Despite all efforts, obesity remains a major health concern worldwide, with continuously increasing rates, affecting approx. 14% of the total world population, being as high as 43% in some countries. As obesity is related to numerous comorbidities, including type 2 diabetes, cardiovascular diseases, and some types of cancer, the consequences for the individual and society at large are drastic. Therefore, it is crucial to understand and predict who is at risk of developing obesity in order to implement early prevention strategies. Many individual risk factors have been emphasized. However, as obesity is a rather multifactorial complication, single markers/biomarkers have thus far not allowed for an efficient prediction of obesity. In addition to less modifiable parameters, such as environment and socio-demographics, studies have revealed that obesity is related to several interacting aspects, including host factors such as genetics/epigenetics or gut microbiota, and more readily modifiable factors, including nutrition and physical activity, as well as sleep patterns and psychological well-being. It is likely that combining markers from across different domains, that is, multimodal markers, allows for better predictability for the risk of developing obesity. However, it must be considered that not all markers are fully predictive; many are rather reactive or even both. In this review and position paper, we emphasize the state-of-the-art regarding (bio)markers that have successfully been employed for predicting obesity risk. An emphasis will rest on novel, emerging biomarkers, and the need for a more integrative, multimodal assessment of obesity risk for a combined assessment aimed at improving risk prediction.

Tuberculosis and cardiovascular disease (CVD) are significant health concerns in developing countries. Evidence indicates a link between tuberculosis infection and CVD development. The immune response to Mycobacterium tuberculosis, involving monocytes, macrophages, lymphocytes, and cytokines, promotes atheroma formation and atherosclerosis, leading to cardiovascular complications. This study aimed to assess mortality patterns among tuberculosis patients due to CVD, describe the proportion and types of CVD-related deaths in a Malaysian tertiary care facility, and examine associated demographic and clinical characteristics.

This retrospective cohort study used an observational analytic design and descriptive mortality analysis at Penang General Hospital, Malaysia. Medical records of adult tuberculosis (TB) patients who died between January 2015 and December 2022 were reviewed. Patients with pre-existing cardiovascular disease were excluded. Causes of death were determined from clinical records and death certificates, with cardiovascular deaths classified based on clinical, laboratory, and imaging findings. Descriptive statistics were used, and exploratory unadjusted associations were assessed using chi-square or Fisher's exact tests as appropriate.

Of 657 TB patient deaths analyzed, 82 (12.5%) were attributed to cardiovascular causes. Acute coronary syndrome was the most frequent (8.37%), followed by acute pulmonary embolism (1.37%). Exploratory analyses suggested associations between cardiovascular deaths and clinical factors such as anemia and drug resistance.

These findings align with global evidence that cardiovascular diseases are a leading cause of death among tuberculosis patients. Prior studies support the elevated risk of CVDrelated mortality in this population. This research provides detailed data on specific cardiovascular disorders, particularly acute coronary syndrome as the primary cause of death. Intravenous drug use showed a strong correlation with CVD mortality (p < 0.001), while anemia was a notable comorbidity despite its low prevalence. The lack of significant associations with diabetes and hypertension suggests that inflammatory or infectious processes may play a greater role in CVD development among TB patients. Regional differences in CVD mortality rates highlight the influence of sociodemographic factors and healthcare resources. The study's exclusion of patients with pre-existing CVD allows for a focused assessment of TB's impact on cardiovascular outcomes.

In this tertiary-care cohort, cardiovascular disease represented a significant proportion of deaths among tuberculosis patients, with acute coronary syndrome as the leading subtype. These results reinforce the need for cardiovascular risk awareness in TB care and highlight the importance of prospective studies to clarify risk factors and causality.

Cardiovascular diseases are more prevalent and have created an alarming situation worldwide. Nutraceuticals are a class of nutrients that include common foods and fruits for managing various diseases. This paper adopts a narrative review approach, focusing on recent advances in nutraceutical-based interventions and nanotechnology applications for cardiovascular diseases.

Extensive literature research on bioactive nutraceuticals was conducted using databases, such as WOS, PubChem, and Scopus, suggesting their potential for target validation and disease identification. Different keywords were used for searching database: Cardiovascular diseases, Nutraceuticals, Antioxidants, Nanoformulations, Targeted drug delivery.

Nutraceuticals play a significant role in reducing cardiovascular risk through antioxidant and free-radical scavenging mechanisms. Regular adherence to medicinal foods, such as nutraceuticals, improves health and significantly reduces the risk of chronic diseases. Several free radicals are generated during physiological and pathological reactions in the body, which are responsible for the degradation of organs.

Nutraceuticals scavenge reactive oxygen species via antioxidant mechanisms. Various novel nanotechnology approaches have been employed to enhance the therapeutic potential of nutraceuticals. Furthermore, nanotechnology has opened new doors for improving the bioavailability, stability, and targeted delivery of nutraceutical compounds. Nanoformulations, such as liposomes, niosomes, and nanoparticles, are employed to address issues of bioavailability, penetration, solubility, and therapeutic efficacy. It offers researchers cost-effective treatment approaches to improve cardiovascular outcomes.

Novel approaches in the field of nutraceuticals possess significant activity in the management of cardiovascular diseases by enhancing stability, bioavailability, solubility, and therapeutic efficacy. Future research should focus on well-designed clinical studies and standardized nanoformulation protocols to facilitate clinical translation.

Worldwide, cardiovascular diseases remain the leading contributors to illness and death, which hinders rapid diagnosis and efficient treatment. Recent developments in artificial intelligence (AI) have transformed cardiovascular medicine by enabling the integration and analysis of large and complex data sets from portable sensors, electronic health records, and medical images. AI algorithms, such as machine learning and deep learning models, excel in detecting detailed patterns and forecasting disease progression, improving risk assessment and diagnostic accuracy. These technologies enable the early diagnosis of disorders such as heart failure, arrhythmias, and coronary artery disease, resulting in more personalized treatment approaches and better patient outcomes. Automated image processing reduces human error and simplifies procedures, while continuous cardiac function can be monitored remotely. As AI systems advance further, they have the potential to revolutionize clinical decision-making by providing real-time information and predictive analyses that anticipate adverse cardiac events. Despite ongoing challenges with data quality, model transparency, and ethical considerations, the use of AI in cardiovascular care is expected to optimize resource allocation, reduce healthcare costs, and ultimately improve survival rates. Adopting this cutting-edge technology represents a crucial step toward a more precise, proactive, and patient-centered strategy with significant potential.

Ferroptosis is an iron-dependent regulated form of cell death characterized by lethal lipid peroxidation and is increasingly implicated in cancer, neurodegenerative diseases, cardiovascular injury, and metabolic disorders. Metformin, a widely prescribed antidiabetic biguanide, exerts pleiotropic effects beyond glucose lowering and has emerged as a context-dependent regulator of ferroptosis. In malignant cells, metformin may enhance ferroptotic susceptibility through activation of AMP-activated protein kinase (AMPK), suppression of mechanistic target of rapamycin (mTOR) signaling and SLC7A11, induction of ferritinophagy, mitochondrial complex I stress, and promotion of lipid peroxidation. Conversely, in normal or stressed non-malignant tissues, metformin may limit ferroptotic injury by activating nuclear factor erythroid 2-related factor 2 (NRF2), supporting glutathione peroxidase 4 (GPX4) and SLC7A11-dependent antioxidant defenses, improving mitochondrial quality control, and stabilizing iron homeostasis. This review synthesizes the molecular basis of this duality, evaluates therapeutic opportunities in oncology and cytoprotection, and outlines biomarker-driven and clinical trial strategies required for translation. Overall, metformin should not be regarded as a universal ferroptosis inducer or inhibitor, but rather as a context-dependent metabolic regulator whose effects are shaped by cell type, dose, exposure duration, transporter expression, iron status, and antioxidant capacity.

Chronic inflammation is a key contributor to the pathogenesis of numerous diseases, including cardiovascular, metabolic, and neurodegenerative disorders. Nutraceutical strategies targeting inflammatory pathways are of increasing interest, particularly those based on omega-3 fatty acids. The objective of this study was to evaluate the anti-inflammatory effects of two omega-3-based nutraceutical formulations, Omega 3 Plus and Omega 3 Orange, in primary human monocytes. Primary human monocytes were isolated from peripheral blood of a healthy donor and cultured under standardized conditions. Cells were pre-treated with different concentrations of the test formulations and subsequently stimulated with lipopolysaccharide (LPS, 10 ng/mL) for 24 h. Cell viability was assessed using the AlamarBlue assay. The release of pro-inflammatory mediators, including TNF-α, IL-1β, IL-6, MCP-1, IL-8, and prostaglandin E2 (PGE2), as well as the anti-inflammatory cytokine IL-10, was quantified using ELISA. Both formulations were well tolerated at concentrations up to 2.5%, with no significant cytotoxic effects. LPS stimulation induced a robust increase in inflammatory mediator release. Pre-treatment with Omega 3 Plus and Omega 3 Orange resulted in a significant, dose-dependent inhibition of pro-inflammatory cytokines, including TNF-α, IL-1β, and IL-6 (up to ~70% reduction). MCP-1 was moderately reduced, whereas IL-8 was only minimally affected. Notably, Omega 3 Orange exhibited a pronounced inhibition of PGE2 production (up to ~95%), while Omega 3 Plus reduced PGE2 levels by approximately 80%. Neither formulation induced IL-10 production in unstimulated cells. These findings demonstrate that both omega-3-based nutraceutical formulations exert potent anti-inflammatory effects in primary human monocytes, primarily through the inhibition of pro-inflammatory cytokines and PGE2. The strong suppression of PGE2 is consistent with a possible modulation of pathways involved in prostaglandin synthesis. These results support the potential application of such formulations in inflammation-associated conditions and warrant further mechanistic and clinical investigation.

Background/Objectives: Arterial hypertension (AH) and hepatitis C virus (HCV) infection are interlinked, with AH increasing the risk of severe liver disease and HCV contributing to cardiovascular issues. Treating HCV in hypertensive patients is critical, though data on direct-acting antivirals (DAAs) in this group remain limited. Methods: This retrospective study evaluated the effects of DAAs in AH patients with HCV using data from the 2015-2023 EpiTer-2 project, a multicenter study in Poland. Results: Among the 18,968 HCV-infected DAA-treated patients, 5976 had AH. These patients were older, predominantly women, and had higher rates of obesity, comorbidities, cirrhosis, hepatocellular carcinoma, and genotype 1b infection. Sustained virologic response rates were high and comparable between the AH and non-AH groups in the intent-to-treat (94.8% vs. 94.2%) and per-protocol analyses (97.6% vs. 97.6%). AH was not independently associated with treatment failure (OR 0.87, 95% CI: 0.69-1.10). Predictors of failure included genotype 3, decompensated liver function, cirrhosis, thrombocytopenia, and treatment with asunaprevir + daclatasvir. While therapy discontinuation was more common in the AH patients, most completed treatment, with fatigue being the most frequent adverse event. Although not directly evaluated, the overall safety outcomes suggest that potential drug-drug interactions with antihypertensive therapies are unlikely to have a major clinical impact in routine practice. Conclusions: This study highlights the safety and efficacy of DAAs in AH patients and emphasizes the importance of early HCV detection and treatment in this population.

Background: Gender differences in aging among people with HIV (PWH) remain poorly characterized. Women with HIV (WWH) may experience more complex aging trajectories, due to the interplay of biological, clinical, and psychosocial factors. In this context, we aimed to investigate gender-specific determinants of frailty among older people with HIV, with a particular focus on women, to better inform tailored clinical care. Methods: Cross-sectional analysis of the Over50 Cohort, including PWH aged ≥50 years from two tertiary hospitals in Spain. Participants underwent a comprehensive geriatric assessment across demographic, clinical, functional, cognitive, psychological, and social domains. Gender-stratified multivariable analyses examined frailty (by Fried criteria) and associated factors. Results: Among 588 participants, 139 (23.6%) were cisgender WWH. Despite younger age and better immune status, WWH showed higher prevalence of frailty (17% vs. 9%), musculoskeletal disease (47% vs. 28%), depressive symptoms (45% vs. 30%), sleep disturbances (10% vs. 5%), and cognitive complaints (23% vs. 11%). Men with HIV (MWH) more frequently had cardiovascular (48% vs. 35%) and renal disease (22% vs. 15%). In multivariable models, frailty in WWH was independently associated with musculoskeletal disease (OR 3.85), cognitive impairment (OR 3.21), depressive symptoms (OR 2.67), and malnutrition (OR 2.14). In MWH, frailty was associated with musculoskeletal disease, cognitive impairment, malnutrition, and older age. Conclusions: Frailty exhibits gender-specific patterns: a multidimensional phenotype in WWH versus age-driven in MWH, supporting tailored, gender-responsive care integrating geriatric, mental, and musculoskeletal health.

Background: Bartonella henselae infection has been associated with a broad spectrum of neurological and autonomic manifestations, although its impact on autonomic nervous system function remains insufficiently characterized, and the aim of this study was to evaluate autonomic function in patients with polymorphic symptoms and Bartonella henselae IgM seroreactivity. Methods: In this cross-sectional study, 75 patients were compared with 75 age- and sex-matched healthy controls, and all participants underwent cardiovascular autonomic reflex testing, short-term (5 min) and long-term (24 h) heart rate variability analysis, and 24 h ambulatory blood pressure monitoring, while head-up tilt testing was performed in the Bartonella group. Results: Abnormal autonomic reflex tests were significantly more frequent in the Bartonella IgM-seroreactive group, particularly those reflecting parasympathetic function, while heart rate variability analysis demonstrated reduced high-frequency components and lower long-term variability indices, and head-up tilt testing revealed heterogeneous hemodynamic responses including orthostatic hypotension and pronounced blood pressure variability, with ambulatory monitoring additionally showing higher nighttime blood pressure values and reduced nocturnal dipping. Conclusions: These findings indicate a consistent pattern of autonomic imbalance characterized predominantly by parasympathetic impairment and altered blood pressure regulation in patients with Bartonella henselae IgM seroreactivity, although further studies are required to clarify underlying mechanisms and clinical implications.

No previous sub-Saharan studies have compared patients with community-acquired pneumonia (CAP) and COVID-19 pneumonia, the focus of this study. Consecutive adult patients hospitalized with CAP (n = 59) or COVID-19 pneumonia (n = 74) were compared regarding multiple characteristics, including cardiac biomarkers. In multivariable logistic regression analysis, differences were noted among various clinical features. Troponin I concentrations (p = 0.00028) and the Troponin I/NT-pro BNP ratio (p = 0.00048) were significantly higher in COVID-19 compared with CAP. After adjustment for age, these differences remained significant (troponin I p = 0.0019; ratio p = 0.00054), while BNP concentrations were now higher in CAP (p = 0.009). PCA demonstrated that BNP and NT-pro BNP contributed most strongly to the dominant cardiac biomarker signature, suggesting shared cardiopulmonary stress across both diseases. Exploratory subgroup analyses suggested higher troponin I levels among people living with HIV and COVID-19, although interaction modelling did not demonstrate significant effect modification by HIV status. Both CAP and COVID-19 pneumonia were associated with evidence of cardiac stress; however, COVID-19 demonstrated a relatively stronger myocardial injury signature characterized by higher troponin I concentrations and an increased Troponin I/NT-pro BNP ratio while CAP had evidence of greater hemodynamic cardiac strain, as evidenced by the higher levels of BNP. The findings suggest that the mechanisms of cardiac involvement may differ between viral and bacterial respiratory infections.