicators significant for clinical trials is crucial for the early detection of CRC. This advancement also aids in establishing new objectives for interventional therapeutic strategies against the disease. Currently, research is exploring various proteins, glycoproteins, and cellular and humoral substances involved in cellular homeostasis mechanisms as potential cancer markers. This review examines the potential utility of fucosylation and sialylation processes, as well as sex hormones, as biomarkers in the diagnosis and prognosis of CRC. A comprehensive search was conducted in PUBMED, MEDLINE, and Google Scholar, supplemented by a manual search of relevant journals. The keywords were L-fucose, sialic acid, fucosyltransferase-4, galectin-3, and steroid hormones in CRCs. [ABSTRACT FROM AUTHOR]

Gender is one of the most essentialized social categories, with putative differences between cisgender men and cisgender women often framed in biological terms. We propose that the consequences of inaccurate and widely held essentialist beliefs about gonadal hormones (EBAGHs) in particular—that is, that androgens signify "men" and estrogens signify "not-men"—have yet to be fully appreciated. For example, placebo effects such as increased strength, sexual desire, and irritability have been documented for the androgen testosterone. Accumulating research also suggests that lay understandings exaggerate the causal importance of testosterone in men's aggression. Consequently, testosterone is often either eschewed (i.e., men are "poisoned" by it) or enshrined ("more is good, less is bad"). Moreover, the efficacy-bolstering role of estrogens such as estradiol across the physical, cognitive, and sexual health domains for men has been downplayed or ignored by those who assert pejorative links between estrogen and weakness or effeminacy. Critically, EBAGHs may fuel "hypermasculine" behaviors such as excessive red meat consumption, problematic alcohol intake, and anabolic steroid misuse as well as treatment seeking for "low T" in the absence of proper medical diagnosis—which can all, ironically, result in disrupting men's optimal hormonal balance. Implications of our analysis for research (e.g., EBAGHs as predictors men's health behaviors, use of bogus "hormonal profiles" to induce or assuage threats to masculinity in experimental studies) and interventions (e.g., "hormone education" to offset the adverse effects of EBAGHs) are discussed. Public Significance Statement: Inaccurate beliefs about gonadal hormones may cause testosterone to be either valued or devalued—and estrogen to be portrayed as the enemy—in men. Such beliefs may contribute to hypermasculine behaviors, poor diet, misguided health care, and other negative outcomes for men. Biologically accurate hormone education may therefore have beneficial consequences for men's self-perception, perception by others, and overall well-being. [ABSTRACT FROM AUTHOR]

The relationship between meningiomas and gonadal steroid hormones has been the subject of debate, and there is limited understanding of the connection between patient, tumor characteristics, and progesterone receptor (PGR) status. This retrospective observational study aims to explore the prognostic correlation between PGR+ and PGR-meningiomas in terms of various clinical, radiological, and surgical predictors. The analysis included 270 patients, divided into 2 groups: group A (PGR-, 194 patients), and group B (PGR+, 76 patients). The analysis showed no significant differences in terms of age, sex, clinical debut, postsurgical complications, total resection, and grading between the 2 groups. However, a significant difference was observed in the mean Karnofsky performance status at all stages of follow-up. Peritumoral edema measured in preoperative magnetic resonance imaging significantly influences the value of Karnofsky performance status in both preoperative (ANOVA, P = 0.05) and postoperative evaluation (postoperative ANOVA, P = 0.014) only in group A. In the multivariate analysis, there are no significant factors related to the clinical, biological, and surgical parameters previously examined for each measurement time (P = 0.826). The study found that PGR + meningioma patients tend to have better postoperative recovery and earlier clinical debut without any association with age prevalence or grading. [ABSTRACT FROM AUTHOR]

In this research, we aimed to determine the antioxidant activity of an atomized extract of Cnidoscolus diacanthus (Pax & K. Hoffm.) J.F. Macbr., known in Peru as "huanarpo hembra", and its effect on sex hormone levels. Its phytochemical profile was determined using liquid chromatography–mass spectrometry (LC–MS), while its total phenol content (TPC) and total flavonoids (TFs) were determined using the Folin–Ciocalteu method and the aluminum chloride method. Its antioxidant activity was determined using 2,2-diphenyl-1-picrylhydrazyl (DPPH), the radical 2,2-azino-bis-3-ethylbenzthiazolin-6 sulfonic acid (ABTS), and ferric-reducing antioxidant power (FRAP). The biological activity of C. diacanthus and its effect on sexual hormones were determined in Holtzman rats of both sexes. Phytochemical analysis revealed the presence of flavonoids and phenolic compounds in its leaves and stems, mainly rutin, quercetin, chlorogenic acid, and genistein. However, the stem extract contained higher total phenol (464.38 ± 4.40 GAE/g) and flavonoid (369.17 ± 3.16 mg QE/g of extract) contents than the leaf extract (212.38 ± 3.19 mg GAE/g and 121.49 ± 2.69 mg QE/g). For DPPH, ABTS, and FRAP, the Trolox-equivalent antioxidant capacity (TEAC) was 597.20 ± 5.40 µmol/g, 452.67 ± 5.76 µmol/g, and 535.91 ± 1.56 µmol/g, respectively, for the stems, while for the leaves, it was 462.39 ± 3.99 µmol/g, 202.32 ± 5.20 µmol/g, and 198.13 ± 1.44 µmol/g, respectively. In terms of the values for hormonal levels, at a dose of 100 mg/kg of the extract, testosterone levels of 1.430 ng/mL (with the leaf extract) and 1.433 ng/mL (with the stem extract), respectively, were found in the male rats. Regarding estradiol levels, in the female rats, these were 10.425 ng/mL (leaf extract) and 8.775 ng/mL (stem extract), while their levels of luteinizing hormone were 0.320 mIU/mL (leaf extract) and 0.273 mIU/mL (stem extract). For the follicle-stimulating hormone, levels of 0.858 mIU/mL (leaf extract) and 0.840 mIU/mL (stem extract) were found in the female rats, and levels of 0.220 mIU/mL (leaf extract) and 0.200 mIU/mL (stem extract) were found in the male rats. It is concluded that the C. diacanthus stem extract had a greater antioxidant capacity than the leaf extract, while both extracts had a superior effect on the sex hormone levels in the female rats compared to the male rats. [ABSTRACT FROM AUTHOR]

Background: Polycystic ovarian syndrome (PCOS) is a metabolic disorder, and its pathogenesis is still unclear, but the changes in the hypothalamicpituitary-gonadal (HPG) axis are considered one of the main causes in the development of PCOS. Kisspeptin is a peptide encoded by the KISS gene that regulates the hypothalamus-pituitary-gonadal (HPG), which may be concerned with the pathogenesis of PCO. Aim: To identify the relation between serum Kisspeptin and sex hormones and metabolic parameters among normal and PCO women. Methods: A prospective case-control study was conducted among 64 subjects (32 with PCO and 32 with the control group). The serum Kisspeptin level was measured using enzyme-linked immunosorbent assay (ELISA) and correlated with other hormones such as LH, FSH, DHEA, testosterone, and prolactin. Results: Serum kisspeptin level was significantly higher in the PCOS group when compared to the control group. There was a statistically significant positive correlation between kisspeptin and each of HOMA IR, LH, FSH, DHEA, testosterone, and prolactin. Conclusions: The increase in kisspeptin level may play a role in pathogenesis of PCOS, and may represent a novel link between metabolic and hormonal disturbance in PCOS females since this peptide was correlated with HOMA-IR, LH, FSH, DHEA, testosterone and prolactin. [ABSTRACT FROM AUTHOR]

Oral contraceptive (OC) use can increase resting blood pressure (BP) in females as well as contribute to greater activation of group III/IV afferents during upper body exercise. It is unknown, however, whether an exaggerated BP response occurs during lower limb exercise in OC users. We sought to elucidate the group III/IV afferent activity-mediated BP and heart rate responses while performing lower extremity tasks during early and late follicular phases in young, healthy females. Females not taking OCs (NOC: n = 8; age: 25 ± 4 yr) and those taking OCs (OC: n = 10; age: 23 ± 2 yr) completed a continuous knee extension/flexion passive stretch (mechanoreflex) and cycling exercise with subsystolic cuff occlusion (exercise pressor reflex), which was followed by a 2-min postexercise circulatory occlusion (PECO) (metaboreflex). Data collection occurred on two occasions: once during the early follicular phase (days 1–4) and once during the late follicular phase (days 10–14) of their menstrual cycle (NOC) or during the placebo and active pill phases (OC). Resting mean arterial BP and heart rate were not different between phases in NOC and OC participants (P > 0.05). Hemodynamic responses to metaboreflex, mechanoreflex, and collective exercise pressor reflex activation were not different between phases in both groups (P > 0.05). In conclusion, although OCs are known to increase BP at rest, our findings indicate that neither endogenous nor exogenous (OC) sex hormones modulate BP during large, lower limb muscle exercise with or without group III/IV afferent activation in young, healthy females. NEW & NOTEWORTHY: Sex differences in the cardiovascular response to exercise have been demonstrated and may be dependent on sex hormone levels. Furthermore, oral contraceptives (OCs) have been shown to exaggerate the blood pressure response to upper extremity exercise. The results of this study indicate that neither endogenous nor exogenous (OC) sex hormones modulate BP during lower extremity dynamic exercise or with group III/IV afferent activation in young, healthy females. [ABSTRACT FROM AUTHOR]

Anabolic‐androgenic steroids (AASs) impairment of reproduction has been reported. We investigated dose‐ and time‐dependent effects of Nandrolone decanoate (ND) on reproductive system in comparison with Testosterone enanthate (TE). Male Wistar rats were administrated with 1, 3, and 9 mg/kg/weeks ND or 1 and 3 mg/kg/weeks TE for 8 weeks, and testicular phenotype and reproductive hormones were assessed at 4 and 8 weeks post‐treatments. AASs × treatment period interaction was significant for gonadosomatic index (GSI), testosterone (T), 17β‐estradiol (E2), and luteinizing hormone (LH). At 4 weeks post‐treatment, GSI was decreased in rats treated with 3 mg/kg/weeks ND and T was decreased in all ND‐treated groups, while no significant changes in LH levels were observed. At 8 weeks post‐treatment, GSI was decreased in rats treated with 1 and 3 mg/kg/weeks ND and with 3 mg/kg/weeks TE, T was decreased in all groups, and E2 and LH were increased and decreased, respectively, in rats treated with 9 mg/kg/weeks ND and with 3 mg/kg/weeks TE. The testes showed histopathological defects in both ND‐ and TE‐treated rats suggesting a delay in seminiferous cycle. This study shows AASs‐induced hypogonadism at low‐dose that coincided with inhibition of T biosynthesis and disruption of T feedback on pituitary. [ABSTRACT FROM AUTHOR]

Historical exclusion of females in research has been, in part, due to the perceived influence of natural menstrual (NAT) and oral contraceptive pill (OCP) cycles on vascular outcomes. NAT and OCP cycle phases may influence brachial artery (BA) endothelial function, however, findings are mixed. Minimal research has examined arterial stiffness, smooth muscle, and lower limb endothelial function. The purpose of this study was to investigate the influence of NAT and OCP cycles on cardiovascular outcomes and cellular regulation. Forty-nine premenopausal females (n = 17 NAT, n = 17 second generation OCP, n = 15 third generation OCP) participated in two randomized order visits in the low (LH, early follicular/placebo) and high (HH, midluteal/active) hormone cycle phases. BA and superficial femoral artery (SFA) endothelial function [flow-mediated dilation (FMD) test], smooth muscle function (nitroglycerine-mediated dilation test), and carotid and peripheral (pulse wave velocity) arterial stiffness were assessed. Cultured female human endothelial cells were exposed to participant serum for 24 h to examine endothelial nitric oxide synthase (eNOS) and estrogen receptor-α (ERα) protein content. BA FMD was elevated in the HH vs. LH phase, regardless of group (HH, 7.7 ± 3.5%; LH, 7.0 ± 3.3%; P = 0.02); however, allometric scaling for baseline diameter resulted in no phase effect (HH, 7.6 ± 2.6%; LH, 7.1 ± 2.6%; P = 0.052, d = 0.35). SFA FMD, BA, and SFA smooth muscle function, arterial stiffness, and eNOS and ERα protein content were unaffected. NAT and OCP phases examined have minimal influence on vascular outcomes and ERα-eNOS pathway, apart from a small effect on BA endothelial function partially explained by differences in baseline artery diameter. NEW & NOTEWORTHY: Comprehensive evaluation of the cardiovascular system in naturally cycling and second and third generation OCP users indicates no major influence of hormonal phases examined on endothelial function and smooth muscle function in the arteries of the upper and lower limbs, arterial stiffness, or underlying cellular mechanisms. Study findings challenge the historical exclusion of female participants due to potentially confounding hormonal cycles; researchers are encouraged to consider the hormonal environment in future study design. [ABSTRACT FROM AUTHOR]

Diabetes leads to testicular damage and infertility. Mesenchymal stem cells and their secretory trophic factors have shown potential as regenerative therapies for diabetes and its associated complications. This study examined the effects of conditioned medium derived from Wharton's jelly mesenchymal stem cells (WJMSCs‐CM) on sperm parameters, reproductive hormones, biochemical parameters, and histological changes in the testes of diabetic rats. Fifty‐six male Sprague–Dawley rats (250–300 g) were assigned to eight groups: control, diabetes, and six diabetic groups receiving early or late treatments with WJMSCs‐CM (D‐CME, D‐CML), insulin (D‐INSE, D‐INSL), or DMEM (D‐DME, D‐DML). In the early treatment groups, insulin (3 U/day, subcutaneously) and WJMSCs‐CM (10 mg/week, intraperitoneally) were administered immediately after diabetes induction; in the late treatment groups, these interventions began 30 days postinduction. Blood glucose and insulin levels, along with sperm parameters, were assessed. Sex hormones, testicular antioxidant enzyme activity, malondialdehyde (MDA), and glutathione (GSH) concentrations were measured using colorimetric methods. Real‐time PCR detected Bax, Bcl‐2, and tumor necrosis factor‐alpha (TNF‐α) gene expression. Our results showed that diabetes increased blood glucose levels, decreased insulin and sex hormone levels, induced testicular oxidative stress and apoptosis, and reduced sperm parameters compared to the control. WJMSCs‐CM significantly ameliorated hyperglycemia, increased insulin and sex hormone levels, and improved sperm quality. In WJMSCs‐CM‐treated diabetic rats, MDA levels were reduced, while GSH and antioxidant enzyme activity increased. Furthermore, WJMSCs‐CM decreased the testicular Bax/Bcl‐2 ratio and TNF‐α expression, as well as enhanced spermatogenic, Sertoli, and Leydig cells. In conclusion, WJMSC‐CM administration effectively mitigated diabetes‐induced testicular damage by reducing oxidative stress, inflammation, and apoptosis. Early treatment with WJMSCs‐CM was more effective than late treatment for diabetes‐induced reproductive dysfunction. [ABSTRACT FROM AUTHOR]

Background: Although sex hormones are recognized to induce immune variations, the effect of hormonal therapy use on immunity is only poorly understood. Here, we quantified how hormonal therapy use affects HIV‐1 immune markers in cis women (CW) and trans women and non‐binary people (TNBP) with HIV. Methods: We considered CD4, CD8 and lymphocyte measurements from cis men (CM), CW and TNBP in the Swiss HIV Cohort Study. We modelled HIV‐1 markers using linear mixed‐effects models with an interaction between 'gender' (CW, TNBP) and 'hormonal therapy use' (yes/no). Models were adjusted on age, ethnicity, education level, time since start of antiretroviral therapy and use of intravenous drugs. We assessed the inflammatory effect of hormonal therapy use in 31 TNBP using serum proteomics measurements of 92 inflammation markers. Results: We included 54 083 measurements from 3092 CW and 83 TNBP, and 147 230 measurements from 8611 CM. Hormonal therapy use increased CD4 count and CD4:CD8 ratio in TNBP more than in CW (pinteraction = 0.02 and 0.007, respectively). TNBP with hormonal therapy use had significantly higher CD4 counts [median = 772 cells/μL, interquartile range (IQR): 520–1006] than without (617 cells/μL, 426–892). This was similar to the effect of CW versus CM on CD4 T cells. Hormonal therapy use did not affect serum protein concentrations in TNBP. Conclusion: This study highlights the potential role of hormonal therapy use in modulating the immune system among other biological and social factors, especially in TNBP with HIV. [ABSTRACT FROM AUTHOR]

The mechanisms regulating plumage coloration appear to be phylogenetically conserved in avian species: the plesiomorphic character state is estrogen-dependent regulation, while testosterone, luteinizing hormone, and non-hormonal control are derived states. Limited data exist on the underlying regulatory processes of sexual dichromatism in the Eared Dove (Zenaida auriculata (Des Murs, 1847)). Since the Columbiformes order is close to basal branches, we hypothesized that estrogen and testosterone play a central role in the regulation of crown plumage coloration in the Eared Dove. To test this, we subjected adult males to a forced molt accompanied by an exogenous increase of estradiol and testosterone to determine whether the presence of these hormones during molting modified the spectrophotometric characteristics of the plumage. No significant differences were found between treatments and controls in the colorimetric variables hue, ultraviolet saturation, and brightness. Similarly, the avian visual model showed no perceptible changes in chromatic and achromatic signals in the individual male adults. We also analyzed the effects of estrogen and testosterone on the growth speed of the new feathers. The hormone-treated groups increased in the speed of molting compared to the control group. These results suggest that the Eared Dove is an exception to basal branch models: rather than regulating coloration, sex hormones speed up the growth of the new feathers. [ABSTRACT FROM AUTHOR]

Oral hormonal contraception (OHC) is a widely employed method in females for the prevention of unintended pregnancies, as well as for the treatment of menstrual disorders, endometriosis, and polycystic ovarian syndrome. However, it is believed that with OHCs use, some females may have higher risk of cardiovascular diseases, such as hypertension, diabetes, myocardial infarction, thrombosis, and heart failure. Although such risks are infrequently detected in healthy young females with the use of oral contraceptives, slightly elevated risks of cardiovascular diseases have been observed among reproductive-aged healthy females. However, prolonged use of OHC has also been claimed to have protective cardiac effects and may contribute to reduced risk of cardiovascular disease. In fact, the debate on whether OHC administration increases the risk of cardiovascular diseases has been ongoing with inconsistent and controversial viewpoints. Nevertheless, a great deal of work has been carried out to understand the relationship between OHC use and the occurrence of cardiovascular risk in females who use OHC for preventing the unwanted pregnancy or treatment of other disorders. Therefore, in this review we summarize the most recent available evidence regarding the association between the use of oral hormonal contraceptives and the risk for cardiovascular disease in females who are using OHC to prevent unintended pregnancy. [ABSTRACT FROM AUTHOR]

Disordered eating refers to a range of eating behaviours and attitudes towards weight and food that can negatively influence physical and psychosocial well-being. The menopausal transition could be a vulnerable period for disordered eating due to major hormonal fluctuations, menopausal symptoms, common body composition shifts, and an increased risk of psychological challenges. This systematic review aimed to summarize evidence on the associations between the menopausal transition and disordered eating. Records published before October 2023 were identified through MEDLINE, PsycINFO, Scopus, Embase, and CINAHL. Studies investigating associations between menopausal status, menopausal symptoms, or reproductive hormone levels, and disordered eating during the menopausal transition were sought. A total of 1301 non-duplicate records were screened, with 10 studies deemed eligible for inclusion. Most included studies used a cross-sectional design (n = 9). Findings include potentially higher levels of binge eating during the perimenopausal stage, whereas restrictive eating behaviours appeared more common during postmenopause compared to premenopause. Both studies investigating menopausal symptoms found strong positive associations with disordered eating. Nonetheless, findings are equivocal with contrasting results and limited methodological quality across studies. Further research is needed to verify these findings and better assist health professionals in supporting healthy eating behaviours in menopausal women during this complex transition. (PROSPERO ID: CRD42021290736) [ABSTRACT FROM AUTHOR]

The article focuses on the impact of an educational intervention regarding anti-Müllerian hormone (AMH) testing on patient interest and knowledge. Topics include the finding that participants who received evidence-based information showed lower interest in AMH testing; the differences in attitudes and intentions to discuss the test with doctors between intervention and control groups; and the common misconceptions about AMH testing's predictive capabilities regarding fertility.