Background: Over the past decade, the gut microbiome (GM) has progressively demonstrated to have a central role in human metabolism, immunity, and cardiometabolic risk. Likewise, sleep disorders showed an impact on individual health and cardiometabolic risk. Recent studies seem to suggest multi-directional relations among GM, diet, sleep, and cardiometabolic risk, though specific interactions are not fully elucidated. We conducted a systematic review to synthesize the currently available evidence on the potential interactions between sleep and GM and their possible implications on cardiometabolic risk. Methods: A systematic review was conducted following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) statement for reporting systematic reviews and meta-analyses, including articles from January 2016 until November 2022. Narrative syntheses were employed to describe the results. Results: A total of 8 studies were selected according to these criteria. Our findings indicated that the sleep disorder and/or the acute circadian rhythm disturbance caused by sleep–wake shifts affected the human GM, mainly throughout microbial functionality. Conclusions: Sleep disorders should be viewed as cardiovascular risk factors and targeted for preventive intervention. More research and well-designed studies are needed to completely assess the role of sleep deprivation in the multi-directional relationship between GM and cardiometabolic risk.

Chronic endometritis (CE) is a persistent inflammatory condition of the endometrium characterized by abnormal infiltration of plasma cells into the endometrial stroma. Frequently associated with repeated implantation failure, recurrent pregnancy loss, and infertility, CE significantly impacts women’s health, contributing to conditions such as abnormal uterine bleeding and endometriosis. Treatment typically involves antibiotic therapy; however, the efficacy of these treatments is increasingly compromised by the rise of antimicrobial resistance (AMR). This paper examines the critical links between AMR and CE, proposing strategies to enhance clinical management and optimize treatment outcomes.

Pregnancy represents a critical eco-biological window during which maternal physiology integrates environmental exposures, lifestyle factors, and interconnected microbial ecosystems to shape fetal development and long-term health. From a One Health perspective, defined here as the interconnection between maternal health, environmental determinants, and microbial ecosystems across generations, the maternal microbiome functions as a dynamic interface linking the external environment to the intrauterine milieu, translating ecological signals into immunological, metabolic, and neuroendocrine pathways that influence placental function and developmental programming. Across gut, vaginal, oral, and mammary niches, maternal microbial communities operate as an integrated network regulating systemic inflammation, metabolic homeostasis, and the production of bioactive metabolites, including short-chain fatty acids, bile acids, and tryptophan derivatives. This review proposes an integrated systems framework in which pregnancy is viewed as a transient ecological system shaped by ten interconnected maternal determinants, encompassing microbial niches, nutrition, lifestyle factors, medical interventions, mode of delivery, and postnatal microbial transmission, that converge on shared microbiome-mediated signaling pathways affecting fetal and neonatal immune, metabolic, and neurodevelopmental trajectories. Broader macro-environmental drivers, including biodiversity loss, urbanization, pollution, and industrialized lifestyles, are considered as upstream modulators of maternal microbial ecology within a One Health context. A systems model is presented to illustrate how environmental inputs are biologically transduced through maternal microbial networks to influence placental function, fetal development, and early-life health trajectories. Framing pregnancy as an integrated eco-biological continuum highlights the maternal microbiome as a central hub of intergenerational health and may support microbiome-informed preventive strategies and public health approaches aimed at reducing the burden of non-communicable diseases (NCDs) of early-life origin.

Background: Serum uric acid (UA) is increasingly recognized as a cardiovascular (CV) risk factor, with evidence suggesting that CV risk may occur at levels below conventional hyperuricemia thresholds. However, real-world comparative data on the effects of dietary interventions on UA are limited. Objective: The primary objective of this study was to compare the effects of a very low-calorie ketogenic diet (VLCKD), intermittent fasting (IF), and standard dietary advice (free diet, FD) on UA levels and UA-defined CV risk in hypertensive postmenopausal women. Methods: In this prospective, single-center, real-world clinical study, 43 women with essential hypertension and obesity underwent dietary interventions. UA levels were assessed at baseline and after 6 months. Hyperuricemia was defined using both the conventional threshold (≥6.0 mg/dL) and the CV risk-oriented Uric Acid Right for Heart Health (URRAH) cut-off (≥4.7 mg/dL). Analyses included paired tests and ANCOVA adjusted for baseline UA. Results: At baseline, over half of participants exceeded the URRAH threshold. Only VLCKD significantly reduced UA levels (−1.23 mg/dL; p < 0.001), remaining independently associated after adjustment (β = −0.95 mg/dL; p = 0.007). URRAH-defined CV risk decreased significantly only in the VLCKD group (55.6% to 22.2%), with one-third transitioning to lower risk. Conclusions: VLCKD significantly reduced UA levels and UA-defined CV risk, supporting its role as a potentially effective lifestyle intervention in this population.