Obesity is a multifactorial chronic disease resulting from complex genetic, molecular, environmental, and behavioral interactions. Its prevalence rises worldwide, affecting cardiovascular, metabolic, oncological, hepatic, respiratory, and skeletal health. Beyond caloric excess, genetic predisposition, epigenetic modifications, gut microbiota dysbiosis, endocrine-disrupting agents, circadian misalignment, and intergenerational and prenatal influences are critical determinants of obesity risk. Core pathophysiological mechanisms include insulin resistance, dyslipidemia, chronic low-grade inflammation, and neuroendocrine dysregulation of appetite and energy balance. These processes are linked to comorbidities such as type 2 diabetes, hypertension, atherosclerosis, fatty liver disease, sleep apnea, osteoporosis, and cancer. Advances in molecular profiling, metabolic phenotyping, and body composition analysis are refining obesity classification and enabling precise risk stratification. Current therapeutic strategies include behavioral interventions addressing stress-related mechanisms, pharmacological therapies such as GLP-1 receptor agonists, emerging gene therapy approaches, and bariatric surgery. Gut-derived hormones (leptin, ghrelin, GLP-1, PYY, CCK) are recognized as pivotal regulators of appetite and weight. Preventive strategies increasingly emphasize circadian alignment, while epigenetic inheritance and prenatal exposures such as maternal obesity or smoking highlight early-life programming in future metabolic health. Additionally, artificial intelligence-based platforms and personalized nutrition provide innovative opportunities for individualized prevention and management. This review synthesizes contemporary evidence on the biological basis, systemic consequences, preventive strategies, and evolving therapeutic modalities of obesity, affirming its recognition as a complex chronic disease requiring personalized, multidisciplinary care.

Cardiovascular diseases (CVDs) remain the leading cause of death worldwide, with growing evidence indicating that epigenetic mechanisms play a central role in their onset and progression. This review provides a comprehensive overview of current knowledge on the epigenetic regulation and molecular mechanisms involved in CVDs, as well as their potential therapeutic implications. The findings demonstrate that DNA methylation, histone modifications, and non-coding RNAs are key regulators of gene expression associated with cardiac hypertrophy, atherosclerosis, myocardial infarction, and heart failure. Interactions between epigenetic alterations and inflammatory or oxidative stress pathways further contribute to endothelial dysfunction and vascular remodeling. Emerging therapeutic strategies targeting these mechanisms, including histone deacetylase inhibitors, DNA methyltransferase inhibitors, and RNA-based therapeutics, show promising cardioprotective effects in experimental and early clinical studies. Overall, this review underscores the significance of epigenetic regulation in cardiovascular pathophysiology and highlights the potential of epigenetic-based interventions as a foundation for precision medicine and novel therapeutic approaches in cardiology.

Background: After a failed endoscopic retrograde cholangiopancreatography (ERCP) for malignant biliary obstruction (MBO), second-line drainage is performed with endoscopic ultrasound-guided biliary drainage (EUS-BD) or percutaneous transhepatic biliary drainage (PTBD). We compared their effectiveness, safety, and short-term survival. Methods: We conducted a single-center retrospective cohort of 101 adults with MBO after they had experienced a failed ERCP (EUS-BD n = 37; PTBD n = 64). Allocation was non-randomized and driven by operational availability. Baseline laboratory tests (complete blood count, platelets, and C-reactive protein) and derived indices (neutrophil-to-lymphocyte ratio [NLR], platelet-to-lymphocyte ratio [PLR], lymphocyte-to-monocyte ratio [LMR], systemic immune-inflammation index [SII], systemic inflammation response index [SIRI], neutrophil-to-platelet score [NPS], and lymphocyte-to-CRP ratio [LCR]) were compared. Outcomes that were a technical success include: an early biochemical response (bilirubin reduction), complications (Clavien–Dindo), length of stay (LOS), and overall survival (OS). Between-group comparisons used the two-sided Mann–Whitney U test (continuous) and Fisher’s exact (binary) test. Survival was assessed by the Kaplan–Meier estimator using log-rank testing. To address later adoption of EUS-BD, we also estimated a restricted mean survival time of 180 days (RMST_0–180) with 95% confidence intervals (CIs). Results: Baseline inflammatory markers and composite indices were similar; baseline total bilirubin was higher in PTBD. The technical success was 100% in both groups. Early biochemical response was 86.5% after EUS-BD vs. 78.1% after PTBD (p = 0.43). Any complication occurred in 29.7% vs. 12.5% (p = 0.04); major complications (Clavien–Dindo ≥ III) occurred in 10.8% vs. 0% (p = 0.02), respectively; and the LOS did not differ (p = 0.21). OS favored EUS-BD (median 143 vs. 54 days and log-rank p = 0.012). RMST_0–180 was 111.1 days for EUS-BD vs. 71.4 days for PTBD (difference + 39.6 days; 95% CI 11.3–65.9). Conclusions: After a failed ERCP for MBO, EUS-BD and PTBD achieved universal technical success and similar early biochemical responses, but EUS-BD was associated with higher complication rates and a significantly longer six-month survival. These findings support the individualized selection balancing procedural risk with the anticipated survival benefit and highlight the need for prospective comparative studies.

Background. Air pollution has become one of the most significant environmental threats to human health worldwide. Increasing evidence suggests that exposure to air pollutants may adversely affect skin homeostasis and contribute to the development or exacerbation of inflammatory skin diseases. Aim. The aim of this narrative review was to summarize current evidence regarding the relationship between air pollution and selected inflammatory skin diseases, particularly acne vulgaris, atopic dermatitis, and psoriasis. Material and methods. A narrative review of scientific literature published within the last ten years was conducted to evaluate the association between air pollution and inflammatory skin diseases. Results. Available evidence indicates that exposure to pollutants such as particulate matter, nitrogen dioxide, ozone, and polycyclic aromatic hydrocarbons may damage the skin through mechanisms including oxidative stress, disruption of the epidermal barrier, and activation of inflammatory pathways. Epidemiological studies suggest that higher air pollution levels are associated with increased incidence or severity of acne vulgaris, atopic dermatitis, and psoriasis. Conclusions. Air pollution appears to be an important environmental factor influencing skin health and inflammatory skin diseases. Further research is needed to clarify causal relationships and support development of preventive and therapeutic strategies.

Background: In contemporary society, an increase in the demand for night-shift workers is anticipated. However, this mode of employment entails potential health hazards. Aim: To demonstrate the correlation between night-shift work and obesity, with a particular emphasis on the link between sleep deprivation and obesity occurring among night-shift employees. Furthermore, this paper describes the mechanisms contributing to the emergence of these dependencies. Methodology: A systematic review of scientific literature was conducted. A systematic search was carried out in PubMed,Google Scholar using keywords. The review examined various populations and age groups, focusing on night shift work, sleep deprevation, hormones and obesity. Results: Night-shift work is positively correlated with an increased risk of high BMI, overweight, and obesity; specifically, the risk of developing central obesity is nearly three times higher compared to day-shift workers. Simultaneously, it has been observed that the specific nature of night work adversely affects sleep quality, rendering it shorter, less restorative, and overall poorer in quality. These physiological sleep disturbances lead to the dysregulation of the HPA axis, the orexin system, and the synchronization between central and peripheral clocks. Furthermore, they disrupt the secretion patterns of various hormones—including cortisol, growth hormone, and melatonin—which collectively impair the metabolic profile and drive the progression of obesity. Conclusions: Poor sleep quality induced by night-shift work contributes to the development of obesity and disturbances in lipid profiles, HbA1c levels, and inflammatory markers among night-shift employees. The increased prevalence of obesity in this population is associated with a higher potential risk of cardiovascular diseases, type 2 diabetes, and other life-threatening conditions. Emerging research on the modulation of light intensity during both working hours and subsequent sleep offers hope that the negative consequences of nocturnal labor can be mitigated. However, it is essential to expand research in this field to develop effective preventative strategies.

Background: Obesity has become a serious problem among children in recent decades. This condition causes metabolic and cardiovascular complications, as well as affects the kidneys. The role of excessive weight has been established as a risk factor for renal disease among adults, but more and more research shows similar outcomes in obese children. The incidence of diagnosed cases of obesity-related nephropathy is constantly on the rise. Aim of the study: This research aims to highlight the importance of renal complications and their monitoring among the group of high-risk patients in the pediatric population. It also presents the latest evidence supporting the use of early biomarkers for detecting and further monitoring the progression of kidney damage among this group of patients.Material and methods: Review of scientific literature published within the last fifteen years was conducted to evaluate the influence of obesity among children on renal complications, especially chronic kidney disease. Results: Complications of obesity, such as hypertension and diabetes, as well as metabolic syndrome, are factors that contribute to the development of chronic kidney disease in children. However, if this condition is not monitored, it can lead to severe kidney damage and rapid disease progression, ultimately resulting in end-stage renal failure. Although researchers view obesity-related glomerulopathy as the result of various mechanisms, the most significant factors are considered to be lipid accumulation, insulin resistance, dysfunction of the renin-angiotensin-aldosterone system, and podocyte damage. Conclusions: Early detection of nephropathy allows slowing disease progression through lifestyle modification and pharmacotherapy, although the existing changes are not reversible. Chronic, progressive kidney disease can reduce not only the quality but also the length of life for young patients.