Maturitas最新文献

Background: The triglyceride-glucose frailty index integrates metabolic load and physiological vulnerability. Its association with incident stroke among individuals at cardiovascular-kidney-metabolic syndrome stages 0-3 remains unclear.

Methods: We performed an observational cohort analysis in the China Health and Retirement Longitudinal Study. Adults at cardiovascular-kidney-metabolic syndrome stages 0-3 who were free of stroke at baseline were included. The exposure of interest was the triglyceride-glucose frailty index, and the outcome was incident stroke during follow-up. Cox proportional hazards models estimated adjusted associations. Nonlinearity was assessed with restricted cubic splines. Effect modification by baseline cognitive function was tested using interaction terms. Regression-based mediation evaluated self-rated health and hypertension.

Results: A total of 6882 adults without stroke at baseline were included, among whom 583 incident strokes occurred during follow-up, an incidence of 8.47%. Stroke incidence increased across tertiles of the triglyceride-glucose frailty index, from 5.14% to 8.24% and 12.03%, with clear separation of Kaplan-Meier curves. In Cox proportional hazards models, each 5-unit increase in the triglyceride-glucose frailty index was associated with a higher hazard of stroke, with a hazard ratio of 1.46 and a 95% confidence interval of 1.31 to 1.64. Compared with the lowest tertile, the hazard ratios were 1.54 (95% confidence interval 1.22 to 1.95) and 2.16 (95% confidence interval 1.71 to 2.73) for the middle and highest tertiles, respectively. Restricted cubic spline analyses indicated a nonlinear association, with an inflection point at a triglyceride-glucose frailty index value of approximately 8.31. Below this level, stroke risk increased more steeply, whereas the association was attenuated above this threshold. Baseline cognitive function significantly modified the association, with stronger effects observed among individuals with better cognitive function. Exploratory mediation analyses suggested that self-rated health and hypertension accounted for approximately 23.0% and 7.6% of the overall statistical association, respectively. Subgroup and sensitivity analyses yielded results that were broadly consistent with the primary findings.

Conclusions: Among adults at cardiovascular-kidney-metabolic syndrome stages 0-3, a higher triglyceride-glucose frailty index was associated with an increased risk of incident stroke. This association was nonlinear, varied by baseline cognitive function, and was partially mediated by self-rated health and hypertension.

Background: Global population aging has made frailty a critical public health concern. While a frailty index (FI) is able to quantify frailty effectively, its association with fall risk needs further validation across diverse populations and cultural contexts.

Methods: This study analyzed data from 24,526 participants aged ≥45 years from national cohorts in the China Health and Retirement Longitudinal Study, the English Longitudinal Study of Aging, and the US Health and Retirement Study. The association between a health deficit-based frailty index and self-reported falls over two years was assessed using a model with multivariable adjustment logistic regression, restricted cubic splines, and stratified analyses.

Results: The mean baseline score on the frailty index was 0.1 in China Health and Retirement Longitudinal Study, 0.2 in English Longitudinal Study of Aging, and 0.4 in Health and Retirement Study. A significant positive association was observed between frailty score and fall risk after multivariable adjustment (P < 0.001), with adjusted odds ratios of 1.45, 1.51, and 1.86 per unit increase in score, respectively. A nonlinear dose-response relationship (P < 0.001) and significant sex interaction (P < 0.001) were identified, with a stronger association in men.

Conclusion: The frailty index is a significant predictor of fall risk in middle-age and older adults, with variations across countries and sexes, supporting its utility as a practical screening tool for targeted interventions to promote healthy aging.

Breast cancer remains a prevalent health concern, affecting approximately one in eight women during their lifetime. While screening mammography has significantly reduced mortality through early detection, its sensitivity is compromised in women with dense breast tissue-a factor that not only increases cancer risk but also obscures malignancies on imaging. Digital breast tomosynthesis has enhanced screening capabilities over traditional 2D mammography, yet limitations persist for dense breasts. In response, recent US federal legislation mandates that mammography lay summaries inform patients about the implications of breast density, including reduced detection rates and elevated risk. Additionally, insurance coverage for supplemental imaging is expanding across the United States. Supplemental screening modalities such as magnetic resonance imaging, whole-breast ultrasound, contrast-enhanced mammography, and molecular breast imaging offer improved detection in dense tissue, but guidance for average-risk women remains unclear. This lack of consensus can lead to confusion among patients and providers. This article aims to equip clinicians with a comprehensive understanding of breast density's impact on screening efficacy, the available supplemental imaging options, and current societal recommendations. By clarifying these considerations, clinicians can better navigate shared decision-making with average-risk patients regarding breast cancer screening.

Background: Intratumoral estrogens may contribute to the growth of breast cancer. Risk factors for breast cancer, including reproductive factors, may influence intratumoral hormone levels.

Methods: This cross-sectional study of 146 postmenopausal women with breast cancer investigated associations of reproductive factors, including parity and breastfeeding history, with serum and intratumoral (tissue) hormone levels, as well as aromatase activity, by hormone receptor subtype classified as estrogen receptor-positive or estrogen receptor-negative and progesterone receptor-negative, using analysis of covariance. Hormone levels and aromatase activity in paired serum and tumor tissue samples were measured using liquid chromatography-tandem mass spectrometry and the tritiated water-release assay. Epidemiological data were collected through a self-administered questionnaire.

Findings: Among women with estrogen receptor-positive cancer, parity history (nulliparous vs. parous) was not significantly associated with serum or tissue hormone levels. No linear association was observed between parity number (nulliparous, 1, 2, ≥3) and tissue estradiol levels (age- and stage-adjusted means: 109.2, 76.7, 85.9, and 113.2 pg/g, respectively; p = 0.58). Tissue estradiol levels were significantly higher among parous women with breastfeeding history (age- and stage-adjusted mean: 103.2 pg/g) than among those without (64.5 pg/g, p = 0.01). In estrogen receptor-negative and progesterone receptor-negative cancers, no associations were observed between these reproductive factors and hormone levels or aromatase activity.

Conclusions: Reproductive history, particularly breastfeeding, may be associated with intratumoral estradiol levels in postmenopausal women with estrogen receptor-positive breast cancer. These findings suggest the importance of considering reproductive factors when investigating biological mechanisms underlying breast cancer progression and prognosis.

Vaginal estrogen is widely used to manage the genitourinary syndrome of menopause. However, its use by breast cancer survivors remains controversial, since some labeling indicates that it may increase the risk of recurrence, based on the known risks of systemic hormone therapy. This review synthesizes current evidence on breast cancer incidence and the use of vaginal estrogen in postmenopausal women, and its systemic absorption, as well as recurrence, mortality, and comparative data among vaginal estrogen formulations in breast cancer survivors, including those receiving aromatase inhibitors. Our findings show that vaginal estrogen results in minimal systemic absorption, and no demonstrated increase in the incidence of breast cancer, its recurrence, or mortality from breast cancer. In breast cancer survivors treated with aromatase inhibitors, vaginal estrogen has not been associated with increased mortality, although evidence on its effect on recurrence remains controversial and the issue warrants further investigation. The absence of head-to-head comparisons of different formulations of vaginal estrogen in breast cancer survivors emphasizes the need for comparative studies to guide individualized treatment strategies. Recent updates from the US Food and Drug Administration, which removed boxed warnings related to breast cancer and acknowledged that vaginal estrogens have a safety profile that is distinct from that of systemic hormone therapy, reinforce our findings and represent an important step toward evidence-based regulation. Building on these regulatory advances, the increasing diagnosis of breast cancer in younger women and the prolonged burden of genitourinary syndrome of menopause underscore the need to translate this evidence into clinical practice by strengthening clinical confidence and supporting individualized, patient-centered decision-making for breast cancer survivors.

Objectives: Mortality from age-related diseases has risen in the last decade. MicroRNAs are key regulators of gene expression linked to these diseases, and their expression can be modulated by diet. This study examined how age and diet influence the expression of microRNAs associated with cardiovascular disease in patients with coronary heart disease.

Methods: From the CORDIOPREV cohort (n = 1002), 120 participants under 56 years and 120 over 66 years were selected through propensity score matching. To assess dietary effects, 60 individuals per age group followed either a low-fat or a Mediterranean diet. Expression of 28 microRNAs in peripheral blood mononuclear cells was analyzed by RT-PCR at baseline and after 5 years.

Results: Younger participants (those aged under 56 years at baseline) showed increased expression of miR-1, miR-150, and miR-145 over time, while no significant changes were observed in older subjects (those over 66 years). Among younger individuals on the Mediterranean diet, miR-1 and miR-145 levels significantly increased after 5 years. Pathway analysis indicated that these microRNAs target genes (CCL2, ED1, SMAD3, PLCE1) related to inflammation, cell adhesion, and coagulation.

Conclusion: The Mediterranean diet may positively modulate the expression of microRNAs associated with cardiovascular disease, with this effect being particularly influenced by age in patients with coronary heart disease.

Objectives: To investigate the controversial association between exogenous hormone use (EHU) and dementia, with a focus on subtype-specific risks.

Study design: This prospective cohort study followed 273,069 women in the UK Biobank over 3,802,608 person-years, identifying 4,710 dementia cases.

Main outcome measures: Cox models assessed use of oral contraceptive (OC) and hormone replacement therapy (HRT) in relation to all-cause dementia, Alzheimer's disease (AD), vascular dementia (VaD), and frontotemporal dementia (FTD) across treatment durations. Subgroup analyses were stratified by age, ethnicity, APOE status, education, income, and reproductive factors. A systematic review was conducted to synthesize existing evidence.

Results: In the cohort study, OC use was associated with reduced risks of all-cause dementia (HR 0.90, 95%CI 0.84-0.95), AD (HR 0.87, 95%CI 0.79-0.95), and VaD (HR 0.81, 95%CI 0.70-0.93), particularly after 4-14 years of use. HRT showed no significant association with increased dementia risk. Synthesized results largely corroborated these findings: OC use was associated with reduced risks of dementia (HR 0.90, 95%CI 0.89-0.92); and although four European studies reported a moderately increased AD risk after post-menopausal HRT use, neither cohort-based studies (HR 0.98, 95%CI 0.90-1.06) nor traditional case-control studies (OR 1.00, 95%CI 0.90-1.11) found an association between HRT and dementia.

Conclusions: Our combined evidence does not support an increased risk of dementia associated with OC use; similarly, no clear association was observed between HRT and increased dementia risk. Clinical decisions on EHU should be individualized, balancing overall benefits against potential risks.

Background and aim: Pregnancy-related exposures have been proposed as potential risk factors for breast cancer later in life, but findings remain inconclusive. This study aimed to update evidence on the associations between the exposure to pregnancy-related factors occurring up to birth-maternal and paternal age, gestational age at birth, twin status, and maternal preeclampsia-and breast cancer risk in daughters.

Material and methods: A systematic review and meta-analysis were conducted. Searches were performed in MEDLINE (via PubMed), Web of Science, and Scopus. We included observational analytical studies assessing associations between parental age, gestational age, twin status, and maternal preeclampsia and breast cancer risk in daughters, reporting effect measures with 95% confidence intervals (CI) or sufficient data for calculation. Study quality was assessed using the Newcastle-Ottawa Scale. A dose-response meta-analysis evaluated the effects of maternal and paternal age, while random-effects models assessed the effects of gestational age, twin status, and maternal preeclampsia. Heterogeneity was assessed using the I² statistic and publication bias through funnel plots and Egger's tests.

Results: Fifty-two studies met the inclusion criteria; 57.7% were high quality. Breast cancer risk increased with maternal age up to 30 years (I² = 10.7%, P = .26). A possible association for paternal age (I² = 33.8%, P = .08) disappeared in subgroup analysis (I² = 1.0%). No associations were found for gestational age (pooled OR [pOR] 0.96, 95% CI 0.84 to 1.10), twin status (pOR 1.19, 95% CI 0.97 to 1.46), or maternal preeclampsia (pOR 1.08, 95% CI 0.71 to 1.64).

Conclusions: Increased maternal age may influence breast cancer risk in daughters. No associations were found for paternal age, gestational age, or twin status; conclusions for maternal preeclampsia remain uncertain due to heterogeneity.