Cardiovascular diseases (CVDs) remain the leading cause of mortality worldwide and constitute a substantial economic burden. Despite population aging, recent years have witnessed an increasing prevalence of conditions such as heart failure (HF), including among young adults. In this context, coronary artery disease (CAD) has also become an increasingly discussed issue. It has long been recognized that control of risk factors is crucial for prevention. Researchers stress the need to monitor these factors from the earliest stages of life, and detailed analyses indicate an influence of the prenatal period on the development of chronic diseases, including cardiovascular disorders. Transgenerational and intergenerational epigenetic mechanisms are also taken into account. This review aims to systematically evaluate the existing literature and summarize the mechanisms that may link these factors. We consider epigenetic, metabolic, immunological, and inflammatory influences. We describe examples of environmental exposures, such as air pollution, maternal diet, toxins, and infections, and analyze data derived from clinical studies. We discuss gaps in the literature and identify limitations, outlining directions for future research and emphasizing the need for CVD prevention initiated at the earliest stages of life.

Endometriosis is a prevalent condition, affecting 10-15% of women of reproductive age and approximately 70% of those with chronic pelvic pain. An estimated 176 million women worldwide are affected by this disease. The condition occurs predominantly between menarche and menopause, with peak incidence between the ages of 25 and 45. Endometriosis is characterized by the presence of endometrial-like tissue outside the uterine cavity, leading to the formation of lesions most commonly in the ovaries but also in the fallopian tubes, gastrointestinal tract, and occasionally in distant locations like the pleura and central nervous system. Symptoms include chronic pelvic pain, heavy and painful menstrual periods, dyspareunia, painful urination, and defecation. Diagnosis involves a combination of medical history, physical examination, imaging techniques, and the gold standard, diagnostic laparoscopy. There is an average delay of 6.7 years between symptom onset and diagnosis, often due to variable and confusing symptoms resembling other conditions. The pathogenesis of endometriosis involves genetic, hormonal, and environmental factors, with significant roles played by estrogens and progesterone. Treatment strategies focus on managing symptoms through pain relief, hormonal therapy, and surgical interventions, although no permanent cure exists. Hormonal imbalances, particularly the interaction of progesterone and estrogens, play a crucial role in disease progression. Current research explores various treatment options, including hormonal therapy, nonsteroidal anti-inflammatory drugs, antioxidants, and surgical methods to improve the quality of life for patients.

Objective: The study aims to evaluate the diagnostic and prognostic efficacy of gut-derived trimethylamine N-oxide (TMAO) as a molecular biomarker for heart failure (HF) in comparison to the N-terminal pro-B-type natriuretic peptide. Background: The clinical value of N-terminal pro-B-type natriuretic peptide (NT-proBNP) is frequently affected by non-cardiac physiological variables, including adiposity, advanced age, and renal clearance rates. Consequently, there is a compelling need for additional biomarkers. This analysis investigates TMAO as a critical mediator within the gut–heart axis, reflecting systemic inflammation and myocardial fibrosis secondary to intestinal dysbiosis. Methods: A comprehensive literature search was conducted using PubMed. Keywords such as “trimethylamine N-oxide”, “heart failure”, “heart failure with preserved ejection fraction” and “N-terminal pro-B-type natriuretic peptide” were used. The inclusion criteria comprised original research and literature reviews describing the pathophysiological mechanisms and clinical utility of TMAO in the context of HF diagnosis and prognosis. Results: The analyzed literature suggests that TMAO functions as an independent predictor of major adverse cardiovascular events, correlating with all-cause mortality and rehospitalization risk across all HF phenotypes. Furthermore, data indicate that using TMAO alongside NT-proBNP measurements may predict patient risk more accurately, particularly in patients where natriuretic peptide interpretation is traditionally obscured by comorbidities such as diabetes mellitus and chronic kidney disease. Conclusions: Although NT-proBNP remains the gold standard for acute diagnosis, TMAO provides significant value for long-term clinical management. By serving as a metabolic–inflammatory indicator, TMAO complements standard diagnostic panels, offering deeper insights into the prognostic trajectory and the underlying intestinal barrier integrity of patients with HF.

Growing evidence indicates that the gut–brain axis plays a central role in cognitive regulation, with microbial metabolites acting as important mediators of neuronal function. This review examines how postbiotics—bioactive compounds produced by microorganisms, including short-chain fatty acids, indole derivatives, bacterial peptides, and extracellular vesicles—may influence memory-related processes and cognitive resilience. Particular attention is given to the molecular and intracellular mechanisms through which postbiotics interact with host targets, including G-protein–coupled receptors, the aryl hydrocarbon receptor, and epigenetic regulators. Activation of these pathways modulates signaling cascades such as mitogen-activated protein kinase/extracellular signal-regulated kinase (MAPK/ERK), phosphoinositide 3-kinase/protein kinase B (PI3K–Akt), and cyclic AMP response element-binding protein (CREB), which are associated with synaptic plasticity, neuronal survival, neurogenesis, and brain-derived neurotrophic factor activity. The review also highlights the role of postbiotics in regulating neuroinflammation, microglial activation, and blood–brain barrier integrity. Despite promising findings, the precise intracellular mechanisms remain incompletely understood and require further investigation to support future therapeutic strategies for cognitive disorders.